GLUTAMINE, AN ANTIAPOPTOTIC AGENT THAT PROTECTS THE INTESTINAL CALCIUM ABSORPTION AFFECTED BY MENADIONE

MOINE L; DÍAZ DE BARBOZA GE; PEREZ AV; TOLOSA DE TALAMONI N

Jornada; XVI Jornadas de Investigación Científica de la Facultad de Ciencias Médicas (JIC), UNC; 2015

We have previously shown that vitamin K3 or menadione(MEN) treatment produces oxidative stress and apoptosis of enterocytes, leadingto a decrease in the intestinal Ca2+ absorption. Since glutamine(GLN) is an amino acid with antiapoptotic properties, its administration might preventthe inhibitory effect of MEN. In fact, preliminary studies have earlier shownthat GLN prevented the inhibitory effect of MEN on the intestinal absorption ofthe cation. The aim of this study was to evaluate the anti-apoptotic ability ofGLN to protect the intestinal Ca2+ absorption inhibited by MEN. Todo this, the dose and time dependency of GLN effects were evaluated in Gallus gallus domesticus adult chicks. The intestinal Ca2+ absorptionwas measured by the in situ ligated intestinalloop technique. Apoptosis was assessed by DNA fragmentation using the TUNELtechnique, expression of pro- and anti-apoptotic proteins by western blot andcaspase 3 activity by ELISA. Data were analyzed by one way ANOVA and Bonferronipost hoc test, consideringsignificant differences at p <0.05. The results indicate that the lowestdose and time of treatment for the prevention of intestinal Ca2+ absorptionwas 0.5 g GLN / kg of body weight (b.w.) supplied orally 30 min before 2.5 molof MEN / kg b.w. per via intraperitoneal. GLN avoided the increase in the TUNELpositive cells and in the caspase 3 activity produced by the quinone. Inaddition, GLN blocked the enhancement in the protein expression ofpro-apoptotic molecule FAS induced by MEN. GLN did not prevent the decreasedexpression of anti-apoptotic protein calbindin D28k. Bax protein expression wasnot changed by any treatment. In conclusion, 0.5 g GLN / kg b.w. 30 min beforeMEN treatment protects enterocyte apoptosis triggered by MEN. Probably, thiseffect is due to the blockage of the extrinsic apoptotic pathway mediated byFAS. GLN would protect the intestinal Ca2+ absorption through maintenanceof the number of cells with absorptive capacity of the cation.