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Toxicity and Carcinogenicity of Dichlorodiphenyltrichloroethane (DDT)

机译:二氯二苯基三氯乙烷(DDT)的毒性和致癌性

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摘要

Dichlorodiphenyltrichloroethane (DDT) is still used in certain areas of tropics and subtropics to control malaria and other insect-transmitted diseases. DDT and its metabolites have been extensively studied for their toxicity and carcinogenicity in animals and humans and shown to have an endocrine disrupting potential affecting reproductive system although the effects may vary among animal species in correlation with exposure levels. Epidemiologic studies revealed either positive or negative associations between exposure to DDT and tumor development, but there has been no clear evidence that DDT causes cancer in humans. In experimental animals, tumor induction by DDT has been shown in the liver, lung, and adrenals. The mechanisms of hepatic tumor development by DDT have been studied in rats and mice. DDT is known as a non-genotoxic hepatocarcinogen and has been shown to induce microsomal enzymes through activation of constitutive androstane receptor (CAR) and to inhibit gap junctional intercellular communication (GJIC) in the rodent liver. The results from our previously conducted 4-week and 2-year feeding studies of p,p′-DDT in F344 rats indicate that DDT may induce hepatocellular eosinophilic foci as a result of oxidative DNA damage and leads them to hepatic neoplasia in combination with its mitogenic activity and inhibitory effect on GJIC. Oxidative stress could be a key factor in hepatocarcinogenesis by DDT.
机译:在热带和亚热带的某些地区,二氯二苯基三氯乙烷(DDT)仍用于控制疟疾和其他昆虫传播的疾病。滴滴涕及其代谢物在动物和人类中的毒性和致癌性已得到广泛研究,并显示具有内分泌干扰潜力,可能影响生殖系统,尽管其影响可能因动物种类而与暴露水平有关。流行病学研究表明,DDT暴露与肿瘤发展之间存在正相关或负相关,但尚无明确证据表明DDT会导致人类癌症。在实验动物中,已在肝脏,肺部和肾上腺中发现了DDT诱导的肿瘤。已经在大鼠和小鼠中研究了滴滴涕引起的肝肿瘤发展机制。滴滴涕被称为一种非遗传毒性的肝致癌物,已被证明可通过激活组成型雄烷受体(CAR)诱导微粒体酶,并抑制啮齿动物肝脏中的间隙连接细胞间通讯(GJIC)。我们先前对F344大鼠进行的p,p'-DDT的4周和2年喂养研究的结果表明,DDT可能由于氧化DNA损伤而诱导肝细胞嗜酸性病灶,并与其结合导致肝肿瘤有丝分裂活性和对GJIC的抑制作用。氧化应激可能是滴滴涕在肝癌发生中的关键因素。

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