Journal
TOXICOLOGY MECHANISMS AND METHODS
Volume 25, Issue 3, Pages 223-228Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/15376516.2015.1034334
Keywords
Arsenic trioxide; buthionine sulfoximine; genotoxicity; glutathione; mouse bone marrow cells; N-acetyl-L-cysteine
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Funding
- UGC-DAE-CSR Kolkata
- UGC
- NASI
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Generation of reactive oxygen species is one of the major contributors in arsenic-induced genotoxicity where reduced glutathione (GSH) could be an important determining factor. To understand the role of endogenous GSH, arsenic trioxide (As2O3) was administered in buthionine sulfoximine (BSO)- and N-acetyl-L-cysteine (NAC)-treated mice. As2O3-induced significant chromosome aberrations (CAs) in all treatment groups compared with the control. BSO-treated mouse bone marrow cells showed significant CAs at a dose of 2 mg As2O3 kg(-1) b.w. Similar induction was not evident at 4 mg As2O3 kg(-1) b.w. and exhibited antagonistic effect at 8 mg As2O3 kg(-1) b.w. To understand this differential effect, expression pattern of Nrf2 was observed. Nrf2 expression increased following As2O3 treatment in a dose-dependent manner up to 4 mg As2O3 kg(-1) b.w after which no further increase was noticed. NAC pre-treatment significantly reduced the extent of As2O3-induced CAs suggesting the protective role of endogenous GSH against arsenic-induced genotoxicity.
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