林丹的[毒性伽马异构体六氯环己烷)。

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林丹的[毒性伽马异构体六氯环己烷)。

J Soc杂志。2002;196 (4):339 - 48。

PubMed ID

12645305 (在PubMed

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文摘

目前的审查的目的是收集信息关于林丹中毒引起的膜效应,y的异构体hexachiorocyclohexane(林丹),主要用作杀虫剂和杀菌剂在农业和进入一些乳液的组成、霜和洗发水用来对付寄生虫(虱子和疥疮)。通过呼吸,消化吸收或经皮的通路,林丹在脂质积累丰富的组织。林丹积累取决于暴露的持续时间和影响组织按照以下顺序:脂肪组织>脑>肾>肌肉>肺>心>肝>血。无论林丹吸收模式,它在血液和积累分布到全身。它可以通过施加系统影响人类健康,免疫,产生畸形的,和/或致癌的影响。林丹中毒的症状是不同的根据中毒的模式,急性或慢性。高剂量的吸收林丹特别有毒的中枢神经系统和女性和男性生殖器官在林丹的哺乳动物被认为是内分泌干扰物)。林丹是高度亲脂性的,包含了生物膜根据下列顺序:大脑线粒体>肌浆网>髓>微粒体>红细胞。林丹在突触传导产生刺激作用,抑制氯电流激活gamma-amino丁酸(GABA)的许多肌肉和神经的准备与受体GABA-chloride通道交互复杂。它似乎影响钙稳态的组织。 The similarity between lindane and inositol (1, 4, 5) phosphate (IP3) suggested that lindane releases Ca2+ from IP3-sensitive intracellular stores in macrophages and myometrial cells. Ca2+ release from reticulum endoplasmic, mitochondria and other Ca2+ stores has been reported in cat kidney cells. Lindane altered energetic metabolism of hepatic mitochondria and the inositol-phosphate synthesis in neuronal cells. However, lindane does not compete with the IP3 receptor. Lindane produces a Ca2+ influx in mice peritoneal macrophage cells responsible for the Ca2+ induced Ca2+ release produced by phospholipase C via IP3 pathway and resulting in a maintained increase of the free cytosolic Ca2+ concentration. Lindane decreased the membrane erythrocyte and cerebral cell concentration of phosphatidyl inositol PI, PIP and PIP2 in rats repetitively exposed to lindane for 3 or 6 months. Lindane induces oxidative stress; it modifies the activity of the scavenger enzymes. This effect is involved in the inhibition of intercellular gap junctions. Modifications of the electrocardiogram (ECG), sinusal rhythm alteration and negative and dysphasic variations of T wave, similar to those produced by hyperkaliemia, have been reported after lindane absorption. During acute lindane poisoning, the activities of serum transaminases (SGOT, SGTP), and lactate deshydrogenase (LDH) increase. Lindane produces histological alterations of cardiac tissues and a cardio-vascular dystrophy (contracture, degenerescence and necrosis) mainly in the left ventricular wall and a hypertrophy of the left ventricle. Chronic application of residual doses of lindane shortened the action potential duration in rat papillary muscle. These effects were similar to those induced by hyperthyroidism. Lindane increases the triiodothyronine (T3) serum level in hyperthyroid rats. T3 plays an important role in the postnatal development of the rat ventricle by increasing the density of potassium channels which contribute to action potential shortening during the development. Thyroid hormones influence the regulation and the expression of messengers ARN which encode different potassium channels involved in action potential repolarization (Kvl.2; Kvl.4; Kvl.5; Kv2.1; Kv4; HCN2). The thyrotropine-releasing hormone (TRH) modulates the HERG-type rapid delayed potassium channel (IKr) encoded by the human gene ether-a-go-go in rat anterior pituitary cells GH3/B6. This channel is involved in the cardiac long QT syndrome. TRH modifies the current kinetics of human HERG potassium channel co-expressed in Xenopus oocytes with the TRH receptor, whose activity is modulated via the protein kinase C pathway linked to a G protein-coupled receptor and is regulated by changes in the PIP2 concentration in the membrane. IKr channels regulation is also dependent on sexual hormones. In conclusion, lindane affects the excitable membranes and the cardio circulatory system. These alterations (may) represent a potential risk for human health.

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药物靶点

药物	目标	类	生物	药理作用	行动
林丹	γ-氨基丁酸受体亚基beta 1	蛋白质	人类	是的	拮抗剂	细节