Glutamine protects intestinal calcium absorption against oxidative stress and apoptosis

DÍAZ DE BARBOZA, GABRIELA; TOLOSA DE TALAMONI, NORI; MOINE, LUCIANA; BENEDETTO, MERCEDES; PÉREZ, ADRIANA

COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-MOLECULAR AND INTEGRATIVE PHYSIOLOGY

ELSEVIER SCIENCE INC

Lugar: Amsterdam; Año: 2017 vol. 212 p. 64 - 71

1095-6433

The aim of this study is to investigate whether glutamine (GLN) could block the inhibition of the intestinal Ca2+ absorption caused by menadione (MEN), and dilucidate the underlying mechanisms. To do this, one-month old chicks were divided in four groups: 1) controls, 2) MEN treated, 3) GLN treated and 4) GLN treated before or after MEN treatment. Intestinal Ca2+ absorption as well as protein expression of molecules involved in the transcellular Ca2+ pathway were determined. Glutathione (GSH) and superoxide anion and activity of enzymes of the antioxidant system were evaluated. Apoptosis was measured by the TUNEL technique, expression of FAS and FASL and caspase-3 activity. A prior dose of 0.5 g GLN/kg of b.w. was necessary to show its protector effect and a dose of 1 g/kg of b.w. could restore the intestinal Ca2+ absorption after MEN treatment. GLN alone did not modify the protein expression of calbindin D28k and plasma membrane Ca2+-ATPase, but blocked the inhibitory effect of the quinone. GLN avoided changes in the intestinal redox state provoked by MEN such as a decrease in the GSH content and increases in the superoxide anion and in the SOD and CAT activities. GLN abrogated apoptotic effects caused by MEN in intestinal mucosa, as indicated by the reduction of TUNEL (+) cells and the FAS/FASL/caspase-3 pathway. In conclusion, GLN could be a drug of choice to normalize the redox state and the proliferation/cell death ratio in the small intestine improving the intestinal Ca2+ absorption altered by oxidative stress.