Cadmium induced lipid peroxidation in kidney function.
Since the kidney is the main target organ for many metals including cadmium, the generation of the products of lipid peroxidation due to accumulation of these toxic metals in the kidney may have importance in the mechanism of their nephrotoxicity. In order to test this hypothesis, we carried out an experimental study in rats. The functions and the levels of tiobarbituric acid reactive substances (TBARS) of the kidney were investigated in animals receiving 15 micrograms/ml aqueous Cd solution for 30 days. Due to cadmium accumulation in kidney cortex, the ratio of Cd/Zn increased significantly and this increase was associated with elevated TBARS in both renal cortex and medulla. The content of TBARS in renal cortex rose from 211.6 +/- 64.2 to 303.4 +/- 46.4 nmol/g protein (p<0.01) and GFR decreased to 390.5 +/- 109.4 from 1008.7 +/- 4.8 microliters/min (p<0.01) in cadmium exposed animals. Daily coadministration of selenium, vitamins A, C, E did not reverse the adverse effect of cadmium on kidney function, despite the significant decrease in cortex TBARS levels (p<0.01). In conclusion, these data suggest to us that lipid peroxidation assessed by TBA test may not be the only mechanism in cadmium induced nephrotoxicity.
Sentürk
U K
UK
Akdeniz University, Faculty of Medicine, Department of Physiology, Antalya, Turkey.
Oner
G
G
Izgüt-Uysal
V M
VM
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D002104:Cadmium / Q000494:pharmacology*; D007668:Kidney / Q000187:drug effects*; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D051381:Rats
D000975:Antioxidants; D002104:Cadmium