Korean J Physiol Pharmacol 2004; 8(6): 345-350
Published online December 30, 2004
Copyright © Korean J Physiol Pharmacol.
Hwa Jin Jung, Won Hye Ka, Jee Na Hwang, and Young Rok Seo
Department of Pharmacology, Medical Research Center (MRC), Kyung Hee University School of Medicine, Seoul 130-701, South Korea
Heat shock (43oC for 60 minutes) is sufficient to induce apoptosis in a wide number of cell lines. In this study, we asked whether DNA strand breaks are responsible for this phenomenon. Using the highly sensitive comet assay for DNA damage detection, we were unable to demonstrate DNA breaks immediately after heat shock in Raji human lymphoid cells. It showed that DNA breaks were not necessary for hyperthermic apoptosis, since its activity is indicative of DNA lesions. Here, we present a suggestion that a protein(s) is the major target for heat shock apoptosis. We firstly found glycerol, which reportedly stabilizes protein structure, showed a protective effect in Raji cells against hyperthermic apoptosis. In addition, quercetin, which modulates transcription of the heat shock protein family members, enhanced apoptotic death induced by hyperthermia. Furthermore, Raji cells are protected by a pre-mild heat treatment prior to the killing dose of heat shock.
Keywords: Apoptosis, Hyperthermia, DNA damage, Heat shock protein, Comet assay
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