Since the kidney is a main target for cadmium, its accumulation in the
kidney tissue by increasing peroxidative damage make the kidney funct
ions vulnerable to stress. For this reason, the effect of cadmium-indu
ced peroxidative damage to kidney responses to stress was investigated
in this study. Two-month-old albino rats receiving 15 mu g/mL contain
ing Cd drinking water for 30 d were exposed to restraint and cold stre
ss for 6 h, and their responses were compared with those of unstressed
counterparts. Lipid peroxidation was found to be significantly higher
in the cortical portion of kidney in cadmium-exposed rats than that o
f unexposed animals. The mean thiobarbutyric acid reactive substance (
TEARS) level rose from 211.6 +/- 64.2 to 303.4 +/- 46.4 nmol/g protein
(p < 0.01). Six hours of cold and restraint stress caused an elevatio
n in the cortical TEARS level in control animals without affecting its
level in cadmium-exposed rats. Despite unaltered cortical TBARS, its
medullar levels increased significantly in cadmium-exposed rats becaus
e of stress. These results suggested that cadmium accumulation in the
kidney increases the susceptibility of medulla against peroxidative da
mage. However, further functional studies are necessary to explain the
role of cadmium in the stress-induced deterioration of medullar funct
ions.