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Titolo:
Pyruvate released by astrocytes protects neurons from copper-catalyzed cysteine neurotoxicity
Autore:
Wang, XF; Cynader, MS;
Indirizzi:
Univ British Columbia, Brain Res Ctr, Vancouver, BC V5Z 3N9, Canada Univ British Columbia Vancouver BC Canada V5Z 3N9 ver, BC V5Z 3N9, Canada Univ British Columbia, Dept Ophthalmol, Vancouver, BC V5Z 3N9, Canada UnivBritish Columbia Vancouver BC Canada V5Z 3N9 ver, BC V5Z 3N9, Canada Vancouver Hosp & Hlth Sci Ctr, Vancouver, BC V5Z 3N9, Canada Vancouver Hosp & Hlth Sci Ctr Vancouver BC Canada V5Z 3N9 V5Z 3N9, Canada
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 10, volume: 21, anno: 2001,
pagine: 3322 - 3331
SICI:
0270-6474(20010515)21:10<3322:PRBAPN>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
BLOOD-BRAIN-BARRIER; AMYOTROPHIC-LATERAL-SCLEROSIS; CEREBROSPINAL-FLUID; RAT-BRAIN; TRANSITION-METALS; HYDROGEN-PEROXIDE; WILSONS-DISEASE; GLUTATHIONE DISULFIDE; GLUCOSE DEPRIVATION; PARKINSONS-DISEASE;
Keywords:
glia; glutathione; toxicity; oxidative stress; transition metal; autoxidation; conditioned medium;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
69
Recensione:
Indirizzi per estratti:
Indirizzo: Wang, XF Univ British Columbia, Brain Res Ctr, 2550 Willow St, Vancouver, BC V5Z 3N9, Canada Univ British Columbia 2550 Willow St Vancouver BC CanadaV5Z 3N9
Citazione:
X.F. Wang e M.S. Cynader, "Pyruvate released by astrocytes protects neurons from copper-catalyzed cysteine neurotoxicity", J NEUROSC, 21(10), 2001, pp. 3322-3331

Abstract

We have found previously that astrocytes can provide cysteine to neurons. However, cysteine has been reported to be neurotoxic although it plays a pivotal role in regulating intracellular levels of glutathione, the major cellular antioxidant. Here, we show that cysteine toxicity is a result of hydroxyl radicals generated during cysteine autoxidation. Transition metal ionsare candidates to catalyze this process. Copper substantially accelerates the autoxidation rate of cysteine even at submicromolar levels, whereas iron and other transition metal ions, including manganese, chromium, and zinc,are less efficient. The autoxidation rate of cysteine in rat CSF is equal to that observed in the presence of similar to0.2 muM copper. In tissue culture tests, we found that cysteine toxicity depends highly on its autoxidation rate and on the total amount of cysteine being oxidized, suggesting that the toxicity can be attributed to the free radicals produced from cysteine autoxidation, but not to cysteine itself. We have also explored the in vivo mechanisms that protect against cysteinetoxicity. Catalase and pyruvate were each found to inhibit the production of hydroxyl radicals generated by cysteine autoxidation. In tissue culture,they both protected primary neurons against cysteine toxicity catalyzed bycopper. This protection is attributed to their ability to react with hydrogen peroxide, preventing the formation of hydroxyl radicals. Pyruvate, but not catalase or glutathione peroxidase, was detected in astrocyte-conditioned medium and CSF. Our data therefore suggest that astrocytes can prevent cysteine toxicity by releasing pyruvate.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 19:49:10