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花生四烯酸诱导的钙离子从分离的肌浆网释放。

Arachidonic acid-induced Ca2+ release from isolated sarcoplasmic reticulum.

作者信息

Dettbarn C, Palade P

机构信息

Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77555-0641.

出版信息

Biochem Pharmacol. 1993 Mar 24;45(6):1301-9. doi: 10.1016/0006-2952(93)90283-3.

Abstract

Arachidonic acid has been shown to release Ca2+ from isolated skeletal and cardiac sarcoplasmic reticulum (SR) vesicles. The release took place nearly equally well from all fractions of the SR and was only partially inhibited by ruthenium red, suggesting that some other pathway is involved in addition to the SR Ca2+ release channel. Arachidonic acid increased SR Ca2+ efflux even in the presence of several different SR Ca2+ pump inhibitors. It also had considerably less effect on uptake measured in the presence of oxalate and did not appear to inhibit Ca(2+)-dependent ATPase activity. Thus, the SR Ca2+ pump also appears to be minimally perturbed by arachidonic acid. Arachidonyl CoA was more effective at releasing Ca2+ than the parent compound. Arachidonic acid effects were not inhibited by lipoxygenase or cyclooxygenase inhibitors, suggesting that no eicosanoids are involved in the effects under study here. Flunarizine, cinnarizine and propyl-methylenedioxyindene inhibited the Ca2+ release induced by arachidonic acid. The effects of arachidonic acid appear to depend on the ratio of arachidonic acid to membrane vesicles.

摘要

花生四烯酸已被证明可从分离的骨骼肌和心肌肌浆网(SR)囊泡中释放Ca2+。从SR的所有组分中释放的情况几乎同样良好,并且仅被钌红部分抑制,这表明除了SR Ca2+释放通道外,还涉及其他一些途径。即使存在几种不同的SR Ca2+泵抑制剂,花生四烯酸也会增加SR Ca2+流出。在草酸盐存在下测量摄取时,它的影响也小得多,并且似乎不会抑制Ca(2+)-依赖性ATP酶活性。因此,SR Ca2+泵似乎也受到花生四烯酸的最小干扰。花生四烯酰辅酶A在释放Ca2+方面比母体化合物更有效。花生四烯酸的作用不受脂氧合酶或环氧化酶抑制剂的抑制,这表明本研究中所涉及的作用不涉及类二十烷酸。氟桂利嗪、桂利嗪和丙基-亚甲二氧基茚抑制花生四烯酸诱导的Ca2+释放。花生四烯酸的作用似乎取决于花生四烯酸与膜囊泡的比例。

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