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Table Of Contents

Information On Toxic Metals -- Including Chelation By Cysteine

Source

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Click On The Number To View The Study Shown Under Description
Number	Description or Title	Comment
...A...	Mercury Being Dumped Into The Atmosphere	WSJ Article, March 2005 The final regulations, which were announced today by the Environmental Protection Agency and expected to take effect in May, would give utilities until 2018 to cut mercury emissions to 15 tons a year from the currently allowed 47 tons, and permit them to use an emissions-trading system to cushion the financial impact of removing mercury, which is released when coal is burned. The move makes the U.S. the first industrial nation to try to reduce power-plant mercury. Fifty one percent of the nation's electricity comes from coal.
...B...	Platinum Toxicity -- Platinum For ChemoTherapy
...C...	Effects Of Metal On Learning
...D...	Measuring For Mercury In The Urine	By Dr. Elmer Cranton
...E...	INTERPRETATION OF TOXIC METALS IN URINE TEST	By Dr. Elmer Cranton
...G...	Metal Detoxification Research and Findings	By Garry Gordon, MD
...H...	Iron and Aluminum Homeostasis in Neural Disorders	The brain is the most compartmentalized organ. It is also highly aerobic. Because nerve cells grow but do not regenerate, the brain is the organ best suited for the accumulation of metabolic errors colocalized in specific areas of the brain over an extended period.
...I...	The Great Oral EDTA Chelation Debate	Oral EDTA definitely removes significant quantities of lead from the human body
	Search Parameters: Results for your query: Search all fields for: toxic metal Published in 1977 through 1999 Only select references with abstracts available Show references published in English only Show references pertaining to humans With an article type of: REVIEW Documents: 1 to 50 of 143
...1...	Cysteine metabolism and metal toxicity.	Here is one of the important references to how cysteine removes toxic metals
...2...	Rheumatoid arthritis and metal compounds--perspectives on the role of oxygen radical detoxification.
...3...	Bacterial resistances to toxic metal ions--a review.
...4...	Effects of micronutrients on metal toxicity.
...5...	Metal-induced developmental toxicity in mammals: a review.
...6...	Experimental research into the pathogenesis of cobalt/hard metal lung disease.
...7...	Health effects of metals: a role for evolution?
...8...	Dimercaptosuccinic acid (DMSA), a non-toxic, water-soluble treatment for heavy metal toxicity.
...9...	Risk assessment in relation to neonatal metal exposure.
...10...	Role of Fenton chemistry in thiol-induced toxicity and apoptosis.
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...11...	Interactions in metal carcinogenicity.
...12...	Glial metallothionein.
...13...	Nutrition and metal toxicity.
...14...	Metal ion homeostasis and intracellular parasitism.
...15...	Toxic and essential metal interactions.
...16...	Carcinogenicity and metallic implants [see comments]
...17...	Shellfish-borne illnesses. A Hong Kong perspective.
...18...	Toxic metal pollution in Africa.
...19...	Toxicity, bioavailability and metal speciation.
...20...	Biological and health implications of toxic heavy metal and essential trace element interactions.
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...21...	Metals and the skin.
...22...	Alzheimer's disease and metal-containing glia.
...23...	Environmental transformation of toxic metals.
...24...	Biological monitoring of toxic metals.
...25...	Ferritin: an expanded role in metabolic regulation.
...26...	The concept of critical levels of toxic heavy metals in target tissues.
...27...	Modulation of metal toxicity by metallothionein.
...28...	Mechanisms of kidney cell injury from metals.
...29...	Lead nephrotoxicity and associated disorders: biochemical mechanisms.
...30...	Modifications of cell signalling in the cytotoxicity of metals.
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...31...	Biological monitoring of metals with special references to the early stages of the life cycle.
...32...	Beyond total element analysis of biological systems with atomic spectrometric techniques.
...33...	The role of vitamin D in toxic metal absorption: a review.
...34...	Interactions of essential and/or toxic metals and metalloid regarding interindividual differences in susceptibility to various toxicants and chronic diseases in man.
...35...	The Great Lakes: a historical overview.
...36...	Human exposure to toxic metals: factors influencing interpretation of biomonitoring results.
...37...	Cobalt myocardiopathy. A critical review of literature.
...38...	Response of higher plants to lead contaminated environment.
...39...	Iron: mammalian defense systems, mechanisms of disease, and chelation therapy approaches.
...40...	Biotransformation and membrane transport in nephrotoxicity.
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...41...	Possible toxicity of herbal remedies.
...42...	The protective role of ceruloplasmin against the activity of free radicals in brain ischaemia.
...43...	A review of drug-induced lysosomal disorders of the liver in man and laboratory animals.
...44...	Occupation- and exposure-related studies on human sperm.
...45...	Measurements of environmental lead contamination and human exposure.
...46...	Molecular physiology, biochemistry, and pharmacology of Alzheimer's amyloid precursor protein (APP).
...47...	Mechanisms for protection against copper toxicity.
...48...	An unusual hypopigmentation in occupational dermatology: presentation of a case and review of the literature.
...49...	Localization of metallothionein in the mammalian central nervous system.
...50...	Neurotoxic effects of selected metals.
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HealthGate Documents

