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

High concentrations of sodium deoxycholate (NaDOC) produce toxic effects. This study explores the effect of a single high concentration of NaDOC on the intestinal Ca2 + 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 Ca2 + absorption was measured as well as the gene and protein expressions of molecules involved in the Ca2 + transcellular pathway. NaDOC inhibited the intestinal Ca2 + absorption, which was concentration dependent. Ca2 +-ATPase mRNA decreased by the bile salt and the same occurred with the protein expression of Ca2 +-ATPase, calbindin D28 k and Na+/Ca2 + 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 Ca2 + 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 Ca2 + absorption through downregulation of proteins involved in the transcellular pathway, as a consequence of oxidative stress and mitochondria mediated apoptosis.