Role of mitochondria in the differential action of sodium deoxycholate and ursodeoxycholic acid on rat duodenum

RODRIGUEZ V; PEREZ A; MARCHIONATTI A; RIVOIRA M; TOLOSA DE TALAMONI N

CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY

NATL RESEARCH COUNCIL CANADA-N R C RESEARCH PRESS

Lugar: Otawa; Año: 2021 vol. 99 p. 270 - 277

0008-4212

Sodiumdeoxycholate (NaDOC) inhibits the intestinal Ca2+ absorption andursodeoxycholic acid (UDCA) stimulates it. The aim of this study was todetermine whether NaDOC and UDCA produce differential effects on the redoxstate of duodenal mitochondria altering the Krebs cycle and the electrontransport chain (ETC) functioning, which could lead to perturbations in themitochondrial dynamics and biogenesis. Rat intestinal mitochondria wereisolated from untreated and treated animals with either NaDOC, UDCA or both. Krebscycle enzymes, ETC components, ATP synthase and mitochondrial dynamics andbiogenesis markers were determined. NaDOC decreased isocitrate dehydrogenase(ICDH) and malate dehydrogenase activities affecting the ETC and ATP synthesis.NaDOC also induced oxidative stress and increased the superoxide dismutaseactivity and impaired the mitochondrial biogenesis and functionality. UDCAincreased the activities of ICDH and complex II of ETC. The combination of bothBA conserved the functional activities of Krebs cycle enzymes, ETC components,oxidative phosphorylation and mitochondrial biogenesis. In conclusion, theinhibitory effect of NaDOC on intestinal Ca2+ absorption is mediatedby mitochondrial dysfunction, which is avoided by UDCA.  The stimulatory effect of UDCA alone isassociated with amelioration of mitochondrial functioning. This knowledge couldimprove treatment of diseases that affect the intestinal Ca2+absorption.