Abstract

Background: Cadmium (Cd) is widespread used in industry and extensively disseminated in the environment. As a result of the extensive use of cadmium (Cd) in industry and its extensive dissemination in the environment, numerous studies have focused on the identification of the early stages of Cd-induced renal injury in exposed persons. Following long-term low-level exposure, nearly one-third of the cadmium in the body will be found in the renal tissue. So, the aim of the present work is to evaluate the disturbed renal functions induced by cadmium exposure and its underlying mechanism. Materials and Methods:Twenty male rats were divided into two main groups, ten rats per each group. Group 1 (n=10) was the Cd group in which rats were treated for 13 days with a daily dose of 1 mg CdCl2/kg body weight in sterile 0.9 % NaCl solution subcutaneously. Group2 (n=10) was the vehicle control, they received equivalent volumes of sterile 0.9 % NaCl solution by subcutaneous injections.Results:cadmium administration led to a decrease in serum sodium and potassium level and increase their level in urine. It led to a significant decrease in creatinine clearance and a significant increase in the oxidative stress biomarker tissue malondialdehyde (MDA), as well as, and a significant decrease in serum total antioxidant capacity. Moreover, cadmium led to a significant decrease in glucose uptake by kidney (mg/gm wet tissue/h.) Conclusion: Cd has detrimental effects on kidney functions and renal handling of glucose and this effect is referred to its oxidative stress effect.

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