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Record 1 from database: MEDLINE
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Title: Cysteine metabolism and metal toxicity.
Author: Quig D
Address: Doctor's Data, Inc., West Chicago, IL, USA. dquig@doctorsdata.com
Source: Altern Med Rev, 1998 Aug, 3:4, 262-70
Abstract: Chronic, low level exposure to toxic metals is an increasing global problem. The symptoms associated with the slow accumulation of toxic metals are multiple and rather nondescript, and overt expression of toxic effects may not appear until later in life. The sulfhydryl-reactive metals (mercury, cadmium, lead, arsenic) are particularly insidious and can affect a vast array of biochemical and nutritional processes. The primary mechanisms by which the sulfhydryl-reactive metals elicit their toxic effects are summarized. The pro-oxidative effects of the metals are compounded by the fact that the metals also inhibit antioxidative enzymes and deplete intracellular glutathione. The metals also have the potential to disrupt the metabolism and biological activities of many proteins due to their high affinity for free sulfhydryl groups.; Cysteine has a pivotal role in inducible, endogenous detoxication mechanisms in the body, and metal exposure taxes cysteine status. The protective effects of glutathione and the metallothioneins are discussed in detail. Basic research pertaining to the transport of toxic metals into the brain is summarized, and a case is made for the use of hydrolyzed whey protein to support metal detoxification and neurological function. Metal exposure also affects essential element status, which can further decrease antioxidation and detoxification processes. Early detection and treatment of metal burden is important for successful detoxification, and optimization of nutritional status is paramount to the prevention and treatment of metal toxicity.
Language of Publication: English
Unique Identifier: 98404750

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MeSH Heading (Major): Arsenic|ME/*PO; Cysteine|DE/*ME; Metals, Heavy|ME/*PO
MeSH Heading: Chronic Disease; Endocrine Glands|DE; Human; Leucine|ME; Mercury|ME; Mercury Poisoning|ME/TH; Oxidation-Reduction|DE; Poisoning|TH

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 1089-5159
Country of Publication: UNITED STATES
CAS Registry/EC Number: 0 (Metals, Heavy); 4371-52-2 (Cysteine); 7005-03-0 (Leucine); 7439-97-6 (Mercury); 7440-38-2 (Arsenic)

Record 2 from database: MEDLINE
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Title: Rheumatoid arthritis and metal compounds--perspectives on the role of oxygen radical detoxification.
Author: Aaseth J; Haugen M; F‡rre O
Address: Medical Department, Kongsvinger Hospital, Norway.
Source: Analyst, 1998 Jan, 123:1, 3-6
Abstract: Rheumatoid arthritis (RA) is characterised by migration of activated phagocytes and other leukocytes into synovial and periarticular tissue. Activated oxygen species and other mediating substances from triggered phagocytes appear to exacerbate and perpetuate the rheumatoid condition. Iron excesses are capable of aggravating the arthritic inflammation, probably through their pro-oxidant potentials. In contrast, therapeutically given gold salts, through a lysosomal loading of the metal, inhibit the triggered cells, thereby reducing the toxic oxygen production. Pharmacological doses of zinc also may immobilise macrophages. Furthermore, the copper-zinc-containing enzyme SOD (superoxide dismutase) can act as a scavenger of toxic oxygen in the tissues. Therapeutic remission of RA has been obtained following intraarticular administration of SOD. Intramuscular administration of copper complexes has induced remission in about 60% of RA patients in open studies. Another drug, penicillamine, that protects cellular membranes against toxic oxygen in vitro, is presumed to act as an antirheumatic via the SOD mimetic activity of its copper complex. Thiomalate and other thiols may possess similar activities. Selenium compounds also may act as oxygen radical scavengers. A significant alleviation of articular pain and morning stiffness was obtained following selenium and vitamin E supplementation in a double-blind study on RA patients. The observations reviewed here indicate that metal compounds and other antioxidants can reduce the rheumatic inflammation by reducing the cellular production and/or concentration of toxic oxygen species.
Language of Publication: English
Unique Identifier: 98242112

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MeSH Heading (Major): Arthritis, Rheumatoid|*DT/ME; Chelating Agents|*TU; Metals|ME/*TU; Reactive Oxygen Species|*ME
MeSH Heading: Cytosol|EN; Human; Superoxide Dismutase|ME

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0003-2654
Country of Publication: ENGLAND

Record 3 from database: MEDLINE
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Title: Bacterial resistances to toxic metal ions--a review.
Author: Silver S
Address: Department of Microbiology and Immunology, University of Illinois at Chicago 60612-7344, USA. U20053@uicvm.uic.edu
Source: Gene, 1996 Nov, 179:1, 9-19
Abstract: Bacterial plasmids encode resistance systems for toxic metal ions, including Ag+, AsO2-, AsO4(3-), Cd2+, Co2+, CrO4(2-), Cu2+, Hg2+, Ni2+, Pb2+, Sb3+, TeO3(2-), Tl+ and Zn2+. The function of most resistance systems is based on the energy-dependent efflux of toxic ions. Some of the efflux systems are ATPases and others are chemiosmotic cation/proton antiporters. The Cd(2+)-resistance ATPase of Gram-positive bacteria (CadA) is membrane cation pump homologous with other bacterial, animal and plant P-type ATPases. CadA has been labeled with 32P from [alpha-32P] ATP and drives ATP-dependent Cd2+ (and Zn2+) uptake by inside-out membrane vesicles (equivalent to efflux from whole cells). Recently, isolated genes defective in the human hereditary diseases of copper metabolism, namely Menkes syndrome and Wilson's disease, encode P-type ATPases that are more similar to bacterial CadA than to other ATPases from eukaryotes. The arsenic resistance efflux system transports arsenite [As(III)], alternatively using either a double-polypeptide (ArsA and ArsB) ATPase or a single-polypeptide (ArsB) functioning as a chemiosmotic transporter. The third gene in the arsenic resistance system, arsC, encodes an enzyme that converts intracellular arsenate [As(V)] to arsenite [As(III)], the substrate of the efflux system. The triple-polypeptide Czc (Cd2+, Zn2+ and Co2+) chemiosmotic efflux pump consists of inner membrane (CzcA), outer membrane (CzcC) and membrane-spanning (CzcB) proteins that together transport cations from the cytoplasm across the periplasmic space to the outside of the cell.
Language of Publication: English
Unique Identifier: 97140153

