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Interleukin‐6 Altered Oxidation Levels of Isolated Adult Rat Ventricular Myocytes During Chronic Exposure
Author(s) -
Liu Shi Jesse,
Liu MeeiYueh G
Publication year - 2007
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.21.5.a446-b
Subject(s) - oxidative stress , chemistry , superoxide dismutase , superoxide , nitric oxide , nitric oxide synthase , antioxidant , pharmacology , endocrinology , medicine , biochemistry , enzyme , biology , organic chemistry
Interleukin (IL)‐6 has been known to increase nitric oxide (NO) production and elicit a negative inotropic effect (NIE) on adult rat ventricular myocytes (ARVM). However, IL‐6‐induced NIE was only partially blocked by L‐NMMA, an NO synthase inhibitor. Present studies tested the hypothesis that IL‐6 also increases oxidative stress, thereby contributing in part to its NIE. ARVM plated in microplates were incubated in the presence or absence of 10 ng/ml IL‐6 for 24–48 h. Oxidative stress was assessed with flurospectrophotometry of dihydroethidium, a membrane‐permeable superoxide‐sensitive dye. The activity of superoxide dismutase (SOD) was assessed under the same experimental conditions. IL‐6 induced a time‐dependent change in superoxide production and SOD activities. The IL‐6‐induced increase in oxidation was inhibited significantly by N‐acetylcysteine (NAC), an antioxidant, but only attenuated by L‐NMMA. By contrast, neither NAC nor L‐NMMA attenuated IL‐6‐induced increase in SOD activities. The results suggest that the NOS pathway contributes partially to IL‐6‐induced increase in oxidation levels, and NAC acts on the downstream of SOD to reduce oxidation induced by IL‐6 (Supported by AHA‐HL‐0550134Z).