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Interplay among superoxide, nitric oxide and hydrogen peroxide in hyperglycemia‐induced endothelial dysfunction (1153.7)
Author(s) -
Patel Hemang,
Chen Juan,
Kavdia Mahendra
Publication year - 2014
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.28.1_supplement.1153.7
Subject(s) - catalase , hydrogen peroxide , superoxide dismutase , nitric oxide , endothelial dysfunction , superoxide , endocrinology , medicine , chemistry , endothelium , radical , reactive oxygen species , endothelial stem cell , biochemistry , oxidative stress , enzyme , in vitro
Free radicals have critical involvement in both physiological and pathological processes in cardiovascular system. Their role is not clear in the regulation of hyperglycemia‐induced endothelial dysfunction. In this study, we investigated the interplay amongst the superoxide (O₂‾), nitric oxide (NO), and hydrogen peroxide (H₂O₂) levels in endothelial cells following 24 hours of hyperglycemia. Furthermore, hyperglycemic‐endothelial cells were treated with superoxide dismutase (SOD) and catalase. Hyperglycemia significantly increased O₂‾ and H₂O₂ levels and decreased NO levels in endothelial cells. Following the exposure to exogenous SOD and catalase, O₂‾ levels decreased to control levels and NO levels significantly increased in hyperglycemic endothelial cells. Regulation of O₂‾, NO and H₂O₂ following SOD and catalase exposure, indicated a tight interplay resulting in increased NO levels upon neutralization of either O₂‾ or H₂O₂. Our findings provide a direct evidence for H₂O₂ led NO level regulation through O₂‾ depletion in hyperglycemia‐induced endothelial dysfunction. Grant Funding Source : NIH R01 HL084337