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MeSH Heading (Major): Gram-Negative Bacteria|GE/*ME; Gram-Positive Bacteria|GE/*ME; Ion Pumps|GE/*ME; Metals|ME/*TO
MeSH Heading: Drug Resistance, Microbial; Genes, Bacterial; Hepatolenticular Degeneration|GE; Human; Kinky Hair Syndrome|GE; Metals, Heavy|ME/TO; Plasmids

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0378-1119
Country of Publication: NETHERLANDS

Record 4 from database: MEDLINE
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Title: Effects of micronutrients on metal toxicity.
Author: Peraza MA; Ayala Fierro F; Barber DS; Casarez E; Rael LT
Address: Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson 85721-0207, USA. peraza@toxic.pharm.arizona.edu
Source: Environ Health Perspect, 1998 Feb, 106 Suppl 1:, 203-16
Abstract: There is growing evidence that micronutrient intake has a significant effect on the toxicity and carcinogenesis caused by various chemicals. This paper examines the effect of micronutrient status on the toxicity of four nonessential metals: cadmium, lead, mercury, and arsenic. Unfortunately, few studies have directly examined the effect of dietary deficiency or supplementation on metal toxicity. More commonly, the effect of dietary alteration must be deduced from the results of mechanistic studies. We have chosen to separate the effect of micronutrients on toxic metals into three classes: interaction between essential micronutrients and toxic metals during uptake, binding, and excretion; influence of micronutrients on the metabolism of toxic metals; and effect of micronutrients on secondary toxic effects of metals. Based on data from mechanistic studies, the ability of micronutrients to modulate the toxicity of metals is indisputable. Micronutrients interact with toxic metals at several points in the body: absorption and excretion of toxic metals; transport of metals in the body; binding to target proteins; metabolism and sequestration of toxic metals; and finally, in secondary mechanisms of toxicity such as oxidative stress. Therefore, people eating a diet deficient in micronutrients will be predisposed to toxicity from nonessential metals.
Language of Publication: English
Unique Identifier: 98199841

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MeSH Heading (Major): Metals|*TO
MeSH Heading: Animal; Arsenic|TO; Cadmium|TO; Calcium|ME; Copper|ME; Diet; Human; Iron|ME; Lead|TO; Mercury|TO; Zinc|ME

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0091-6765
Country of Publication: UNITED STATES

Record 5 from database: MEDLINE
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Title: Metal-induced developmental toxicity in mammals: a review.
Author: Domingo JL
Address: Laboratory of Toxicology and Biochemistry, School of Medicine, Rovira i Virgili University, Reus, Spain.
Source: J Toxicol Environ Health, 1994 Jun, 42:2, 123-41
Abstract: It is well established that certain metals are toxic to embryonic and fetal tissues and can induce teratogenicity in mammals. The main objective of this paper has been to summarize the toxic effects that excesses of certain metals may cause on mammalian development. The reviewed elements have been divided into four groups: (a) metals of greatest toxicological significance (arsenic, cadmium, lead, mercury, and uranium) that are wide-spread in the human environment, (b) essential trace metals (chromium, cobalt, manganese, selenium, and zinc), (c) other metals with evident biological interest (nickel and vanadium), and (d) metals of pharmacological interest (aluminum, gallium, and lithium). A summary of the therapeutic use of chelating agents in the prevention of metal-induced developmental toxicity has also been included. meso-2,3-Dimercaptosuccinic acid (DMSA) and sodium 2,3-dimercaptopropane-1-sulfonate (DMPS) have been reported to be effective in alleviating arsenic- and mercury-induced teratogenesis, whereas sodium 4,5-dihydroxybenzene-1,3-disulfonate (Tiron) would protect against vanadium- and uranium-induced developmental toxicity.
Language of Publication: English
Unique Identifier: 94267830

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MeSH Heading (Major): Abnormalities, Drug-Induced|*/PC; Fetal Development|*DE; Metals|AI/*TO; Teratogens|*TO
MeSH Heading: Animal; Chelating Agents|TU; Environmental Exposure; Female; Fetal Growth Retardation|CI/PC; Human; Mammals; Pregnancy

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
ISSN: 0098-4108
Country of Publication: UNITED STATES

Record 6 from database: MEDLINE
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Title: Experimental research into the pathogenesis of cobalt/hard metal lung disease.
Author: Lison D; Lauwerys R; Demedts M; Nemery B
Address: UnitÆe de Toxicologie Industrielle et MÆedecine du Travail, UCL, Brussels, Belgium.
Source: Eur Respir J, 1996 May, 9:5, 1024-8
Abstract: In recent years clinical, epidemiological and experimental evidence has accumulated indicating that cobalt metal particles, when inhaled in association with other agents such as metallic carbides (hard metals) or diamond dust, may produce an interstitial lung disease termed "hard metal disease" or "cobalt lung". This article summarizes the progress accomplished in our two laboratories to understand the pathogenesis of this disease. Gaps and weaknesses in our current knowledge have also been highlighted in order to suggest potential avenues for further research. Whilst animal models have proved useful for the demonstration of the toxic synergy between cobalt and carbides (e.g. tungsten carbide), most animal models have remained descriptive and have not provided information on the mechanism for this synergy. In particular, the bizarre multinucleated giant cells which are an important hallmark of the human disease, have not been reproduced consistently in experimental animals. Since cobalt is a known sensitizer, there may also be a need to develop experimental models to test the possible involvement of immunological mechanisms in the pathogenesis of the interstitial disease. In vitro systems including macrophage cell cultures and physico-chemical tests have been useful to investigate the mechanism underlying the toxic synergy. The recent finding that, in vitro, cobalt and metallic carbides interact with oxygen to produce toxic activated oxygen species opens a new avenue of research and may offer an alternative interpretation of the fact that only a limited proportion of exposed workers develop interstitial disease. Besides the possible involvement of immunological mechanisms, it may be speculated that individuals with a lower antioxidant defence are more susceptible to the toxic effect of activated oxygen species produced by cobalt-containing dusts from hard metal.
Language of Publication: English
Unique Identifier: 96385623

