Abstract:
:Nitric oxide (NO) has been shown to be cytotoxic for normal and transformed cell lines. One of the intracellular targets for NO action is glutathione (GSH). GSH determinates cellular redox potential and modulates several biological events. During oxidative and nitrosative stress, glutathione system imbalance is associated with the upregulation of gamma-glutamylcysteine synthetase (gamma-GCS) expression, which is mediated by nuclear factor kappaB (NF-kappaB). Our previous studies demonstrated a cytotoxic effect of NO and taxol on human lymphoblastic leukemia cells triggered by inhibition of NF-kappaB activity. In this study, we have demonstrated the involvement of GSH in taxol- and NO-induced cytotoxic effects on human CEM leukemia cells. NO- and taxol-induced a depletion of GSH levels in CEM cells, which was potentialized by l-buthionine-S,R-sulfoximine (BSO), an inhibitor of gamma-GCS. BSO induced an increase in nuclear translocation of NF-kappaB. However, when cells were treated with NO or taxol in association with BSO, these compounds inhibited the constitutive activity of NF-kappaB. These results suggest that oxidative and nitrosative damage in lymphoblastic leukemia cells shall be mediated by NO- and taxol-induced GSH depletion as a consequence of preventing GSH synthesis.
journal_name
Leuk Resjournal_title
Leukemia researchauthors
Santos-Silva MC,Freitas MS,Assreuy Jdoi
10.1016/j.leukres.2005.06.021keywords:
subject
Has Abstractpub_date
2006-02-01 00:00:00pages
145-52issue
2eissn
0145-2126issn
1873-5835pii
S0145-2126(05)00262-6journal_volume
30pub_type
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pub_type: 杂志文章,多中心研究
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pub_type: 杂志文章
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journal_title:Leukemia research
pub_type: 杂志文章
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