Host: The Japan Radiation Research Society
We have proposed that main route of radiation carcinogenesis is not targeted DNA molecules but induced from Long-Lived Radicals in intracellular proteins. Very recently we found Slow-Releasing Long-Lived Radicals (SRLLRs) in culture Syrian golden Hamster embryonic (SHE) cells those levels were gradually increased for 5h after gamma-ray irradiation of 4 Gy. Recent our experiments indicate that hydrogen peroxides derived from dysfunctional mitochondria by ionizing radiation, are responsible for producing SRLLRs. In order to confirm the effect of hydrogen peroxides on SRLLRs generation in the cells. DL-Buthionine-(S,R)-sulfoximine(BSO) or 3-Amino-1H-1,2,4-triazole(AT) for inhibiting glutathione synthesis or catalase, respectively, were treated to the cells for investigating relationships between the treatments and the levels of SRLLRs. Although increment of level of SRLLRs for 4 Gy irradiated cells at 5h after irradiation was 36%, that in BSO(0.1mM) treated cells was much increased as 86%. The treatment of AT and following gamma-ray irradiation of 4 Gy increased those levels 18 and 68%, respectively. These results indicate that glutathione or catalase ,as efficient scavengers of hydrogen peroxides in cells, are responsible for reducing levels of SRLLRs. Because addition of myxothiazole, as an inhibitor of electron transportation in mitochondria, suppressed the level of SRLLRs in irradiated cell, SRLLRs are likely to be produced by hydrogen peroxide from dysfunctional mitochondria by ionizing irradiation.
