NDLI: Methylglyoxal-bis(guanylhydrazone), a polyamine analogue, sensitized Î³-radiation-induced cell death in HL-60 leukemia cells Sensitizing effect of MGBG on Î³-radiation-induced cell death.

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Methylglyoxal-bis(guanylhydrazone), a polyamine analogue, sensitized Î³-radiation-induced cell death in HL-60 leukemia cells Sensitizing effect of MGBG on Î³-radiation-induced cell death.

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Methylglyoxal-bis(guanylhydrazone), a polyamine analogue, sensitized Î³-radiation-induced cell death in HL-60 leukemia cells Sensitizing effect of MGBG on Î³-radiation-induced cell death.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kim, Jin Sik Lee, Jin Chung, Hai Won Choi, Han Paik, Sang Gi Kim, In Gyu
Description	Author Affiliation: Kim JS ( Department of Radiation Biology, Environment Radiation Research Group, Korea Atomic Energy Research Institute, P.O. Box 105, Yusong, Daejon 305-600, Republic of Korea.)
Abstract	Methylglyoxal-bis(guanylhydrazone) (MGBG), a polyamine analogue, has been known to inhibit the biosynthesis of polyamines, which are important in cell proliferation. We showed that MGBG treatment significantly affected Î³-radiation-induced cell cycle transition (G(1)/G(0)âSâG(2)/M) and thus Î³-radiation-induced cell death. As determined by micronuclei and comet assay, we showed that it sensitized the cytotoxic effect induced by Î³-radiation. One of the reasons is that polyamine depletion by MGBG treatment did not effectively protect against the chemical (OH) or physical damage to DNA caused by Î³-radiation. Through in vitro experiment, we confirmed that DNA strand breaks induced by Î³-radiation was prevented more effectively in the presence of polyamines (spermine and spermidine) than in the absence of polyamines. MGBG also blocks the cell cycle transition caused by Î³-radiation (G(2) arrest), which helps protect cells by allowing time for DNA repair before entry into mitosis or apoptosis, via the down regulation of cyclin D1, which mediates the transition from G(1) to S phase of cell cycle, and ataxia telangiectasia mutated, which is involved in the DNA sensing, repair and cell cycle check point. Therefore, the abrogation of G(2) arrest sensitizes cells to the effect of Î³-radiation. As a result, Î³-radiation-induced cell death increased by about 2.5-3.0-fold in cells treated with MGBG. However, exogenous spermidine supplement partially relieved this Î³-radiation-induced cytotoxicity and cell death. These findings suggest a potentially therapeutic strategy for increasing the cytotoxic efficacy of Î³-radiation.
File Format	HTM / HTML
ISSN	13826689
Issue Number	2
Journal	Environmental Toxicology and Pharmacology
Volume Number	22
e-ISSN	18727077
Language	English
Publisher	Elsevier
Publisher Date	2006-09-01
Publisher Place	Netherlands
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Environmental Health Discipline Pharmacology
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Medicine Toxicology Pharmacology

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