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MeSH Heading (Major): Lung Diseases|*/ET/PP; Metals|*AE; Occupational Diseases|*/CI/PP
MeSH Heading: Administration, Inhalation; Animal; Cobalt|AE; Disease Models, Animal; Human; Support, Non-U.S. Gov't

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0903-1936
Country of Publication: DENMARK

Record 7 from database: MEDLINE
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Title: Health effects of metals: a role for evolution?
Author: Clarkson T
Address: Department of Environmental Medicine, University of Rochester School of Medicine, New York 14642, USA.
Source: Environ Health Perspect, 1995 Feb, 103 Suppl 1:, 9-12
Abstract: Metals have been mined and used since ancient times. The industrial era has seen a sharp increase in both the amounts and variety of metals that find applications in industry. The inadvertent release of metals, such as from fossil fuel consumption, also adds to the global burden. A number of catastrophic outbreaks have alerted us to the occupational and environmental health risks. Life on this planet has evolved in the presence of metals. Cells learned to make use of the more abundant metals in the Archean oceans as an integral component in their structure and function. Today, we inherit these as the essential metals. At the same time, evolving life must have developed means of coping with the potentially toxic actions of metals. The appearance of oxygen in the atmosphere in the Precambrian period also resulted in cells both using and developing protective mechanisms against what must have been a highly toxic, reactive gas. Atmospheric oxygen must have increased the solubility of many metals as insoluble metal sulfides were oxidized to the more soluble sulfates. It may be no coincidence that the protective mechanisms for oxygen are also used to protect against a number of toxic metals. Selected examples are given on the role of evolution in metal toxicology, specifically, examples where the normal function of essential metals is deranged by competition with nonessential metals. Examples are also given of protective mechanisms that involve enzymes or cofactors involved in the oxygen defense system.
Language of Publication: English
Unique Identifier: 95347320

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MeSH Heading (Major): Environmental Health|*; Evolution|*; Metals|*TO
MeSH Heading: Human; Support, U.S. Gov't, P.H.S.

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0091-6765
Country of Publication: UNITED STATES

Record 8 from database: MEDLINE
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Title: Dimercaptosuccinic acid (DMSA), a non-toxic, water-soluble treatment for heavy metal toxicity.
Author: Miller AL
Address: Alternative Medicine Review. P.O. Box 25, Dover, ID 83825, USA. alan@thorne.com
Source: Altern Med Rev, 1998 Jun, 3:3, 199-207
Abstract: Heavy metals are, unfortunately, present in the air, water, and food supply. Cases of severe acute lead, mercury, arsenic, and cadmium poisoning are rare; however, when they do occur an effective, non-toxic treatment is essential. In addition, chronic, low-level exposure to lead in the soil and in residues of lead-based paint, to mercury in the atmosphere, in dental amalgams and in seafood, and to cadmium and arsenic in the environment and in cigarette smoke is much more common than acute exposure. Meso-2,3-dimercaptosuccinic acid (DMSA) is a sulfhydryl-containing, water-soluble, non-toxic, orally-administered metal chelator which has been in use as an antidote to heavy metal toxicity since the 1950s. More recent clinical use and research substantiates this compound s efficacy and safety, and establishes it as the premier metal chelation compound, based on oral dosing, urinary excretion, and its safety characteristics compared to other chelating substances.
Language of Publication: English
Unique Identifier: 98331854

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MeSH Heading (Major): Chelating Agents|PK/*TU; Metals, Heavy|*PO; Succimer|PK/*TU
MeSH Heading: Arsenic|PO; Cadmium Poisoning|DT; Human; Lead Poisoning|DT; Mercury Poisoning|DT; Poisoning|DT

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 1089-5159
Country of Publication: UNITED STATES

Record 9 from database: MEDLINE
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Title: Risk assessment in relation to neonatal metal exposure.
Author: Oskarsson A; Palminger Hallén I; Sundberg J; Petersson Grawé K
Address: Department of Food Hygiene, Faculty of Veterinary Medicine, Swedish University of Agricultural Sciences, Uppsala, Sweden.
Source: Analyst, 1998 Jan, 123:1, 19-23
Abstract: Rapid changes in organ development and function occur during the neonatal period. During this period the central nervous system is in a rapid growth rate and highly vulnerable to toxic effects of, e.g., lead and methylmercury. Furthermore, the kinetics of many metals is age-specific, with a higher gastrointestinal absorption, less effective renal excretion as well as a less effective blood-brain barrier in newborns compared to adults. Due to their low body weight and high food consumption per kg of body weight, the tissue levels of contaminants can reach higher levels in newborns than in adults. Generally, there is a low transfer of toxic metals through milk when maternal exposure levels are low. However, knowledge is limited about the lactational transport of metals and the potential effects of metals in the mammary gland on milk secretion and composition. There are some data from rodents on the lactational transfer and the uptake in the neonate of inorganic mercury, methylmercury, lead and cadmium. Metal levels in human breast milk and blood samples from different exposure situations can give information on the correlation between blood and milk levels. If such a relationship exists, milk levels can be used as an indicator of both maternal and neonatal exposure. Better understanding of the neonatal exposure, including kinetics in the lactating mother and in the newborn, and effects of toxic metals in different age groups is needed for the risk assessment. Interactions with nutritional factors and the great beneficial value of breast-feeding should also be considered.
Language of Publication: English
Unique Identifier: 98242115

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MeSH Heading (Major): Infant, Newborn|*ME; Metals|*AE/PK; Milk, Human|*CH
MeSH Heading: Adult; Cadmium|AE/PK; Female; Human; Infant Food; Lactation|ME; Lead|AE/PK; Mercury|AE/PK; Risk Assessment; Water

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0003-2654
Country of Publication: ENGLAND

