Induction of Oxidative Stress by Chronic Administration of Sodium Dichromate [Chromium VI] and Cadmium Chloride [Cadmium II] to Rats
TL;DR: Results clearly indicate that low dose chronic administration of sodium dichromate and cadmium chloride induces an oxidative stress resulting in tissue damaging effects that may contribute to the toxicity and carcinogenicity of these two cations.
About: This article is published in Free Radical Biology and Medicine.The article was published on 1997-01-01. It has received 209 citations till now. The article focuses on the topics: Sodium dichromate & Cadmium chloride.
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TL;DR: This review provides an analysis of arsenic, cadmium, chromium, lead, and mercury's environmental occurrence, production and use, potential for human exposure, and molecular mechanisms of toxicity, genotoxicity, and carcinogenicity.
Abstract: Heavy metals are naturally occurring elements that have a high atomic weight and a density at least five times greater than that of water. Their multiple industrial, domestic, agricultural, medical, and technological applications have led to their wide distribution in the environment, raising concerns over their potential effects on human health and the environment. Their toxicity depends on several factors including the dose, route of exposure, and chemical species, as well as the age, gender, genetics, and nutritional status of exposed individuals. Because of their high degree of toxicity, arsenic, cadmium, chromium, lead, and mercury rank among the priority metals that are of public health significance. These metallic elements are considered systemic toxicants that are known to induce multiple organ damage, even at lower levels of exposure. They are also classified as human carcinogens (known or probable) according to the US Environmental Protection Agency and the International Agency for Research on Cancer. This review provides an analysis of their environmental occurrence, production and use, potential for human exposure, and molecular mechanisms of toxicity, genotoxicity, and carcinogenicity.
4,407 citations
Cites background from "Induction of Oxidative Stress by Ch..."
...demonstrated that rats received Cr(VI) orally in water-induced hepatic mitochondrial and microsomal lipid peroxidation as well as enhanced excretion of urinary lipid metabolites including malondialdehyde [150, 151]....
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TL;DR: This review provides an update of the existing chelating agents and the various strategies available for the treatment of heavy metals and metalloid intoxications.
Abstract: Chelation therapy is the preferred medical treatment for reducing the toxic effects of metals. Chelating agents are capable of binding to toxic metal ions to form complex structures which are easily excreted from the body removing them from intracellular or extracellular spaces. 2,3-Dimercaprol has long been the mainstay of chelation therapy for lead or arsenic poisoning, however its serious side effects have led researchers to develop less toxic analogues. Hydrophilic chelators like meso-2,3-dimercaptosuccinic acid effectively promote renal metal excretion, but their ability to access intracellular metals is weak. Newer strategies to address these drawbacks like combination therapy (use of structurally different chelating agents) or co-administration of antioxidants have been reported recently. In this review we provide an update of the existing chelating agents and the various strategies available for the treatment of heavy metals and metalloid intoxications.
765 citations
TL;DR: This experimental system represents an important new animal model for chromate-induced cancers by ingestion of drinking water, and it suggests by extrapolation that chromate can likely be considered a human carcinogen by ingestion as well.
Abstract: Chromium is a human carcinogen primarily by inhalation exposure in occupational settings. Although lung cancer has been established as a consequence of hexavalent chromium exposure in smokers and nonsmokers, some cancers of other tissues of the gastrointestinal and central nervous systems have also been noted. Except for a few reports from China, little is known about the health risks of environmental exposures to chromium. Likewise, there has been a lack of epidemiological studies of human exposure to hexavalent Cr by drinking water or ingestion, and it has been suggested that humans can perhaps tolerate hexavalent Cr at higher levels than the current drinking water standard of 50 ppb. This review highlights the most recent data on the induction of skin tumors in mice by chronic drinking-water exposure to hexavalent chromium in combination with solar ultraviolet light. This experimental system represents an important new animal model for chromate-induced cancers by ingestion of drinking water, and it suggests by extrapolation that chromate can likely be considered a human carcinogen by ingestion as well. The potential use of this animal model for future risk assessment is discussed.
721 citations
Cites background from "Induction of Oxidative Stress by Ch..."
...…cancers, and based on the knowledge that Cr gets into the central nervous system (CNS), there should also be concern about the possibility that hexavalent Cr may be neurotoxic (Bagchi et al., 1997; Travacio et al., 2000, 2001; Ueno et al., 2001; Attenburrow et al., 2002; Wesseling et al., 2002)....
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TL;DR: This minireview focused on direct evidence for the generation of free radicals in intact animals following acute Cd overload and discussed the association of ROS in chronic Cd toxicity and carcinogenesis.
689 citations
Cites background from "Induction of Oxidative Stress by Ch..."
