Risk assessment of hydroquinone: Differential responses of cell growth and lethality correlated to hydroquinone concentration

Yang Jee Kim, Hae Dong Woo, Byeong Mo Kim, Young Joon Lee, Su Jin Kang, Yoon Hee Cho, Hai Won Chung

Research output: Contribution to journalArticlepeer-review

Abstract

Hydroquinone (HQ) is a major metabolite of benzene and has been used as an antioxidant, a stabilizer, a photographic reducer, and an ingredient in skin lighteners. In this study, the effects of low (5 M) and high (50 M) concentrations of HQ were investigated on cell growth and lethality in Jurkat cells. Intracellular reactive oxygen species (ROS) levels were increased with both HQ concentrations. Fifty micromolar HQ markedly increased phosphorylation of ERK and activation of caspase-9/-3, followed by PARP cleavage. The addition of ERK inhibitor PD98059 or N-acetylcysteine (NAC) abolished HQ-induced apoptosis. Five micromolar HQ activated ERK protein, but not JNK or p38. However, S-phase recruitment was decreased by preincubation with NAC, but not PD98059. Thus, high levels of ROS contributed to HQ-induced apoptosis via ERK signaling and the caspase pathway, whereas low quantities of ROS resulted in S-phase recruitment in the cell-cycle distribution.

Original languageEnglish
Pages (from-to)1272-1278
Number of pages7
JournalJournal of Toxicology and Environmental Health - Part A
Volume72
Issue number21-22
DOIs
StatePublished - Jan 2009

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