Record 10 from database: MEDLINE
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Title: Role of Fenton chemistry in thiol-induced toxicity and apoptosis.
Author: Held KD; Sylvester FC; Hopcia KL; Biaglow JE
Address: Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, 02114, USA.
Source: Radiat Res, 1996 May, 145:5, 542-53
Abstract: Under certain conditions, many radioprotective thiols can be toxic, causing loss of colony-forming ability in cultured mammalian cells in a biphasic fashion whereby the thiols are not toxic at high or low concentrations of the drug, but cause decreased clonogenicity at intermediate (0.2-1.0 mM) drug levels. This symposium paper summarizes our studies using dithiothreitol (DTT) as a model thiol to demonstrate the role of Fenton chemistry in thiol toxicity. The toxicity of DTT in V79 cells has several characteristics: it is dependent on the medium used during exposure of cells to the drug; the toxicity is decreased or prevented by addition of catalase exogenously, but superoxide dismutase has no effect; the toxicity is increased by addition of copper, either free or derived from ceruloplasmin in serum; and the toxicity can be modified intracellularly by altering glucose availability or pentose cycle activity. Thus the data are consistent with a mechanism whereby DTT oxidation produces H2O2 in a reaction catalyzed by metals, predominantly copper, followed by reaction of H2O2 in a metal-catalyzed Fenton reaction to produce the ultimate toxic species, .OH. Studies comparing 12 thiols have shown that the magnitude of cell killing and pattern of dependence on thiol concentration vary among the different agents, with the toxicity depending on the interplay between the rates of two reactions: thiol oxidation and the reaction between the thiol and the H2O2 produced during the thiol oxidation. The addition of other metals, e.g. Zn2+, and metal chelators, e.g. EDTA, can also alter DTT toxicity by altering the rates of thiol oxidation or the Fenton reaction. Recent studies have shown that in certain cell lines thiols can also cause apoptosis in a biphasic pattern, with little apoptosis at low or high drug concentrations but greatly increased apoptosis levels at intermediate (approximately 3 mM) thiol concentrations. There appears to be a good correlation between those thiols that cause loss of clonogenicity and those that induce apoptosis, suggesting similar mechanisms may be involved in both end points. However, thiol-induced apoptosis is not prevented by addition of exogenous catalase. These observations are discussed in relation to the possible role of Fenton chemistry in induction of apoptosis by thiols.
Language of Publication: English
Unique Identifier: 96198949

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MeSH Heading (Major): Apoptosis|*DE; Cell Survival|*DE; Hydrogen Peroxide|*; Iron|*; Sulfhydryl Compounds|*PD/TO
MeSH Heading: Animal; Cell Line; Chelating Agents|PD; Dithiothreitol|PD/TO; Human; Hydroxyl Radical; Metals|PD; Support, U.S. Gov't, P.H.S.

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0033-7587
Country of Publication: UNITED STATES

Record 11 from database: MEDLINE
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Title: Interactions in metal carcinogenicity.
Author: Beyersmann D
Address: Department of Biology and Chemistry, University of Bremen, Germany.
Source: Toxicol Lett, 1994 Jun, 72:1-3, 333-8
Abstract: The carcinogenicity and genotoxicity of cadmium, chromium, cobalt and nickel strongly depend on their chemical ligands (speciation) which modulate their bioavailability and reactivity with biochemical targets. With the exception of hexavalent chromium, carcinogenic metal compounds are only weakly genotoxic. However, the ions of the carcinogenic metals cadmium, cobalt and nickel, and also the noncarcinogenic lead, inhibit the repair of DNA damaged by direct genotoxic agents like UV irradiation and alkylating substances, thereby enhancing the effects of the latter agents. These effects are interpreted by the interference of the toxic metal ions with biochemical functions of magnesium, calcium and zinc ions.
Language of Publication: English
Unique Identifier: 94262088

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MeSH Heading (Major): Carcinogens|*TO; Metals|AE/*TO; Neoplasms, Experimental|*CI
MeSH Heading: Animal; Cocarcinogenesis; Drug Interactions; DNA Damage; DNA Repair|DE; Human; Risk Factors; Support, Non-U.S. Gov't

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0378-4274
Country of Publication: NETHERLANDS

Record 12 from database: MEDLINE
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Title: Glial metallothionein.
Author: Young JK
Address: Department of Anatomy, Howard University, Washington, D.C. 20059.
Source: Biol Signals, 1994 May, 3:3, 169-75
Abstract: The metal-binding protein, metallothionein (MT) has been found to be primarily produced by astrocytes in the rat and human brain. This review discusses the relationship of glial MT to the distribution of metals in the brain, possible roles of MT in the regulation of glial enzymes and other glial proteins, and the possible role of a subset of MT-immunoreactive glia, the Gomori-positive astrocytes, in defending against toxic metals that enter the brain via circumventricular organs. The possible involvement of MT-containing astrocytes in degenerative brain disorders in also briefly discussed.
Language of Publication: English
Unique Identifier: 95152627

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MeSH Heading (Major): Metallothionein|GE/*ME; Neuroglia|*ME
MeSH Heading: Animal; Astrocytes|ME; Brain|DE/ME; Brain Diseases|ET/ME; Human; Metabolic Detoxication, Drug; Metals|ME/PK/TO; Rats; RNA, Messenger|GE/ME; Signal Transduction

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 1016-0922
Country of Publication: SWITZERLAND

