European Cytokine Network
MENURole for glutathione in the hyposensitivity of LPS-pretreated mice to LPS anorexia Volume 18, numéro 2, June 2007
Illustrations
- Mots-clés : reactive oxygen species, cytokine, food intake, liver, brain, mitochondria
- DOI : 10.1684/ecn.2007.0090
- Page(s) : 39-45
- Année de parution : 2007
To study the role of the redox state regulator glutathione (GSH) in bacterial lipopolysaccharide (LPS)-induced anorexia we measured GSH in liver, serum and brain in response to intraperitoneal (ip) lipopolysaccharide (LPS, 4μg/mouse) injection in LPS-naïve and LPS-pretreated (4 μg/mouse) mice. LPS reduced food intake in LPS-naïve mice and LPS pretreatment attenuated this effect. LPS reduced total reduced GSH at 24 hours after injection in LPS-naïve mice. On the other hand, LPS pretreatment caused an upregulation of GSH levels in brain and liver, and this was associated with a significant attenuation of LPS-induced anorexia. In addition, LPS pretreatment increased mitochondrial GSH levels in brain and liver. Pharmacological GSH depletion with diethylmaleate and L-buthionine sulfoximine in LPS-pretreated mice ablated the hyposensitivity to the anorexic effect of LPS. Together, these findings suggest a prominent role for GSH and its intracellular repartition in LPS anorexia.