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林丹对大鼠肠上皮细胞中血管活性肠肽受体/效应系统的影响。

Lindane effect upon the vasoactive intestinal peptide receptor/effector system in rat enterocytes.

作者信息

Carrero I, Fernández-Moreno M D, Pérez-Albarsanz M A, Prieto J C

机构信息

Departmento de Bioquímica y Biología Molecular, Universidad de Alcalá, Alcalá de Henares-Madrid, Spain.

出版信息

Biochem Biophys Res Commun. 1989 Mar 31;159(3):1391-6. doi: 10.1016/0006-291x(89)92264-x.

Abstract

Isolated rat enterocytes exposed to the insecticide lindane (the gamma-isomer of hexachlorocyclohexane, HCCH) showed an important decrease in the efficiency of the neuropeptide vasoactive intestinal peptide (VIP) upon the stimulation of cyclic AMP accumulation. The effect of lindane was time- and dose-dependent, optimal conditions being reached after 5 min incubation of cells at 25 degrees C with 0.5 mM of this organochlorine compound. Lindane action exhibited an important degree of specificity since the isomer alpha-HCCH and endrin reproduced the same inhibitory pattern but beta-HCCH and dieldrin were inactive. The inhibition of VIP-induced cyclic AMP accumulation could not be explained by a lindane-dependent reduction in the binding of VIP to its specific receptors. Among various possibilities, the results suggest the modification of membrane fluidity by lindane and/or the activation of Ca2+-dependent protein kinase C by this compound leading to phosphorylation of Gs/adenylate cyclase.

摘要

暴露于杀虫剂林丹(六氯环己烷的γ异构体,HCCH)的离体大鼠肠上皮细胞,在刺激环磷酸腺苷(cAMP)积累时,神经肽血管活性肠肽(VIP)的效率出现显著下降。林丹的作用具有时间和剂量依赖性,在25℃下将细胞与0.5 mM这种有机氯化合物孵育5分钟后达到最佳条件。林丹的作用表现出高度的特异性,因为α-HCCH异构体和异狄氏剂呈现相同的抑制模式,但β-HCCH和狄氏剂无活性。VIP诱导的cAMP积累的抑制不能用林丹导致VIP与其特异性受体结合减少来解释。在各种可能性中,结果表明林丹改变了膜流动性和/或该化合物激活了钙依赖性蛋白激酶C,导致Gs/腺苷酸环化酶磷酸化。

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