BUBR1 insufficiency in mice increases their sensitivity to oxidative stress

Daisuke Matsuda, Takuya Matsumoto, Kenichi Honma, Ayae Ikawa-Yoshida, Mitsuho Onimaru, Tadashi Furuyama, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Yoshihiko Maehara

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)

Abstract

Background/Aim: Budding uninhibited by benzimidazole-related 1 (BUBR1) plays an important role in the spindle assembly checkpoint to prevent chromosome missegregation and aneuploidy during mitosis. We previously generated mutant mice that express BUBR1 at only 20% of the normal level (BubR1L/L mice). Here, we examined the effect of low BUBR1 expression on oxidative stress-induced carcinogenesis in mice. Materials and Methods: We orally administered either a potassium bromate (KBrO3) solution (2 g/l) or tap water to BubR1L/L and wild-type (BubR1+/+) mice for 16 weeks and examined the subsequent incidence of tumours. Results: KBrO3-treated BubR1L/L mice showed significantly higher mortality than the KBrO3-treated BubR1+/+ and control tap water-treated mice (p=0.0082). Histopathological and immunohistochemical analyses revealed that the spleens of surviving BubR1L/L mice were occupied by non-B-, non-T-cells with high proliferative potential. Conclusion: Our results indicate that low BUBR1 expression increases oxidative stress-induced mortality in mice, possibly caused by splenic neoplasms.

Original languageEnglish
Pages (from-to)769-776
Number of pages8
JournalIn Vivo
Volume30
Issue number6
DOIs
Publication statusPublished - Nov 1 2016

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology

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