Litocholic acid prevents the inhibitory effect produced by sodium deoxycholate on the intestinal calcium absorption

MARCHIONATTI AM; PEREZ A; RIVOIRA M.A; RODRÍGUEZ V. A; TOLOSA DE TALAMONI N.

Congreso; XXXI Reunión Anual de la AAOMM; 2014

Bile acids (BA) and their salts are the major components of bile. Litocholic (LCA) and deoxycholic acids (DOC) are secondary bile acids that originated from the primary bile acids by intestinal microflora action. High concentrations of BA are cytotoxic and are considered to be involved in the pathogenesis of diseases such as colon cancer. In this laboratory, we have demonstrated that the DOC, by an oxidative mechanism, inhibits the intestinal calcium absorption affecting mitochondrial membrane and cell survival (Rivoira col. Comp Biochem Physiol 2012). The objective of this work was to determine whether LCA is capable of preventing the inhibitory effect of DOC and the individual effect that the LCA can trigger in the gut and its implications on the calcium absorption pathway. Four-week old chicks were used: 1) treated with physiological solution (controls), 2) treated with 10 mmol/l NaDOC, 3) treated with 200 μmol/l LCA and 4) treated with LCA + NaDOC in 30 min. Theintestinal Ca2+ absorption was measured as well as protein carbonyl content, alkaline phosphatase activity (AP), changes in mitochondria membrane permeability, Ca2+ pump, Na+/Ca+2 exchanger, calbindin D28K protein and gene expressions. In addition, claudin 2, 12 and TRPV6 gene expressions were determined. LCA alone did not alter the intestinal Ca2+ absorption. The combined treatment prevented the inhibitory effect caused by NaDOC on the intestinal Ca2+ absorption and returned the values of the protein and gene expression to control. LCA avoided the increment in the protein carbonyl content, the decrease in the AP activity and the changes in the mitochondrial membrane permeability produced by NaDOC. In conclusion, LCA prevented the effect produced by NaDOC on the intestinal Ca2+ absorption, at least in part, by blocking of the oxidative stress.