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Glutamine protects intestinal calcium absorption against oxidative stress and apoptosis
Luciana Moine1, Gabriela Díaz de Barboza1, Adriana Pérez1
1Laboratorio "Dr. Fernando Cañas", Cátedra de Bioquímica y Biología Molecular, Facultad de Ciencias Médicas, INICSA, CONICET-Universidad Nacional de Córdoba, Pabellón Argentina, 2do. Piso, Ciudad Universitaria, 5000 Córdoba, Argentina.
Abstract:
The aim of this study was to investigate whether glutamine (GLN) could block the inhibition of the intestinal Ca2+ absorption caused by menadione (MEN), and elucidate 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, the expression of FAS and FASL and the caspase-3 activity. A previous dose of 0.5gGLN/kg of b.w. was necessary to show its protector effect and a dose of 1g/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 an oral nutritional supplement to normalize the redox state and the proliferation/cell death ratio in the small intestine improving the intestinal Ca2+ absorption altered by oxidative stress.
Insights
Glutamine (GLN) supplementation can protect intestinal calcium absorption from menadione (MEN)-induced damage by restoring redox balance and reducing apoptosis in the small intestine.
Area of Science:
- Nutritional biochemistry
- Gastroenterology
- Cellular physiology
Background:
- Menadione (MEN) is known to impair intestinal calcium (Ca2+) absorption.
- Oxidative stress and apoptosis are implicated in MEN-induced intestinal damage.
- The protective role of glutamine (GLN) against such damage requires elucidation.
Purpose of the Study:
- To investigate if glutamine (GLN) can prevent the inhibition of intestinal Ca2+ absorption caused by menadione (MEN).
- To elucidate the underlying mechanisms of GLN's protective effects, focusing on redox state and apoptosis.
Main Methods:
- One-month-old chicks were used, divided into control, MEN-treated, GLN-treated, and combined treatment groups.
- Intestinal Ca2+ absorption, transcellular Ca2+ pathway protein expression, glutathione (GSH) levels, superoxide anion production, antioxidant enzyme activities (SOD, CAT), and apoptosis markers (TUNEL, FAS, FASL, caspase-3) were assessed.
Main Results:
- A dose of 1g/kg body weight glutamine (GLN) restored intestinal Ca2+ absorption inhibited by menadione (MEN).
- GLN prevented MEN-induced alterations in intestinal redox state, including decreased GSH and increased superoxide anion.
- GLN abrogated MEN-induced apoptosis in the intestinal mucosa by reducing TUNEL-positive cells and modulating the FAS/FASL/caspase-3 pathway.
Conclusions:
- Glutamine (GLN) acts as a protective agent against menadione (MEN)-induced intestinal damage.
- GLN normalizes the redox state and the proliferation/cell death ratio in the small intestine.
- GLN supplementation holds potential as an oral nutritional strategy to improve intestinal Ca2+ absorption compromised by oxidative stress.
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