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 Printable version |
Role for glutathione in the hyposensitivity of LPS-pretreated mice to LPS anorexia |
European Cytokine Network. Volume 18, Number 2, 39-45, June 2007, Research papers
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 Free Article
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Author(s) : Noemi Hernadfalvi, Wolfgang Langhans, Claudia von Meyenburg, Brigitte Onteniente, Denis Richard, Denis Arsenijevic |
Summary : 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. |
Keywords : reactive oxygen species, cytokine, food intake, liver, brain, mitochondria |
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