Endocrine disrupters and testicular dysgenesis syndrome
Endocrine disrupters and testicular dysgenesis syndrome
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DOI：
10.1159/000058100
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发表时间：
2002-01-01
期刊：
影响因子：
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通讯作者：
Skakkebæk, NE
中科院分区：
文献类型：
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作者：
Skakkebæk, NE
在过去的几代人中，我们在环境中接触到越来越多的内分泌干扰物，包括二氯二苯三氯乙烷（DDT），多氯联苯，某些杀虫剂，邻苯二甲酸酯DBP，肉类中的合成类固醇和许多其他制剂（表1），它们作为性类固醇的激动剂或拮抗剂。尽管从事野生动物研究的生物学家一直担心这些化学制剂对动物繁殖的可能影响，但临床医生似乎不太关心对人类健康的可能影响。然而，依赖内分泌的癌症，包括乳腺癌、前列腺癌和睾丸癌的发病率不断上升，以及男性生殖健康问题发病率不断上升的迹象，应使我们警惕接触内分泌干扰物与目前生殖问题高发之间可能存在的联系。例如，在丹麦，5%的儿童现在是在辅助生殖（卵胞浆内精子注射、体外受精、供体授精和子宫内授精）后出生的，1%的男性（主要是年轻人）患睾丸癌。有证据支持尿道下裂、隐睾、精液质量差和睾丸癌是潜在的睾丸发育不全综合征的症状，由于不利的环境影响，睾丸发育不全综合征可能变得越来越常见。实验和流行病学证据表明，睾丸发育不全综合征是胎儿生命期间胎儿编程和性腺发育中断的结果。
Over the last couple of generations, we have been exposed to an increasing number of endocrine disrupters in our environment, including dichlorodiphenyltrichloroethane (DDT), PCB, certain pesticides, the phthalate DBP, synthetic steroids in meat and many other agents (table 1), which act as agonists or antagonists of sex steroids. Although biologists working with wildlife have been concerned about the possible effects of these chemical agents on animal reproduction, it appears that clinicians have been less concerned about possible health effects in humans. However, the increasing incidence of hormone-dependent cancers, including cancer of the breast, prostate and testis, and signs of an increasing incidence of male reproductive health problems should alert us to the possible association between exposure to endocrine disrupters and the current high frequency of reproductive problems. In Denmark, for example, 5% of all children are now born after assisted reproduction (intracytoplasmic sperm injection, in vitro fertilization, donor insemination and intrauterine insemination) and 1% of all (mostly young) men develop testicular cancer. Evidence exists to support the concept that hypospadias, undescended testis, poor semen quality and testicular cancer are symptoms of an underlying testicular dysgenesis syndrome, which may be becoming increasingly common due to adverse environmental effects. Experimental and epidemiological evidence suggests that testicular dysgenesis syndrome is a result of disruption of foetal programming and gonadal development during foetal life.