Cadmium, zinc and copper relationships in kidney and liver of humans exposed to environmental cadmium
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Cadmium poisoning
CADMIUM EXPOSURE
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Accumulation, elimination and subcellular distribution of heavy metals in Littorina brevicula exposed to cadmium and zinc separately and concurrently were investigated. When the winkles had been exposed to 400 ㎍/L CdCl₂ and 3000 ㎍/l ZnSO₄ separately for 90 days, each of the metal body burden in the whole sofl parts increased in proportion to time of exposure until 70 days. But it didn't increase after 70 days. But when the winkles had been exposed to cadmium and zinc simultaneously, cadmium body burden decreased but zinc body burden increased as compared to the winkles exposed to each of the metal. We also found that cadmium accumulated in the winkles was not depurated for 42 days, but zinc accumulated in them was depurated. Especially, zinc was depurated faster when they had been exposed to mixture of cadmium and zinc. After the winkles had been exposed to cadmium and zinc separately for 70 days, about 60% cadmium of the total body burden was associated with the soluble fraction, while about 75% zinc of the total body burden was associated with insoluble fraction. And these trends of metal partitioning did not alter when the winkles had been exposed to metal mixture. After the soluble fraction applied to gel-filtration chromatography column, the distribution patterns of cadmium and zinc associated with proteins or ligands were different each other. Most of cadmium (＞90%) in the soluble fraction was bound to MBP-1 (Metal-binding protein-1), about 6.5 kDa), while zinc was distributed evenly to HMW (High molecular weight fraction, >60 kDa), MBP-1, MBP-2 (about 5 kDa), LMW (Low molecular weight fraction,
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Objective To observe subchronic
cadmium-induced liver and kidney injury,and to study the relationship between
Metallothionein(MT)and cadmium toxicity. Methods 0.5mg/kg Cd2+ as CdCl2 solution was
injected intraperitoneally,3 times/week,and the functions of liver and kidney were detected
dynamically in 10 weeks of cadmium exposure. Results After 6-week cadmium exposure,the
injury of liver and kidney was observed functionally and morphologically,and the mole ratio of
Cd over MT in corresponding tissue was greater than 7. The severity of cadmium-induced
damage increased with the increase of CdMT ratio. Conclusion Both liver and kidney are
targets of subchronic cadmium exposure,and non-MT-bound cadmium may be an important
component in cadmium pathogenesis.
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Abstract • Mortality was observed in 4- to 5-week-old Swiss Webster mice exposed to 300 or 3 ppm cadmium as cadmium chloride in the drinking water. Mice receiving 300 ppm cadium suffered 26% mortality as compared with 7% of those on the low cadmium dose. Death did not occur in control mice. Clinical signs and histopathology established Hexamita muris as the causative agent. Cadmium lesions were not observed. It is suggested that mortality due to hexamitiasis resulted from synergism between cadmium and H muris.
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Chronic cadmium poisoning occurs after prolonged exposure to the dust or fumes of cadmium-containing compounds. This paper describes the case of a pigment worker exposed to cadmium carbonate dust who exhibited many of the characteristic features of chronic cadmium poisoning.
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The present study examines the absorption and excretion of chlorella cadmium-binding protein (Ch-CdBP) in rats incomparison to the same functions for inorganic cadmium. Ten daily administrations of inorganic cadmium, significantly curbed increases in body weight but the same number of oral administrations of Ch-CdBP.Cadmium accumlations in the liver, kidneys and spleen were smaller in rats given Ch-CdBP than in those which had received the cadmium. Cadmium concentration in blood maximized 60min after one oral dose, but it did not change significantly after Ch-CdBP administration.Cadmium excretion in urine was more rapid and the amount much greater when Ch-CdBP had been administered than when cadmium had been administered.
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Cadmium is a dangerous occupational and environmental toxin. It accumulates in the human organism mainly in liver and kidneys. Cadmium half-life is about 10 years, so the symptoms of cadmium intoxication may occur several years after the exposure. Until now in treating intoxication with this metal chelating compounds have been used, burdened with numerous undesirable symptoms. In our investigations anthocyanins from Aronia melanocarpa were used to reduce the harmful results caused by cadmium. Administering anthocyanins with cadmium chloride resulted in a statistically significant decrease of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activity, concentration of bilirubin and urea in blood serum and decreased cadmium cumulation in liver and kidneys in relation to animals receiving cadmium chloride only.
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