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首页> 外文期刊>Physiological Research >Involvement of nitric oxide in noradrenaline-induced changes in the activity of antioxidant enzymes and lipid peroxidation in rat brown adipose tissue and heart
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Involvement of nitric oxide in noradrenaline-induced changes in the activity of antioxidant enzymes and lipid peroxidation in rat brown adipose tissue and heart

机译:一氧化氮参与去甲肾上腺素诱导的大鼠棕色脂肪组织和心脏中抗氧化酶活性和脂质过氧化的变化

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The effect of exogenous noradrenaline (NA) (1.6 mg center dot kg(-1) i.p., 35 min prior sacrifice) on the activity of antioxidant enzymes (AOE) copper zinc superoxide dismutase (CuZnSOD), manganese superoxide dismutase (MnSOD) and catalase (CAT), as well as lipid peroxides (LP) concentration were studied in the rat interscapular brown adipose tissue (IBAT) and heart of saline (controls) and N-omega-nitro-L-arginine methyl ester (L-NAME) treated rats (10 mg center dot kg(-1), i.p., during 3 days and 20 min before NA). NA differently affects both AOE activities and LP production in the IBAT and heart. Thus, NA inhibited the activity of all IBAT AOE and LP production while in the heart it markedly increased CAT activity only, but had no effect on any of SODs activities and LP concentration. L-NAME, a nitric oxide synthase blocker, completely abolished the NA-induced inhibition of the IBAT AOE and LP production, whereas in the heart it was without effect. In conclusion, these results indicate that both NA and L-NAME effects on AOE activity and LP production are tissue specific and also suggest that nitric oxide mediates the NA-induced inhibition of AOE activity and LP production in the MAT only.
机译:外源去甲去甲肾上腺素(NA)(1.6 mg中心点kg(-1)ip,处死前35分钟)对抗氧化酶(AOE)铜锌超氧化物歧化酶(CuZnSOD),锰超氧化物歧化酶(MnSOD)和过氧化氢酶活性的影响(CAT)以及脂质过氧化物(LP)的浓度在大鼠肩ular间棕色脂肪组织(IBAT)和盐水心脏(对照)和N-ω-硝基-L-精氨酸甲酯(L-NAME)中进行了研究大鼠(NA前3天和20分钟内,腹腔注射10 mg中心点kg(-1),ip)。 NA对IBAT和心脏中的AOE活动和LP产生都有不同的影响。因此,NA抑制所有IBAT AOE和LP产生的活性,而在心脏中仅显着增加CAT活性,但对任何SOD活性和LP浓度均无影响。一氧化氮合酶阻滞剂L-NAME完全消除了NA诱导的对IBAT AOE和LP产生的抑制作用,而在心脏中则没有作用。总之,这些结果表明,NA和L-NAME对AOE活性和LP产生的影响都是组织特异性的,也表明一氧化氮仅在MAT中介导NA诱导的对AOE活性和LP产生的抑制。

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