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 Lettjournal_title
Neuroscience lettersauthors
Koch TR,Fink JG,Ruan E,Petro A,Opara ECdoi
10.1016/s0304-3940(97)00726-xsubject
Has Abstractpub_date
1997-10-10 00:00:00pages
77-80issue
1-2eissn
0304-3940issn
1872-7972pii
S0304-3940(97)00726-Xjournal_volume
235pub_type
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