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Annotation

Do KQ, Trabesinger AH, Kirsten-Krüger M, Lauer CJ, Dydak U, Hell D, Holsboer F, Boesiger P, Cuénod M. Schizophrenia: glutathione deficit in cerebrospinal fluid and prefrontal cortex in vivo. Eur J Neurosci . 2000 Oct ; 12(10):3721-8. PubMed Abstract

Comments on Paper and Primary News
Primary News: Schizophrenia: a Case of Faulty Redox Detox?

Comment by:  Richard Deth
Submitted 25 November 2007 Posted 28 November 2007
  I recommend this paper

Identification of a limitation in the capacity for glutathione (GSH) synthesis by Gysin and colleagues raises several questions: "How could a redox problem (i.e., oxidative stress) lead to schizophrenia?” and "Does this finding mesh with other hypotheses?"

All cells must maintain sufficient levels of GSH to survive collateral damage from oxidative metabolism, and a number of adaptive mechanisms have evolved to meet this need. One important example is inhibition of the enzyme methionine synthase by oxidative stress. The higher the oxidative stress level, the greater the inhibition of its methylation of homocysteine to methionine, allowing the accumulating homocysteine to be diverted to GSH synthesis via the trans-sulfuration pathway. Homocysteine levels are elevated in schizophrenia, especially, but not exclusively, in first-episode males (Regland et al., 1995; Haidemenos et al., 2007), implying that methionine synthase is inhibited, perhaps by oxidative stress. Importantly,...  Read more


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