BENEDETTO MARIA MERCEDES
Congresos y reuniones científicas
Título:
Oral administration of glutamine prevents oxidative stress triggered by menadione in duodenal enterocytes
Autor/es:
DÍAZ DE BARBOZA G.E; BENEDETTO M.M; TOLOSA DE TALAMONI N.G
Lugar:
Buenos Aires
Reunión:
Otro; XXVIII Reunión Anual de la Asociación Argentina de Osteología y Metabolismo Mineral; 2011
Institución organizadora:
Asociación Argentina de Osteología y Metabolismo Mineral
Resumen:
We have previously demonstrated that menadione (MEN) decreases intestinal calcium
absorption triggering oxidative stress and apoptotic death of enterocytes. The aminoacid
glutamine (GLN) has restorative and protective properties of the redox state in tissues
exposed to oxidant drugs. In this work we studied the possible role of GLN on the oxidative
stress induced by MEN in enterocytes. Chickens (4 weeks old Cobb-Harding) were fed a
commercial diet. Controls were treated with vehicle and the treated group with 1 g GLN/kg
bw per os and with MEN 12.5 μmol/kg bw intraperitoneally (60 or 90 min later). Both drugs
acted together for 30 min. Glutathione (GSH) content was quantified by enzymatic method.
The activity of catalase (CAT) and superoxide dismutase (SOD) was determined in duodenal
mucosa homogenates by spectrophotometry. GLN administration 60 or 90 min before MEN
injection increased 30–35% GSH levels, restoring the control values. GLN prevented the
induction of CAT activity by MEN (Control 14.06±0.69; MEN 23.51±1.94*; GLN60 min+
MEN 17.15±0.96 and GLN90 min+MEN 17.89±1.04 U/mg of protein; *p<0.001 vs
Control). Similarly, GLN avoided the increase in SOD activity produced by MEN (Control
10.95±1.11, MEN 20.34±1.87*, GLN60 min+MEN 12.66±1.08 and GLN90 min+MEN
11.06±2.15 U/mg protein, *p <0.05 vs Control). The data suggest that GLN is capable of
preventing the oxidative effect induced by MEN administration in duodenal enterocytes, as
shown by the restoration of control values in intracellular GSH content and in the activity of
CAT and SOD. Future studies should evaluate if cellular redox state restoration may prevent
the loss of intestinal Ca absorption caused by MEN.
absorption triggering oxidative stress and apoptotic death of enterocytes. The aminoacid
glutamine (GLN) has restorative and protective properties of the redox state in tissues
exposed to oxidant drugs. In this work we studied the possible role of GLN on the oxidative
stress induced by MEN in enterocytes. Chickens (4 weeks old Cobb-Harding) were fed a
commercial diet. Controls were treated with vehicle and the treated group with 1 g GLN/kg
bw per os and with MEN 12.5 μmol/kg bw intraperitoneally (60 or 90 min later). Both drugs
acted together for 30 min. Glutathione (GSH) content was quantified by enzymatic method.
The activity of catalase (CAT) and superoxide dismutase (SOD) was determined in duodenal
mucosa homogenates by spectrophotometry. GLN administration 60 or 90 min before MEN
injection increased 30–35% GSH levels, restoring the control values. GLN prevented the
induction of CAT activity by MEN (Control 14.06±0.69; MEN 23.51±1.94*; GLN60 min+
MEN 17.15±0.96 and GLN90 min+MEN 17.89±1.04 U/mg of protein; *p<0.001 vs
Control). Similarly, GLN avoided the increase in SOD activity produced by MEN (Control
10.95±1.11, MEN 20.34±1.87*, GLN60 min+MEN 12.66±1.08 and GLN90 min+MEN
11.06±2.15 U/mg protein, *p <0.05 vs Control). The data suggest that GLN is capable of
preventing the oxidative effect induced by MEN administration in duodenal enterocytes, as
shown by the restoration of control values in intracellular GSH content and in the activity of
CAT and SOD. Future studies should evaluate if cellular redox state restoration may prevent
the loss of intestinal Ca absorption caused by MEN.
