Protective role of selenium against renal toxicity induced by cadmium in rats.
Cadmium is an environmental toxic metal implicated in human diseases. The mechanism of its toxicity is not fully understood. Therefore, the role of cadmium in renal toxicity, and the protective role of selenium against this toxicity were investigated. Forty-five male rats were used through out the study and divided into three groups of 15. The first group received saline solution daily for 10 days. The second group, received cadmium chloride (CdCl2) (2 mg/kg body weight) intraperitoneally daily for a period of 10 days. The third group, received sodium selenite (1 mg/kg body weight, twice in 10 days) and cadmium chloride (CdCl2) once a day [corrected] The results showed that cadmium treatment increased renal lipid peroxidation (measured as malondialdehyde, MDA) which was associated with a significant decrease in the antioxidant systems such as reduced glutathione levels and the activities of glutathione peroxidase (GPx) and thioredoxin reductase (TrxR). On the other hand, pretreatment of rats with selenium and cadmium led to a significant decrease in MDA concentration, and increased levels of GSH and the activities of GPx and TrxR when compared with those of cadmium-treated group. The total levels of phospholipid, triglyceride, and cholesterolester classes were decreased, while free fatty acids levels were markedly increased after cadmium treatment. In addition, the total levels of both mono- and poly-unsaturated fatty acids of different lipid classes were significantly decreased, while the total saturated fatty acids was significantly increased by cadmium treatment. Pretreatment of rats with selenium, was found to protect kidney tissues of rats against the biochemical changes resulting from cadmium administration. These results suggest that cadmium causes renal toxicity by inducing lipid peroxidation, decreasing antioxidant systems, and also by altering lipid metabolism. In addition, selenium treatment could protect the kidney tissues against the toxicity of cadmium since it reduced MDA levels and increased the activities of antioxidant enzymes in these tissues. These results could be important for the further understanding of the complex mechanisms of cadmium toxicity in kidney tissues and in the development of better treatments for people and/or animals exposed to the heavy metal.
El-Sharaky
A S
AS
Department of Biochemistry, Faculty of Science, Alexandria University, Alexandria, Egypt.
Newairy
A A
AA
Badreldeen
M M
MM
Eweda
S M
SM
Sheweita
S A
SA
D000818:Animals; D002104:Cadmium / Q000633:toxicity*; D005227:Fatty Acids / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D007674:Kidney Diseases / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D020011:Protective Agents / Q000494:pharmacology*; D051381:Rats; D012643:Selenium / Q000494:pharmacology*; D013880:Thioredoxin-Disulfide Reductase / Q000378:metabolism
D005227:Fatty Acids; D020011:Protective Agents; D002104:Cadmium; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013880:Thioredoxin-Disulfide Reductase; D005978:Glutathione; D012643:Selenium