Crews D, Bergeron J M, McLachlan J A
Institute of Reproductive Biology, University of Texas at Austin 78712, USA.
Environ Health Perspect. 1995 Oct;103 Suppl 7(Suppl 7):73-7. doi: 10.1289/ehp.95103s773.
In the current model of vertebrate sex determination and sexual differentiation, gonadal sex is fixed at fertilization by specific chromosomes, a process known as genotypic sex determination (GSD). Only after the gonad is formed do hormones begin to exert an influence that modifies specific structures that eventually will differ the sexes. Many egg-laying reptiles do not exhibit GSD but rather depend on the temperature of the incubating egg to determine the gonadal sex of the offspring, a process termed temperature-dependent sex determination (TSD). Research on TSD indicates that sex determination in these species is fundamentally different in at least one way. Gonadal sex is not irrevocably set by the genetic composition inherited at fertilization but depends ultimately on which genes encoding for steroidogenic enzymes and hormone receptors are activated during the midtrimester of embryonic development by temperature. Incubation temperature modifies the activity as well as the temporal and spatial sequence of enzymes and hormone receptors such that sex-specific hormone milieus, created in the urogenital system of the developing embryo, determine gonad type. Estrogen is the physiologic equivalent of incubation temperature and the proximate cue that initiates female sex determination. There is increasing evidence that some polychlorinated biphenyl (PCB) compounds are capable of disrupting reproductive and endocrine function in fish, birds, and mammals, including humans. Reproductive disorders resulting from exposure to these xenobiotic compounds may include reductions in fertility, hatch rate in fish and birds, and viability of offspring, as well as alterations in hormone levels or adult sexual behaviors, all of which have further implications, particularly in wildlife population dynamics. Research on the mechanism through which these compounds may be acting to alter reproductive function indicates estrogenic activity, by which the compounds may be altering sexual differentiation. In TSD turtles, the estrogenic effect of some PCBs reverses gonadal sex in individuals incubating at an otherwise male-producing temperature. Furthermore, certain PCBs are synergistic in their effect at very low concentrations.
在当前脊椎动物性别决定和性分化模型中，性腺性别在受精时由特定染色体确定，这一过程称为基因型性别决定（GSD）。只有在性腺形成后，激素才开始发挥作用，改变特定结构，最终使两性产生差异。许多产卵爬行动物并不表现出GSD，而是依赖于孵化卵的温度来决定后代的性腺性别，这一过程称为温度依赖性性别决定（TSD）。对TSD的研究表明，这些物种的性别决定至少在一个方面有根本不同。性腺性别并非由受精时遗传的基因组成不可逆转地确定，而是最终取决于在胚胎发育中期哪些编码类固醇生成酶和激素受体的基因被温度激活。孵化温度会改变酶和激素受体的活性以及时间和空间序列，从而在发育中的胚胎泌尿生殖系统中产生特定性别的激素环境，进而决定性腺类型。雌激素相当于孵化温度，是启动雌性性别决定的直接线索。越来越多的证据表明，一些多氯联苯（PCB）化合物能够破坏鱼类、鸟类和哺乳动物（包括人类）的生殖和内分泌功能。接触这些外源性化合物导致的生殖障碍可能包括生育力下降、鱼类和鸟类的孵化率降低、后代的生存能力下降，以及激素水平或成年性行为的改变，所有这些都有进一步的影响，特别是在野生动物种群动态方面。对这些化合物可能改变生殖功能的机制的研究表明其具有雌激素活性，通过这种活性，这些化合物可能会改变性别分化。在TSD海龟中，一些PCB的雌激素作用会使在原本产生雄性的温度下孵化的个体的性腺性别发生逆转。此外，某些PCB在极低浓度下具有协同作用。
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