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

Autor: Rivoira MA; Laboratorio Dr. Fernando Cañas, Cátedra de Bioquímica y Biología Molecular, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Pabellón Argentina, 2do. Piso, Ciudad Universitaria, 5000 Córdoba, Argentina., Marchionatti AM, Centeno VA, Díaz de Barboza GE, Peralta López ME, Tolosa de Talamoni NG
Jazyk: angličtina
Zdroj: Comparative biochemistry and physiology. Part A, Molecular & integrative physiology [Comp Biochem Physiol A Mol Integr Physiol] 2012 Aug; Vol. 162 (4), pp. 397-405. Date of Electronic Publication: 2012 Apr 27.
DOI: 10.1016/j.cbpa.2012.04.016
Abstrakt: 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(28k) 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.
(Copyright © 2012 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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