US EPA

2735236 

Journal Article 

Alterations in rat liver and kidney cortex metabolism after acute and chronic exposure to cadmium 

Merali, Z; Kacew, S; Singhal, RL 

1974 

1 

Toxicology and Applied Pharmacology
ISSN: 0041-008X
EISSN: 1096-0333 

29 

1 

140 

English 

WOS:A1974T653800172 

is part of a larger document 3378179 Abstracts of papers for the Thirteenth Annual Meeting of the Society of Toxicology, Washington, D.C. March 10–14, 1974

Exposure to cadmium has been shown to produce itai-itai disease, hypertension and testicular atrophy, as well as an increase in the excretion of urinary protein and glucose. The purpose of this study was to investigate the acute and chronic effects of cadmium on serum urea, blood glucose and hepatic glycogen, as well as on the activities of the 4 key, rate-limiting enzymes involved in kidney cortex and liver gluconeogenesis. Rats injected ip with an acute dose of cadmium chloride (60 mg/kg) displayed metabolic changes as early as I hr which were reflected in increased blood glucose (4-fold) and serum urea (2-fold) and a decrease in hepatic glycogen content (2-fold). The activities of the 4 gluconeogenic enzymes, pyruvate carboxylase, phosphoenolpyruvate carboxykinase, fructose 1,6-diphosphatase and glucose 6-phosphatase, showed small but consistent increases in both liver and kidney cortex. Chronic exposure to a smaller dose of cadmium (1 mg/kg/day) for 45 days also enhanced blood glucose and serum urea and reduced hepatic glycogen concentrations. Following chronic cadmium treatment, the activities of the 4 hepatic and renal gluconeogenic enzymes also were significantly elevated when compared to the control values. In rats given cadmium (1 mg/kg) for 45 days and then maintained for 28 days without any additional treatment (withdrawal group), the observed increases in blood glucose and serum urea still persisted, as did the drop in liver glycogen. Similarly, enzyme activities in livers and kidney cortices of rats in the "withdrawal" group remained significantly above those seen in the control animals. The results show that exposure to cadmium produces hyperglycemia, hyperuremia and glycogenolysis, as well as stimulating the process of renal and hepatic gluconeogenesis, and that the various biochemical changes persist for a prolonged period even after the cessation of heavy metal treatment. (Supported by a grant from the Department of National Health and Welfare, Canada.) 

Thirteenth Annual Meeting of the Society of Toxicology 

Washington, D.C. 

March 10–14, 1974