Record 13 from database: MEDLINE
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Title: Nutrition and metal toxicity.
Author: Goyer RA
Address: National Institute of Environmental Health Sciences, Research Triangle Park, NC 27707.
Source: Am J Clin Nutr, 1995 Mar, 61:3 Suppl, 646S-650S
Abstract: Lead, cadmium, and mercury are toxic metals that are not essential for nutrition. However, the toxic effects of these metals may be mediated or enhanced by interactions or deficiencies of nutritionally essential metals. Lead competes with calcium, inhibiting the release of neurotransmitters, and interferes with the regulation of cell metabolism by binding to second-messenger calcium receptors, blocking calcium transport by calcium channels and calcium-sodium ATP pumps, and by competing for calcium-binding protein sites and uptake by mitochondria. Dietary deficiencies of calcium, iron, and zinc enhance the effects of lead on cognitive and behavioral development. Iron deficiency increases the gastrointestinal absorption of cadmium, and cadmium competes with zinc for binding sites on metallothionein, which is important in the storage and transport of zinc during development. Selenium protects from mercury and methyl mercury toxicity by preventing damage from free radicals or by forming inactive selenium mercury complexes.
Language of Publication: English
Unique Identifier: 95185439

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MeSH Heading (Major): Metals|*PO; Nutrition|*
MeSH Heading: Animal; Calcium|ME; Diet; Drug Interactions; Human; Iron|DF

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0002-9165
Country of Publication: UNITED STATES

Record 14 from database: MEDLINE
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Title: Metal ion homeostasis and intracellular parasitism.
Author: Agranoff DD; Krishna S
Address: Department of Cellular and Molecular Sciences, St George's Hospital Medical School, London, UK.
Source: Mol Microbiol, 1998 May, 28:3, 403-12
Abstract: Bacteria possess multiple mechanisms for the transport of metal ions. While many of these systems may have evolved in the first instance to resist the detrimental effects of toxic environmental heavy metals, they have since become adapted to a variety of important homeostatic functions. The 'P'-type ATPases play a key role in metal ion transport in bacteria. A Cu+-ATPase from the intracellular bacterium Listeria monocytogenes is implicated in pathogenesis, and similar pumps in Mycobacterium tuberculosis and M. leprae may play a comparable role. Intracellular bacteria require transition metal cations for the synthesis of superoxide dismutases and catalases, which constitute an important line of defence against macrophage-killing mechanisms. The macrophage protein Nramp1, which confers resistance to a variety of intracellular pathogens, has also been shown recently to be a divalent amphoteric cation transporter. Mycobacterial homologues have recently been identified by genomic analysis. These findings suggest a model in which competition for divalent cations plays a pivotal role in the interaction between host and parasite.
Language of Publication: English
Unique Identifier: 98294035

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MeSH Heading (Major): Adenosinetriphosphatase|*ME; Bacteria|*ME/*PY; Metals|*ME
MeSH Heading: Animal; Bacterial Physiology; Carrier Proteins|ME; Homeostasis; Human; Ion Transport; Membrane Proteins|ME; Support, Non-U.S. Gov't

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0950-382X
Country of Publication: ENGLAND
CAS Registry/EC Number: EC 3.6.1.3 (Adenosinetriphosphatase); 0 (Carrier Proteins); 0 (Membrane Proteins); 0 (Metals); 0 (Nramp protein)

Record 15 from database: MEDLINE
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Title: Toxic and essential metal interactions.
Author: Goyer RA
Address
Source: Annu Rev Nutr, 1997, 17:, 37-50
Abstract: Cadmium, lead, mercury, and aluminum are toxic metals that may interact metabolically with nutritionally essential metals. Iron deficiency increases absorption of cadmium, lead, and aluminum. Lead interacts with calcium in the nervous system to impair cognitive development. Cadmium and aluminum interact with calcium in the skeletal system to produce osteodystrophies. Lead replaces zinc on heme enzymes and cadmium replaces zinc on metallothionein. Selenium protects from mercury and methylmercury toxicity. Aluminum interacts with calcium in bone and kidneys, resulting in aluminum osteodystrophy. Calcium deficiency along with low dietary magnesium may contribute to aluminum-induced degenerative nervous disease.
Language of Publication: English
Unique Identifier: 97382927

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MeSH Heading (Major): Metals|*PD/*PO
MeSH Heading: Aluminum|PD/PO; Animal; Cadmium|PD; Cadmium Poisoning; Calcium|ME; Female; Human; Iron|DF; Lead|PD; Lead Poisoning; Mercury|PD; Mercury Poisoning; Pregnancy

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0199-9885
Country of Publication: UNITED STATES

Record 16 from database: MEDLINE
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Title: Carcinogenicity and metallic implants [see comments]
Author: Vahey JW; Simonian PT; Conrad EU 3rd
Address: Department of Orthopaedic Surgery, University of Washington Medical School, Seattle, USA.
Source: Am J Orthop, 1995 Apr, 24:4, 319-24
Abstract: The literature related to the carcinogenetic potential of metallic implants was reviewed. There were 20 cases described in which tumors were identified in proximity to metallic implants. These cases occurred over a 34-year period. Investigators have identified a 70% increased incidence of lymphomas and hematopoietic tumors over that in the general population in patients who had received total hip arthroplasties. Carcinogenicity theories include the potential direct toxicity of materials, the effects of surface properties, the electromotive potential created by dissimilar metals in contact, the immunologic response to implants, and finally, the sustained presence of low-grade infection. Corrosion is a well-documented phenomenon and occurs with any type of metal. The rate of formation of corrosion products and their toxicity varies with the implant composition. Toxic effects of metals, such as malignant potential and other adverse effects, have been demonstrated in animal models. The published information on this controversial and very poignant issue of metallic carcinogenesis is useful for all orthopedic surgeons.
Language of Publication: English
Unique Identifier: 95308062

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MeSH Heading (Major): Neoplasms|*ET; Prostheses and Implants|*AE
MeSH Heading: Animal; Human; Joint Prosthesis|AE; Metals

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 1078-4519
Country of Publication: UNITED STATES

Record 17 from database: MEDLINE
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Title: Shellfish-borne illnesses. A Hong Kong perspective.
Author: Chan TY
Address: Department of Clinical Pharmacology, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong.
Source: Trop Geogr Med, 1995, 47:6, 305-7
Abstract: This article provides an overview of the spectrum of infectious and toxic illnesses that may occur following the consumption of contaminated shellfish in Hong Kong. These include hepatitis A, hepatitis E, infections due to vibrio species, paralytic shellfish poisoning, neurotoxic shellfish poisoning and heavy metal poisoning. Possible preventive measures are discussed.
Language of Publication: English
Unique Identifier: 96209384

