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Cited by 360

The DOI matches its Crossref record; 126 of the 126 references it cites were found in a registry or an index.

Regulation of Neuronal Glutathione Synthesis

Open access
Aoyama, Koji, Watabe, Masahiko, Nakaki, Toshio·2008·Journal of Pharmacological Sciences

Abstract

The brain is among the major organs generating large amounts of reactive oxygen species and is especially susceptible to oxidative stress. Glutathione (GSH) plays critical roles as an antioxidant, enzyme cofactor, cysteine storage form, the major redox buffer, and a neuromodulator in the central nervous system. GSH deficiency has been implicated in neurodegenerative diseases. GSH is a tripeptide comprised of glutamate, cysteine, and glycine. Cysteine is the rate-limiting substrate for GSH synthesis within neurons. Most neuronal cysteine uptake is mediated by sodium-dependent excitatory amino acid transporter (EAAT) systems, known as excitatory amino acid carrier 1 (EAAC1). Previous studies demonstrated EAAT is vulnerable to oxidative stress, leading to impaired function. A recent study found EAAC1-deficient mice to have decreased brain GSH levels and increased susceptibility to oxidative stress. The function of EAAC1 is also regulated by glutamate transporter associated protein 3-18. This review focuses on the mechanisms underlying GSH synthesis, especially those related to neuronal cysteine transport via EAAC1, as well as on the importance of GSH functions against oxidative stress.

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Metadata

Authors
Aoyama, K., Watabe, M., & Nakaki, T.
Venue
Journal of Pharmacological Sciences
Published
2008
Volume
108
Issue
3
Pages
227-238
ISSN
  • 1347-8613 (ISSN-L)
  • 1347-8648
OpenAlex
W2049225057
Cited by
360
References
126
FWCI
8.37
Type
journal article
Language
en
Open access
bronze

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Aoyama, K., Watabe, M., & Nakaki, T. (2008). Regulation of Neuronal Glutathione Synthesis. Journal of Pharmacological Sciences. https://doi.org/10.1254/jphs.08r01cr

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