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N‐acetylcysteine inhibits NADPH oxidase activation and attenuates lipid peroxidation in the heart, lung, liver and kidney in streptozotocin‐induced diabetic rats
Author(s) -
Lei Shaoqing,
Liu Yanan,
Liu Huimin,
Xia Zhongyuan,
Irwin Michael G,
Xia Zhengyuan
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.805.1
Hyperglycemia induced increased production of reactive oxygen species (ROS) and the subsequent oxidative stress is a known mediator of tissue damage and is implicated in the pathogenesis of diabetes‐related complications. The nicotinamide dinucleotide phosphate (NADPH) oxidase family has emerged as one of the major sources of ROS production in diabetes. We postulated that antioxidant N‐aceltylcysteine (NAC) can attenuate tissue oxidative damage by inhibiting NADPH oxidase activation in various tissues, including heart, lung, liver and kidney tissues in diabetes. Control (C) and streptozotocin‐induced diabetic (D) rats were untreated or treated with NAC (1.5g/kg/day) delivered by oral gavage for 4 weeks. The levels of 15‐F2t‐isoprostane, a specific marker of oxidative damage, were significantly increased in the plasma and in the heart, lung, liver and kidney tissues in D rats (p<0.05, vs. C), which is accompanied with significantly increased membrane translocation of the p67phox subunit of NADPH oxidase in all tissues and increased expression of the membrane‐bound NADPH oxidase p22phox subunit in the heart, lung and kidney tissues. All these changes were either prevented or suppressed by NAC treatment. It is concluded that antioxidant NAC may attenuate oxidative damage in various tissues by inhibiting the activation of NADPH oxidase in diabetes. Supported by RGC/GRF grants (781109, 766709) and NSFC grant (30872447)