@Article{ecn.2007.0090,
AUTHOR = {Noemi Hernadfalvi, Wolfgang Langhans, Claudia von Meyenburg, Brigitte Onteniente, Denis Richard, Denis Arsenijevic},
TITLE = {Role for glutathione in the hyposensitivity of LPS-pretreated mice to LPS anorexia},
JOURNAL = {European Cytokine Network},
VOLUME = {18},
YEAR = {2007},
NUMBER = {2},
PAGES = {86--92},
URL = {http://www.techscience.com/ECN/v18n2/66000},
ISSN = {1952-4005},
ABSTRACT = {To study the role of the redox state regulator glutathione (GSH) in bacterial lipopolysaccharide
(LPS)-induced anorexia we measured total reduced GSH (trGSH) in liver, serum and brain in response to
intraperitoneal (ip) lipopolysaccharide (LPS, 4 lg/mouse) injection in LPS-naïve and LPS-pretreated (4 lg/mouse
given 3 days earlier) mice. LPS reduced food intake in LPS-naïve mice and LPS pretreatment attenuated this
effect. LPS decreased trGSH at 24 hours after injection in LPS-naïve mice but 4 days later trGSH levels were
upregulated in brain and liver, and this was associated with a significant attenuation of LPS-induced anorexia. In
addition, LPS increased mitochondrial GSH levels in brain and liver at 4 days after injection. Pharmacological
GSH depletion with diethylmaleate and L-buthionine sulfoximine in LPS-pretreated mice ablated the hyposen-sitivity
to the anorexic effect of LPS. Together, these findings suggest a prominent role for GSH and its
intracellular repartition in LPS anorexia.},
DOI = {10.1684/ecn.2007.0090}
}