N-t-Butyl hydroxylamine regulates heat shock-induced apoptosis in U937 cells

Authors: Kim, Hyun Jeong1; Shin, Seoung Woo1; Oh, Chang Joo1; Lee, Mann Hyung2; Yang, Chae Ha3; Park, Jeen-Woo1

Source: Redox Report, Volume 10, Number 6, December 2005 , pp. 287-293(7)

Publisher: Maney Publishing

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Abstract:

Heat shock may increase oxidative stress due to increased production of reactive oxygen species and/or the promotion of cellular oxidation events. Therefore, compounds that scavenge reactive oxygen species may regulate heat shock-induced cell death. Recently, it has been shown that the decomposition product of the spin-trapping agent α-phenyl-N-t-butylnitrone, N-t-butyl hydroxylamine (NtBHA), mimics α-phenyl-N-t-butylnitrone and is much more potent in delaying reactive oxygen species-associated senescence. We investigated the protective role of NtBHA against heat shock-induced apoptosis in U937 cells. Upon exposure to heat shock, there was a distinct difference between the untreated cells and the cells pre-treated with 0.1 mM NtBHA for 2 h in regard to apoptotic parameters, cellular redox status, and mitochondrial function. Upon exposure to heat shock, NtBHA pre-treated cells showed significant inhibition of apoptotic features such as activation of caspase-3, up-regulation of Bax, and down-regulation of Bcl-2 compared to untreated cells. This study indicates that NtBHA may play an important role in regulating the apoptosis induced by heat shock, presumably through scavenging of reactive oxygen species.

Keywords: HEAT SHOCK; N-T-BUTYL HYDROXYLAMINE; U937; APOPTOSIS; REDOX STATUS

Document Type: Research article

DOI: 10.1179/135100005X83662

Affiliations: 1: School of Life Sciences and Biotechnology, College of Natural Sciences, Kyungpook National University, Taegu, Korea 2: Daegu-Catholic University, Hayang, Korea 3: Daegu Haany University, Taegu, Korea

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