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1 Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine and Dentistry, Okayama, Okayama, Japan; Department of Brain Science, Okayama University Graduate School of Medicine and Dentistry, Okayama, Okayama, Japan
2 Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine and Dentistry, Okayama, Okayama, Japan
3 Department of Public Health, Okayama University Graduate School of Medicine and Dentistry, Okayama, Okayama, Japan
4 Department of Biochemistry, Okayama University Graduate School of Medicine and Dentistry, Okayama, Okayama, Japan
5 Department of Brain Science, Okayama University Graduate School of Medicine and Dentistry, Okayama, Okayama, Japan
* To whom correspondence should be addressed. E-mail: hitoshis{at}md.okayama-u.ac.jp.
Tissue homeostasis is determined by the balance between oxidants and anti-oxidants. Catalase is an important anti-oxidant enzyme regulating the level of intracellular hydrogen peroxide and hydroxyl radicals. The effect of catalase deficiency on renal tubulointerstitial injury induced by unilateral ureteral obstruction (UUO) has been studied in homozygous acatalasemic mutant mice (C3H/AnLCsbCsb) as compared with wild mice (C3H/AnLCsaCsa). Complete UUO caused interstitial cell infiltration, tubular dilation and atrophy, and interstitial fibrosis with accumulation of type IV collagen in obstructed kidneys (OBK) of both mouse groups. However, the degree of injuries showed significant increase in OBK of acatalasemic mice as compared with that of wild mice until day 7. The deposition of lipid peroxidation products including 4-hydroxy-2-hexenal, malondialdehyde, and 4-hydroxy-2-nonenal was severer in dilated tubules of acatalasemic OBK. Apoptosis in tubular epithelial cells significantly increased in acatalasemic OBK at day 4. Expression of caspase-9, a marker of mitochondrial pathway-derived apoptosis, increased in dilated tubules of acatalasemic mice. The level of catalase activity remained low in acatalasemic OBK until day 7 without compensatory upregulation of glutathione peroxidase activity. The data indicate that acatalasemia exacerbated oxidation of renal tissue and sensitized tubular epithelial cells to apoptosis in OBK of UUO. This study demonstrates that catalase deficiency enhanced tubulointerstitial injury and fibrosis in murine model of UUO, thus supports the protective role of catalase in this model.
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