Evaluation of sodium orthovanadate as a radioprotective agent under total-body irradiation and partial-body irradiation conditions in mice

Nishiyama, Yuichi; Morita, Akinori; Wang, Bing; Sakai, Takayuki; Ramadhani, Dwi; Satoh, Hidetoshi; Tanaka, Kaoru; Sasatani, Megumi; Ochi, Shintaro; Tominaga, Masahide; Ikushima, Hitoshi; Ueno, Junji; Nenoi, Mitsuru; Aoki, Shin

doi:10.1080/09553002.2021.1941377

Cited by 4 publications

(2 citation statements)

References 37 publications

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“…The finding from 30-day survival tests that isorhamnetin had no efficacy in reducing TBI lethality supports this conclusion. It has been well documented that p53-dependent apoptosis of bone marrow cells contributes to the pathogenesis of radiation HP syndrome [5,23], and that the syndrome can be effectively suppressed by p53 inhibition [6][7][8][9][10]. Considering the fact that isorhamnetin did not strongly inhibit p53 activity and has no antiapoptotic effect, its ineffectiveness against bone marrow death may be somewhat reasonable.…”

Section: Discussionmentioning

confidence: 99%

“…Tumor suppressor p53 is a primary regulator in radiation response and is well known as a transcription factor which is closely associated with apoptosis [1], cell cycle control [2], and DNA damage response [3]. Several studies demonstrated that p53 functions in a different way between tissues [4][5][6]. p53 causes apoptosis in irradiated hematopoietic lineages that leads to HP syndrome, and some p53 inhibitors have been shown to rescue mice from HP syndrome caused by total-body irradiation (TBI) [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

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Isorhamnetin Promotes 53BP1 Recruitment through the Enhancement of ATM Phosphorylation and Protects Mice from Radiation Gastrointestinal Syndrome

Nishiyama

Morita

Tatsuta

et al. 2021

Genes

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Flavonoids are a subclass of polyphenols which are attractive, due to possessing various physiological activities, including a radioprotective effect. Tumor suppressor p53 is a primary regulator in the radiation response and is involved in the pathogenesis of radiation injuries. In this study, we revealed that isorhamnetin inhibited radiation cell death, and investigated its action mechanism focusing on DNA damage response. Although isorhamnetin moderated p53 activity, it promoted phosphorylation of ataxia telangiectasia mutated (ATM) and enhanced 53BP1 recruitment in irradiated cells. The radioprotective effect of isorhamnetin was not observed in the presence of ATM inhibitor, indicating that its protective effect was dependent on ATM. Furthermore, isorhamnetin-treated mice survived gastrointestinal death caused by a lethal dose of abdominal irradiation. These findings suggested that isorhamnetin enhances the ATM-dependent DNA repair process, which is presumably associated with the suppressive effect against GI syndrome.

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