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MeSH Heading (Major): Infection|EP/*ET; Metals|*PO; Shellfish|*MI/*PO
MeSH Heading: Adolescence; Adult; Aged; Child; Child, Preschool; Cookery; Female; Hong Kong|EP; Human; Infant; Infection Control; Male; Middle Age; Population Surveillance

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0041-3232
Country of Publication: NETHERLANDS

Record 18 from database: MEDLINE
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Title: Toxic metal pollution in Africa.
Author: Nriagu JO
Address: National Water Research Institute, Burlington, Ontario, Canada.
Source: Sci Total Environ, 1992 Jun 30, 121:, 1-37
Abstract: The available information suggests that the concentrations of toxic metals in many ecosystems of Africa are reaching unprecedented levels. Because of the heavy load of contaminated dusts in the air of the overcrowded cities, the ambient concentrations of toxic metals are now among the highest being reported anywhere. Lead pollution from the increasing number of automobiles and cottage industries represents a major health hazard, and it is estimated that 15-30% of the infants in some urban areas may already be suffering from lead poisoning. The cultural and lifestyle determinants of lead exposure and the greater susceptibility of African populations to environmental metal poisoning are highlighted. The suggestion is made that the environmental health criteria for toxic metals in the developed countries may not provide adequate protection for many African communities.
Language of Publication: English
Unique Identifier: 93068194

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MeSH Heading (Major): Environmental Exposure|*; Environmental Pollution|*; Metals|*/AN
MeSH Heading: Africa; Animal; Climate; Diet; Fishes; Health Status; Human; Trace Elements|AN

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
ISSN: 0048-9697
Country of Publication: NETHERLANDS
CAS Registry/EC Number: 0 (Metals); 0 (Trace Elements)

Record 19 from database: MEDLINE
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Title: Toxicity, bioavailability and metal speciation.
Author: Jonnalagadda SB; Rao PV
Address: Department of Chemistry, University of Zimbabwe, Mt. Pleasant, Harare.
Source: Comp Biochem Physiol C, 1993 Nov, 106:3, 585-95
Abstract: 1. Environmental toxicology emphasizes the difference from traditional toxicology in which pure compounds of interest are added to purified diets, or injected into the test animals. When the objective is to study the fate and effects of trace elements in the environment, knowledge of the speciation of the elements and their physico-chemical forms is important. 2. Cadmium salts such as the sulfides, carbonates or oxides, are practically insoluble in water. However, these can be converted to water-soluble salts in nature under the influence of oxygen and acids. Chronic exposure to Cd is associated with renal toxicity in humans once a critical body burden is reached. 3. The solubility of As(III) oxide in water is fairly low, but high in either acid or alkali. In water, arsenic is usually in the form of the arsenate or arsenite. As(III) is systemically more poisonous than the As(V), and As(V) is reduced to the As(III) form before exerting any toxic effects. Organic arsenicals also exert their toxic effects in vivo in animals by first metabolizing to the trivalent arsenoxide form. Some methyl arsenic compounds, such as di- and trimethylarsines, occur naturally as a consequence of biological activity. The toxic effect of arsenite can be potentiated by dithiols, while As has a protective effect against the toxicity of a variety of forms of Se in several species. 4. Selenium occurs in several oxidation states and many selenium analogues of organic sulfur compounds exist in nature. Selenium in selenate form occurs in alkaline soils, where it is soluble and easily available to plants. Selenite binds tightly to iron and aluminum oxides and thus is quite insoluble in soils. Hydrogen selenide is a very toxic gas at room temperature. The methylated forms of Se are much less toxic for the organism than selenite. However, the methylated Se derivatives have strong synergistic toxicity with other minerals such as arsenic. 5. Aquatic organisms absorb and retain Hg in the tissues, as methylmercury, although most of the environmental Hg to which they are exposed is inorganic. The methylmercury in fish arises from the bacterial methylation of inorganic Hg. Methylmercury in the human diet is almost completely absorbed into the bloodstream. The nervous system is the principal target tissue affected by methylmercury in adult human beings, while kidney is the critical organ following the ingestion of Hg(II) salts.
Language of Publication: English
Unique Identifier: 94139253

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MeSH Heading (Major): Metals|CH/*PK/*TO
MeSH Heading: Animal; Biological Availability; Human

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0742-8413
Country of Publication: ENGLAND
CAS Registry/EC Number: 0 (Metals)

Record 20 from database: MEDLINE
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Title: Biological and health implications of toxic heavy metal and essential trace element interactions.
Author: Chowdhury BA; Chandra RK
Address
Source: Prog Food Nutr Sci, 1987, 11:1, 55-113
Abstract: Human civilization and a concomitant increase in industrial activity has gradually redistributed many toxic metals from the earth's crust to the environment and increased the possibility of human exposure. Among the various toxic elements, heavy metals cadmium, lead, and mercury are specially prevalent in nature due to their high industrial use. These metals serve no biological function and their presence in tissues reflects contact of the organism with its environment. They are cumulative poison, and are toxic even at low dose. Studies of metabolism and toxicity of these elements have revealed important interactions between them and some essential dietary elements like calcium, zinc, iron, selenium, copper, chromium, and manganese. In general, a deficiency of these essential elements increases toxicity of heavy metals, whereas an excess appears to be protective. While most of the observations are on laboratory animals, limited human data are in agreement with the results of animal experiments. These suggest that the dietary presence of the essential elements may contribute to the protection of man and animal from the effects of heavy metal exposure, while their deficiency may increase toxicity. Appropriate dietary manipulation thus may be valuable in the prevention and treatment of heavy metal toxicity.
Language of Publication: English
Unique Identifier: 87290638

