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Updated: Jun 8, 2026

Inducing Acute Liver Injury in Rats via Carbon Tetrachloride (CCl4) Exposure Through an Orogastric Tube
Published on: April 28, 2020
Calretinin immunoreactivity in normal and carbon tetrachloride-induced nephrotoxic rats
Ki Young Kang1, Jin Nam Kim, In Youb Chang
1Department of Anatomy, College of Medicine, Seonam University, Namwon, Republic of Korea.
Abstract:
Carbon tetrachloride (CCl(4)) is a potent hepatotoxic and nephrotoxic chemical. Little, however, is known about the association of CCl(4)-induced nephrotoxicity and calretinin. We hypothesized that calretinin might be localized in the proximal tubule cells and play a role against CCl(4)-induced nephrotoxicity, since the target of CCl(4) is the brush border-bearing tubule cells. CCl(4) (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 CCl(4)-treated kidneys. Calretinin was clearly immunolocalized in the apical surface of proximal convoluted tubule in the deeper cortex of normal kidney and blurred after CCl(4) administration, with only minor changes of calbindin D-28k immunoreactivity in the distal convoluted tubules and collecting ducts, irrelevant to the CCl(4) treatment. These findings might have significance since decreased immunolocalization of calretinin with CCl(4)-induced nephrotoxicity may contribute to the toxicity-related decrease in calcium transport or calcium buffering activity in the kidney.
