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环磷酸腺苷(cAMP)和环磷酸鸟苷(cGMP)参与蜕皮抑制激素(MIH,一种抑制蟹类类固醇生成的神经肽)的作用模式。

Involvement of cAMP and cGMP in the mode of action of molt-inhibiting hormone (MIH) a neuropeptide which inhibits steroidogenesis in a crab.

作者信息

Saïdi B, de Bessé N, Webster S G, Sedlmeier D, Lachaise F

机构信息

Laboratoire de Biochimie et Physiologie du Développement, ENS, URA 686, Paris, France.

出版信息

Mol Cell Endocrinol. 1994 Jun;102(1-2):53-61. doi: 10.1016/0303-7207(94)90097-3.

Abstract

In crustaceans, production of molting hormones (or ecdysteroids) by the molting glands (Y-organs; YO), is under negative control exerted by a neuropeptide, the molt-inhibiting hormone (MIH). MIH of the crab Carcinus maenas inhibits in vitro steroidogenesis of basal (intermolt crab) or activated (premolt crab) YO. MIH inhibits secretion of the two ecdysteroids synthesized by crab YO, ecdysone (E) secreted throughout the molting cycle, and 25-deoxyecdysone (25dE), secreted during the premolt period. At a MIH concentration of 10(-8) M, E is reduced about 50% and 25dE 94%. Regardless of the molting stage, this inhibition of steroidogenesis is reversible, dose dependent and measurable after 5 min. On intermolt YO, MIH induced cGMP increase and 8BrcGMP mimics the effect of MIH: at this stage cGMP seems to be involved with MIH inhibition of steroidogenesis. On premolt YO MIH induced a transient increase of cAMP (2-fold) and a long-lasting enhancement of cGMP (60-fold). On active YO, we demonstrated that a low concentration (10(-5) M) of dbcAMP, 8BrcAMP, 8BrcGMP, or agents increasing intracellular cAMP, mimic MIH effects and inhibit steroidogenesis. From these observations it is concluded that both cyclic nucleotides are involved in the mode of action of MIH on activated YO. At this premolt period, MIH/cAMP may act cooperatively with MIH/cGMP in the inhibitory control of steroidogenesis by crab YO.

摘要

在甲壳类动物中,蜕皮腺(Y器官;YO)产生蜕皮激素(或蜕皮甾类)受一种神经肽——蜕皮抑制激素(MIH)的负调控。海蟹的MIH可在体外抑制基础状态(蜕皮间期蟹)或激活状态(蜕皮前期蟹)的YO的类固醇生成。MIH抑制蟹YO合成的两种蜕皮甾类的分泌,即整个蜕皮周期都分泌的蜕皮酮(E)和蜕皮前期分泌的25 - 脱氧蜕皮酮(25dE)。在MIH浓度为10^(-8) M时,E减少约50%,25dE减少94%。无论蜕皮阶段如何,这种对类固醇生成的抑制都是可逆的、剂量依赖性的,且在5分钟后可测量。对于蜕皮间期的YO,MIH诱导cGMP增加,8 - 溴 - cGMP模拟MIH的作用:在此阶段,cGMP似乎参与了MIH对类固醇生成的抑制。对于蜕皮前期的YO,MIH诱导cAMP短暂增加(2倍)和cGMP持久增强(60倍)。对于激活状态的YO,我们证明低浓度(10^(-5) M)的二丁酰环磷腺苷(dbcAMP)、8 - 溴 - cAMP、8 - 溴 - cGMP或增加细胞内cAMP的试剂模拟MIH的作用并抑制类固醇生成。从这些观察结果得出结论,两种环核苷酸都参与了MIH对激活状态的YO的作用方式。在这个蜕皮前期,MIH/cAMP可能与MIH/cGMP协同作用,对蟹YO的类固醇生成进行抑制性调控。

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