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MeSH Heading (Major): Metals|*TO; Trace Elements|*ME
MeSH Heading: Animal; Bone and Bones|DE/ME; Cadmium|ME/TO; Calcium|ME; Copper|ME; Diet; Drug Interactions; Environmental Exposure; Human; Iron|ME; Lead|ME/TO; Lung|DE/ME; Manganese|ME; Mercury|ME/TO; Metallothionein|ME; Selenium|ME; Smoking; Tissue Distribution; Zinc|ME

Publication Type: JOURNAL ARTICLE; REVIEW
ISSN: 0306-0632
Country of Publication: ENGLAND
CAS Registry/EC Number: 0 (Metals); 0 (Trace Elements); 7439-89-6 (Iron); 7439-92-1 (Lead); 7439-96-5 (Manganese); 7439-97-6 (Mercury); 7440-43-9 (Cadmium); 7440-50-8 (Copper); 7440-66-6 (Zinc); 7440-70-2 (Calcium); 7782-49-2 (Selenium); 9038-94-2 (Metallothionein)

Record 21 from database: MEDLINE
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Title: Metals and the skin.
Author: Hostýnek JJ; Hinz RS; Lorence CR; Price M; Guy RH
Address: E.T.R.I., Lafayette, CA 94549.
Source: Crit Rev Toxicol, 1993, 23:2, 171-235
Abstract: Certain metals, and many metal-based compounds, are inherently toxic, and their presence in occupational and environmental settings raises appropriate questions concerning human exposure. Contact of these materials with the skin represents an important route of exposure, which is not well characterized. The purpose of this review, therefore, is to assemble the available, useful information pertinent to risk assessment following dermal contact. Specifically, we summarize here: (1) data relevant to the qualitative and (where possible) quantitative evaluation of metal compound permeation through the skin; (2) the role of each metal in metabolism, particularly with respect to the skin, and the potentially toxic effects that may result from dermal contact; and (3) the immunological characteristics (including allergenicity) of the metals and their derivatives. In total, information on 31 metals has been reviewed. It is clear that many diverse factors determine the ability of metal-based species to permeate biological membranes, not all of which have been fully defined. Therefore, considerably more experimentation, targeted at the development of high-quality transport data, will be required before the specification of practically useful structure-activity relationships are possible.
Language of Publication: English
Unique Identifier: 93319628

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MeSH Heading (Major): Metals|IM/PK/*TO; Skin Absorption|*
MeSH Heading: Animal; Dermatitis, Contact|PP; Human; Support, U.S. Gov't, Non-P.H.S.

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
ISSN: 1040-8444
Country of Publication: UNITED STATES
CAS Registry/EC Number: 0 (Metals)

Record 22 from database: MEDLINE
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Title: Alzheimer's disease and metal-containing glia.
Author: Young JK
Address: Department of Anatomy, Howard University, Washington DC 20059.
Source: Med Hypotheses, 1992 May, 38:1, 1-4
Abstract: Considerable evidence suggests that in Alzheimer's disease, olfactory bulb damage may be a primary factor, causing degeneration and neurofibrillary tangles primarily in neurons connected with this brain area. Also, deposits of amyloid may involve an improper regulation of the cleavage of a precursor protein by glia. Finally, toxic effects of aluminium may be an etiological factor. This review proposes that all these seemingly unrelated aspects of Alzheimer's disease could be related to a disturbed function of metal-containing glia. Such a disturbance, initiated by or aggravating toxic effects of aluminum, may underlie initial damage in the olfactory bulb and/or other brain areas with a weakened blood-brain barrier and may be responsible for amyloid deposition.
Language of Publication: English
Unique Identifier: 92310300

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MeSH Heading (Major): Aluminum|*TO; Alzheimer's Disease|*ET/PA; Metals|AN/*TO; Neuroglia|DE/*PA
MeSH Heading: Brain|DE/PA; Human

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN: 0306-9877
Country of Publication: ENGLAND
CAS Registry/EC Number: 0 (Metals); 7429-90-5 (Aluminum)

Record 23 from database: MEDLINE
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Title: Environmental transformation of toxic metals.
Author: Wade MJ; Davis BK; Carlisle JS; Klein AK; Valoppi LM
Address: Department of Toxic Substances Control, California Environmental Protection Agency Sacramento 95812-0806.
Source: Occup Med, 1993 Jul-Sep, 8:3, 574-601
Abstract: Because toxicity varies enormously with the chemical state of metals, transformations in the environment control the level of the human health hazard. Important transformation processes include adsorption and desorption from soils and sediments, oxidation and reduction (redox) reactions, biotic metabolism, formation of organic metal compounds, and bioaccumulation. The six metals detailed in this chapter--arsenic, cadmium, chromium, lead, mercury, and selenium--were chosen because of their toxicity, frequency of occurrence at hazardous waste sites, and involvement in environmental contamination.
Language of Publication: English
Unique Identifier: 94098443

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MeSH Heading (Major): Environmental Exposure|*; Environmental Pollution|*; Hazardous Substances|*; Metals|*CH/PK
MeSH Heading: Animal; Biological Availability; Ecosystem; Human

Publication Type: JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
ISSN: 0885-114X
Country of Publication: UNITED STATES
CAS Registry/EC Number: 0 (Hazardous Substances); 0 (Metals)

Record 24 from database: MEDLINE
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Title: Biological monitoring of toxic metals.
Author: Friberg L; Elinder CG
Address: Department of Environmental Hygiene, Karolinska Institute, Stockholm, Sweden.
Source: Scand J Work Environ Health, 1993, 19 Suppl 1:, 7-13
Abstract: The biological monitoring of metals, when used properly, allows total exposure to a particular metal to be measured from various media. It takes into consideration inter- and intraindividual variations in uptake due to differences in metabolism and physical work load and can be used to ident