...Cd-induced ROS could overwhelm the antioxidant defenses, leading to increased lipid peroxidation and oxidative DNA damage (Bagchi et al., 1997; Waisberg et al., 2003)....
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...…increases lipid peroxidation (as determined by the formation of thiobarbituric acid reactive substances) in liver mitochondria and microsomes 15 days after administration, reaching peak between 60 and 75 days of treatment, with increased urinary excretion of lipid metabolites (Bagchi et al., 1997)....
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...It has been suggested that the mechanisms of acute Cd toxicity involve the depletion of glutathione and protein-bound sulfhydryl groups, resulting in enhanced production of ROS such as superoxide ion, hydrogen peroxide, and hydroxyl radicals (Manaca et al., 1994; Bagchi et al., 1997; Liu and Jan, 2000)....
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...…been suggested that the mechanisms of acute Cd toxicity involve the depletion of glutathione and protein-bound sulfhydryl groups, resulting in enhanced production of ROS such as superoxide ion, hydrogen peroxide, and hydroxyl radicals (Manaca et al., 1994; Bagchi et al., 1997; Liu and Jan, 2000)....
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...4 mg/kg in drinking water increases lipid peroxidation (as determined by the formation of thiobarbituric acid reactive substances) in liver mitochondria and microsomes 15 days after administration, reaching peak between 60 and 75 days of treatment, with increased urinary excretion of lipid metabolites (Bagchi et al., 1997)....
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TL;DR: Comparative studies demonstrate that a cascade of cellular events including oxidative stress, genomic DNA damage and modulation of apoptotic regulatory gene p53 are involved in chromium(VI)-induced toxicity and carcinogenesis.
604 citations
References
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Book•
01 Jan 1950
TL;DR: In this article, Cardinal Manifestations of Disease Genetics and Disease Clinical Pharmacology Nutrition Infectious Disease Disorders Of The Cardiovascular System Disorders Of the Kidney And Urinary Tract Disorders Of Gastrointestinal System Disorders of The Immune System, Connective Tissue And Joints Hematology And Oncology Endocrinology And Metabolism Neurologic Disorders Environmental And Occupational Hazards.
Abstract: Introduction To Clinical Medicine Cardinal Manifestations Of Disease Genetics And Disease Clinical Pharmacology Nutrition Infectious Disease Disorders Of The Cardiovascular System Disorders Of The Kidney And Urinary Tract Disorders Of The Gastrointestinal System Disorders Of The Immune System, Connective Tissue And Joints Hematology And Oncology Endocrinology And Metabolism Neurologic Disorders Environmental And Occupational Hazards.
12,186 citations
TL;DR: This chapter discusses microsomal lipid peroxidation, a complex process known to occur in both plants and animals that involves the formation and propagation of lipid radicals, the uptake of oxygen, a rearrangement of the double bonds in unsaturated lipids, and the eventual destruction of membrane lipids.
Abstract: Publisher Summary This chapter discusses microsomal lipid peroxidation Lipid peroxidation is a complex process known to occur in both plants and animals It involves the formation and propagation of lipid radicals, the uptake of oxygen, a rearrangement of the double bonds in unsaturated lipids, and the eventual destruction of membrane lipids, producing a variety of breakdown products, including alcohols, ketones, aldehydes, and ethers Biological membranes are often rich in unsaturated fatty acids and bathed in an oxygen-rich, metal-containing fluid Lipid peroxidation begins with the abstraction of a hydrogen atom from an unsaturated fatty acid, resulting in the formation of a lipid radical The formation of lipid endoperoxides in unsaturated fatty acids containing at least 3 methylene interrupted double bonds can lead to the formation of malondialdehyde as a breakdown product Nonenzymic peroxidation of microsomal membranes also occurs and is probably mediated in part by endogenous hemoproteins and transition metals The direct measurement of lipid hydroperoxides has an advantage over the thiobarbituric acid assay in that it permits a more accurate comparison of lipid peroxide levels in dissimilar lipid membranes
11,945 citations
TL;DR: Some mechanisms associated with the toxicities of metal ions are very similar to the effects produced by many organic xenobiotics, related to differences in solubilities, absorbability, transport, chemical reactions, and the complexes that are formed within the body.
4,084 citations
TL;DR: It is suggested that LPO is an early and sensitive consequence of Cd exposure as determined in various organs and investigated as assessed by the measurement of thiobarbituric acid reactive substances (TBARS).
325 citations
TL;DR: Results indicate that sodium chromate(VI) reacts with hydrogen peroxide to form tetraperoxochromate(V), leading to the production of the hydroxyl radical, which causes every base alteration and deoxyribose-phosphate backbone breakage.
299 citations