Open AccessDetection of antioxidant enzyme activities in renal tissues of early stage IgA nephropathy in ddY mice
Author(s) -
Wang Li Ning,
Fukui Mitsumine,
Shou Ichiyu,
Yaguchi Yutaka,
Funabiki Kazuhiko,
Horikoshi Satoshi,
Shirato Isao,
Tomino Yasuhiko
Publication year - 1996
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/(sici)1098-2825(1996)10:6<394::aid-jcla13>3.0.co;2-s
Subject(s) - nephropathy , catalase , endocrinology , medicine , renal cortex , antioxidant , kidney , mesangial cell , enzyme , oxidative stress , chemistry , biochemistry , diabetes mellitus
The purpose of this study was to determine the antioxidant enzyme activities in renal tissues of early stage ddY mice, an animal model for primary IgA nephropathy. Eight‐ and 40‐week‐old ddY female mice and normal healthy Balb/c female mice were used in this study. The levels of Cu/Zn‐SOD, Mn‐SOD, and GSH‐PX activities in the renal cortex were significantly higher in 40‐week‐old ddY mice than in Balb/c control mice of the same age; no change of catalase activity was observed. There were no significant differences in the levels of Cu/Zn‐SOD, MT‐SOD, GSH‐PX, and catalase activities between the ddY mice and Balb/c mice at 8 weeks of age. Urinary protein was slightly higher in 40‐week‐old ddY mice. IgA or C3 was deposited at low levels in the glomerular mesangial areas of 8‐week‐old ddY mice. Marked depositions of IgA and C3 extended from the glomerular mesangial areas to the capillary walls of 40‐week‐old ddY mice. Expansion of glomerular mesangial matrices and mild mesangial cell proliferation was observed in 40‐week‐old ddY mice. Antioxidant enzyme activities in the renal cortex were already increased in the early stage IgA nephropathy in 40‐week‐old ddY mice. These findings suggest that measurements of antioxidant enzyme activities in the renal cortex of 40‐week‐old ddY mice was useful for evaluation of the pathogenesis of renal involvement in the early stage of IgA nephropathy. © 1996 Wiley‐Liss, Inc.