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Molecular basis of cadmium toxicity

Journal Article:

Abstract

Cadmium has been shown to manifest its toxicity in human and animals by mainly accumulating in almost all of the organs. The kidney is the main target organ where it is concentrated mainly in the cortex. Environmental exposure of cadmium occurs via food, occupational industries, terrestrial and aquatic ecosystem. At molecular level, cadmium interferes with the utilization of essential metals e.g. Ca, Zn, Se, Cr and Fe and deficiencies of these essential metals including protein and vitamins, exaggerate cadmium toxicity, due to its increased absorption through the gut and greater retention in different organs as metallothionein (Cd-Mt). Cadmium transport, across the intestinal and renal brush border membrane vesicles, is carrier mediated and it competes with zinc and calcium. It has been postulated that cadmium shares the same transport system. Cadmium inhibits protein synthesis, carbohydrate metabolism and drug metabolizing enzymes in liver of animals. Chronic environmental exposure of cadmium produces hypertension in experimental animals. Functional changes accompanying cadmium nephropathy include low molecular weight proteinuria which is of tubular origin associated with excess excretion of proteins such as beta 2 microglobulin, metallothionein and high molecular weight proteinuria of glomerular origin (excretion of proteins such as albumin IgG, transferrin etc.). Recent data has  More>>
Publication Date:
Jan 01, 1984
Product Type:
Journal Article
Reference Number:
EDB-85-069282
Resource Relation:
Journal Name: Prog. Food Nut. Sci.; (United Kingdom); Journal Volume: 8:1-2
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; CADMIUM; MEMBRANE TRANSPORT; TOXICITY; BIOLOGICAL ACCUMULATION; CARBOHYDRATES; CENTRAL NERVOUS SYSTEM; IMMUNE REACTIONS; INHIBITION; INTESTINAL ABSORPTION; KIDNEYS; LUNGS; METABOLISM; METALLOTHIONEIN; NUTRITIONAL DEFICIENCY; PROTEINS; ABSORPTION; BODY; ELEMENTS; METALLOPROTEINS; METALS; NERVOUS SYSTEM; ORGANIC COMPOUNDS; ORGANS; RESPIRATORY SYSTEM; UPTAKE; 560306* - Chemicals Metabolism & Toxicology- Man- (-1987); 560305 - Chemicals Metabolism & Toxicology- Vertebrates- (-1987)
OSTI ID:
5820753
Research Organizations:
Postgraduate Inst. of Medical Education and Research, Chandigarh, India
Country of Origin:
United Kingdom
Language:
English
Other Identifying Numbers:
Journal ID: CODEN: PFNSD
Submitting Site:
HEDB
Size:
Pages: 109-163
Announcement Date:

Journal Article:

Citation Formats

Nath, R, Prasad, R, Palinal, V K, and Chopra, R K. Molecular basis of cadmium toxicity. United Kingdom: N. p., 1984. Web.
Nath, R, Prasad, R, Palinal, V K, & Chopra, R K. Molecular basis of cadmium toxicity. United Kingdom.
Nath, R, Prasad, R, Palinal, V K, and Chopra, R K. 1984. "Molecular basis of cadmium toxicity." United Kingdom.
@misc{etde_5820753,
title = {Molecular basis of cadmium toxicity}
author = {Nath, R, Prasad, R, Palinal, V K, and Chopra, R K}
abstractNote = {Cadmium has been shown to manifest its toxicity in human and animals by mainly accumulating in almost all of the organs. The kidney is the main target organ where it is concentrated mainly in the cortex. Environmental exposure of cadmium occurs via food, occupational industries, terrestrial and aquatic ecosystem. At molecular level, cadmium interferes with the utilization of essential metals e.g. Ca, Zn, Se, Cr and Fe and deficiencies of these essential metals including protein and vitamins, exaggerate cadmium toxicity, due to its increased absorption through the gut and greater retention in different organs as metallothionein (Cd-Mt). Cadmium transport, across the intestinal and renal brush border membrane vesicles, is carrier mediated and it competes with zinc and calcium. It has been postulated that cadmium shares the same transport system. Cadmium inhibits protein synthesis, carbohydrate metabolism and drug metabolizing enzymes in liver of animals. Chronic environmental exposure of cadmium produces hypertension in experimental animals. Functional changes accompanying cadmium nephropathy include low molecular weight proteinuria which is of tubular origin associated with excess excretion of proteins such as beta 2 microglobulin, metallothionein and high molecular weight proteinuria of glomerular origin (excretion of proteins such as albumin IgG, transferrin etc.). Recent data has shown that metallothionein is more nephrotoxic to animals. Cadmium is also toxic to central nervous system. It causes an alterations of cellular functions in lungs. Cadmium affects both humoral and cell mediated immune response in animals. Cadmium induces metallothionein in liver and kidney but under certain nutritional deficiencies like protein-calorie malnutrition and calcium deficiency, enhanced induction and greater accumulation of cadmium metallothionein has been observed.}
journal = {Prog. Food Nut. Sci.; (United Kingdom)}
volume = {8:1-2}
journal type = {AC}
place = {United Kingdom}
year = {1984}
month = {Jan}
}