Calretinin immunoreactivity in normal and carbon tetrachloride-induced nephrotoxic rats

Carbon tetrachloride (CCl4) is a potent hepatotoxic and nephrotoxic chemical. Little, however, is known about the association of CCl4-induced nephrotoxicity and calretinin. We hypothesized that calretinin might be localized in the proximal tubule cells and play a role against CCl4-induced nephrotoxicity, since the target of CCl4 is the brush border-bearing tubule cells. CCl4 (1 ml/kg) was administrated by oral gavage to 8-week old male Sprague–Dawley rats once a week for 4 weeks. A significant increase in serum blood urea nitrogen and creatinine was confirmed by serum analysis. Calretinin immunolocalization was compared with the calbindin D-28k immunoreactivity in normal and CCl4-treated kidneys. Calretinin was clearly immunolocalized in the apical surface of proximal convoluted tubule in the deeper cortex of normal kidney and blurred after CCl4 administration, with only minor changes of calbindin D-28k immunoreactivity in the distal convoluted tubules and collecting ducts, irrelevant to the CCl4 treatment. These findings might have significance since decreased immunolocalization of calretinin with CCl4-induced nephrotoxicity may contribute to the toxicity-related decrease in calcium transport or calcium buffering activity in the kidney.