Calretinin immunoreactivity in normal and carbon tetrachloride-induced nephrotoxic rats

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• 作者：Ki Young Kang^a ; ¹ ; Jin Nam Kim^b ; ¹ ; In Youb Chang^c ; ^d ; Sung Ho Park^e ; Sang Pil Yoon^c ; ^f ; ^{spyoon@jejunu.ac.kr"" rel=""nofollow}
• 关键词：Calretinin ; Carbon tetrachloride ; Kidney ; Proximal tubule ; Rat
• 刊名：Acta Histochemica
• 出版年：2011
• 出版时间：November 2011
• 年：2011
• 卷：113
• 期：7
• 页码：712-716
• 全文大小：989 K

文摘

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.