| First Author | Matsuda D | Year | 2016 |
| Journal | In Vivo | Volume | 30 |
| Issue | 6 | Pages | 769-776 |
| PubMed ID | 27815460 | Mgi Jnum | J:312177 |
| Mgi Id | MGI:6783206 | Doi | 10.21873/invivo.10993 |
| Citation | Matsuda D, et al. (2016) BUBR1 Insufficiency in Mice Increases their Sensitivity to Oxidative Stress. In Vivo 30(6):769-776 |
| abstractText | 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 (BubR1(L/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 BubR1(L/L) and wild-type (BubR1(+/+))mice for 16 weeks and examined the subsequent incidence of tumours. RESULTS: KBrO3-treated BubR1(L/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. |
