Sodium deoxycholate inhibits chick duodenal calcium absorption through oxidative stress and apoptosis

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• 作者：Marí ; a A. Rivoira ; Ana M. Marchionatti ; Viviana A. Centeno ; Gabriela E. Dí ; az de Barboza ; Marí ; a E. Peralta Ló ; pez ; Nori G. Tolosa de Talamoni ; ^{ntolosa@biomed.fcm.unc.edu.ar}
• 关键词：BAs ; bile acids ; BBM ; brush border membrane ; BLM ; basolateral membrane ; CAT ; catalase ; CB ; calbindin D28k ; DAB ; 3 ; 3&prime ; -diaminobenzidine ; ESR ; electron spin resonance ; GAPDH ; glyceraldehyde-3-phosphate dehydrogenase ; GI ; gastrointestinal ; GPx ; glutathi
• 刊名：Comparative Biochemistry and Physiology - Part A ; Molecular & Integrative Physiology
• 出版年：2012
• 期刊代码：23_10956433
• 类别：abs
• 出版时间：August, 2012
• 卷：162
• 期：4
• 页码：397-405
• 文件大小：3995 K

摘要

High concentrations of sodium deoxycholate (NaDOC) produce toxic effects. This study explores the effect of a single high concentration of NaDOC on the intestinal Ca^2 + absorption and the underlying mechanisms. Chicks were divided into two groups: 1) controls and 2) treated with different concentrations of NaDOC in the duodenal loop for variable times. Intestinal Ca^2 + absorption was measured as well as the gene and protein expressions of molecules involved in the Ca^2 + transcellular pathway. NaDOC inhibited the intestinal Ca^2 + absorption, which was concentration dependent. Ca^2 +-ATPase mRNA decreased by the bile salt and the same occurred with the protein expression of Ca^2 +-ATPase, calbindin D_28 k and Na⁺/Ca^2 + exchanger. NaDOC produced oxidative stress as judged by ROS generation, mitochondrial swelling and glutathione depletion. Furthermore, the antioxidant quercetin blocked the inhibitory effect of NaDOC on the intestinal Ca^2 + absorption. Apoptosis was also triggered by the bile salt, as indicated by the TUNEL staining and the cytochrome c release from the mitochondria. As a compensatory mechanism, enzyme activities of the antioxidant system were all increased. In conclusion, a single high concentration of NaDOC inhibits intestinal Ca^2 + absorption through downregulation of proteins involved in the transcellular pathway, as a consequence of oxidative stress and mitochondria mediated apoptosis.