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[应激期间脂质过氧化在抑制心脏钠钾 -ATP 酶中的作用]

[Role of lipid peroxidation in inhibiting cardiac Na, K-ATPase during stress].

作者信息

Meerson F Z, Sazontova T G, Kagan V E, Tverdokhlib V P, Arkhipenko Iu V

出版信息

Biull Eksp Biol Med. 1983 Dec;96(12):42-4.

PMID:6140965
Abstract

Induction of lipid peroxidation (LPO) under emotional painful stress in rats in vivo and by the Fe2+ plus ascorbate system in vitro results in inactivation of Na,K-ATPase in the sarcolemma-rich membrane fraction of the heart. Activity of Mg-ATPase remains practically unchanged. The scavenger of lipid free radicals 4-methyl-2,6-ditertbutylphenol (ionol) prevents Na,K-ATPase inactivation in both cases. It is concluded that LPO plays the key role in the impairment of the heart Na-pump function under stress and that such impairment can be prevented by free radical scavengers. The stress-induced shifts in the ionic homeostasis in cardiomyocytes are discussed.

摘要

体内情绪性疼痛应激下以及体外通过亚铁离子加抗坏血酸系统诱导大鼠脂质过氧化(LPO),会导致心脏富含肌膜的膜部分中钠钾-ATP酶失活。镁-ATP酶的活性实际上保持不变。脂质自由基清除剂4-甲基-2,6-二叔丁基苯酚(生育酚)在两种情况下均可防止钠钾-ATP酶失活。得出的结论是,LPO在应激状态下心脏钠泵功能受损中起关键作用,并且这种损伤可以被自由基清除剂预防。讨论了应激诱导的心肌细胞离子稳态变化。

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