Chronic glutathione depletion alters expression of enteric inhibitory neurochemicals in the mouse.

Abstract:

:Antioxidants may delay or prevent neural diseases. Depletion of the non-enzymatic antioxidant, glutathione, in a mouse model was produced by inhibiting its rate-limiting enzyme, gamma-glutamylcysteine synthetase, for 7 weeks. Ileum and colon were obtained from treated and control (saline) mice. Glutathione levels and nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase activity were determined by spectrophotometric assays; vasoactive intestinal peptide (VIP) levels were measured by radioimmunoassay. Glutathione levels were higher in ileum than colon. Colonic glutathione was decreased in treated mice compared to controls; there were no differences in ileal glutathione levels. VIP was decreased in ileum compared to controls, while NADPH diaphorase activity was decreased in colon compared to controls. In this chronic mouse model, glutathione appeared to regulate expression of enteric inhibitory nerve cell products.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Koch TR,Fink JG,Ruan E,Petro A,Opara EC

doi

10.1016/s0304-3940(97)00726-x

subject

Has Abstract

pub_date

1997-10-10 00:00:00

pages

77-80

issue

1-2

eissn

0304-3940

issn

1872-7972

pii

S0304-3940(97)00726-X

journal_volume

235

pub_type

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