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N-t-Butyl hydroxylamine regulates ionizing radiation-induced apoptosis in U937 cells.
Biochimie. 2007 Dec; 89(12):1509-16.B

Abstract

Ionizing radiation induces the production of reactive oxygen species, which play an important causative role in apoptotic cell death. Therefore, compounds that scavenge reactive oxygen species may confer regulatory effects on apoptosis. Recently, it has been shown that the decomposition product of the spin-trapping agent alpha-phenyl-N-t-butylnitrone, N-t-butyl hydroxylamine (NtBHA), mimics alpha-phenyl-N-t-butylnitrone and is much more potent in delaying reactive oxygen species-associated senescence. We investigated the effects of NtBHA on ionizing radiation-induced apoptosis. Upon exposure to 2Gy of gamma-irradiation, there was a distinct difference between the control cells and the cells pre-treated with 0.1mM NtBHA for 2h in regard to apoptotic parameters, cellular redox status, mitochondria function, and oxidative damage to cells. NtBHA effectively suppressed morphological evidence of apoptosis and DNA fragmentation in U937 cells exposed to ionizing radiation. The generation of intracellular reactive oxygen species was higher and the GSH level was lower in control cells compared to NtBHA-treated cells. The ionizing radiation-induced mitochondrial damage reflected by the altered mitochondrial permeability transition, the increase in the accumulation of reactive oxygen species, and the reduction of ATP production were significantly higher in control cells compared to NtBHA-treated cells. NtBHA pre-treated cells showed significant inhibition of apoptotic features such as activation of caspase-3, up-regulation of Bax and p53, and down-regulation of Bcl-2 compared to control cells upon exposure to ionizing radiation. This study indicates that NtBHA may play an important role in regulating the apoptosis induced by ionizing radiation presumably through scavenging of reactive oxygen species.

Authors+Show Affiliations

School of Life Sciences and Biotechnology, College of Natural Sciences, Kyungpook National University, Taegu 702-701, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17764803

Citation

Lee, Jin Hyup, et al. "N-t-Butyl Hydroxylamine Regulates Ionizing Radiation-induced Apoptosis in U937 Cells." Biochimie, vol. 89, no. 12, 2007, pp. 1509-16.
Lee JH, Tak JK, Park KM, et al. N-t-Butyl hydroxylamine regulates ionizing radiation-induced apoptosis in U937 cells. Biochimie. 2007;89(12):1509-16.
Lee, J. H., Tak, J. K., Park, K. M., & Park, J. W. (2007). N-t-Butyl hydroxylamine regulates ionizing radiation-induced apoptosis in U937 cells. Biochimie, 89(12), 1509-16.
Lee JH, et al. N-t-Butyl Hydroxylamine Regulates Ionizing Radiation-induced Apoptosis in U937 Cells. Biochimie. 2007;89(12):1509-16. PubMed PMID: 17764803.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - N-t-Butyl hydroxylamine regulates ionizing radiation-induced apoptosis in U937 cells. AU - Lee,Jin Hyup, AU - Tak,Jean Kyoung, AU - Park,Kwon Moo, AU - Park,Jeen-Woo, Y1 - 2007/07/24/ PY - 2007/03/31/received PY - 2007/07/18/accepted PY - 2007/9/4/pubmed PY - 2008/4/9/medline PY - 2007/9/4/entrez SP - 1509 EP - 16 JF - Biochimie JO - Biochimie VL - 89 IS - 12 N2 - Ionizing radiation induces the production of reactive oxygen species, which play an important causative role in apoptotic cell death. Therefore, compounds that scavenge reactive oxygen species may confer regulatory effects on apoptosis. Recently, it has been shown that the decomposition product of the spin-trapping agent alpha-phenyl-N-t-butylnitrone, N-t-butyl hydroxylamine (NtBHA), mimics alpha-phenyl-N-t-butylnitrone and is much more potent in delaying reactive oxygen species-associated senescence. We investigated the effects of NtBHA on ionizing radiation-induced apoptosis. Upon exposure to 2Gy of gamma-irradiation, there was a distinct difference between the control cells and the cells pre-treated with 0.1mM NtBHA for 2h in regard to apoptotic parameters, cellular redox status, mitochondria function, and oxidative damage to cells. NtBHA effectively suppressed morphological evidence of apoptosis and DNA fragmentation in U937 cells exposed to ionizing radiation. The generation of intracellular reactive oxygen species was higher and the GSH level was lower in control cells compared to NtBHA-treated cells. The ionizing radiation-induced mitochondrial damage reflected by the altered mitochondrial permeability transition, the increase in the accumulation of reactive oxygen species, and the reduction of ATP production were significantly higher in control cells compared to NtBHA-treated cells. NtBHA pre-treated cells showed significant inhibition of apoptotic features such as activation of caspase-3, up-regulation of Bax and p53, and down-regulation of Bcl-2 compared to control cells upon exposure to ionizing radiation. This study indicates that NtBHA may play an important role in regulating the apoptosis induced by ionizing radiation presumably through scavenging of reactive oxygen species. SN - 0300-9084 UR - https://www.unboundmedicine.com/medline/citation/17764803/N_t_Butyl_hydroxylamine_regulates_ionizing_radiation_induced_apoptosis_in_U937_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0300-9084(07)00186-1 DB - PRIME DP - Unbound Medicine ER -