Ankley Gerald T, Miller David H, Jensen Kathleen M, Villeneuve Daniel L, Martinović Dalma
US Environmental Protection Agency, Mid-Continent Ecology Division, 6201 Congdon Boulevard, Duluth, MN 55804 USA.
Aquat Toxicol. 2008 Jun 2;88(1):69-74. doi: 10.1016/j.aquatox.2008.03.005. Epub 2008 Mar 18.
Concentration and/or production of sex steroids such as 17beta-estradiol (E2) and testosterone (T) in fish have commonly been measured in field studies concerned with endocrine-active chemicals. There is a reasonable mechanistic basis for using E2 or T as biomarkers, as chemicals can alter steroid production through both direct and indirect effects on the hypothalamic-pituitary-gonadal (HPG) axis. There is uncertainty, however, as to what changes in steroid status may mean relative to apical endpoints, such as reproduction, that directly affect population status. In this study, we analyzed data from fathead minnow (Pimephales promelas) reproduction studies in which decreases in fecundity were associated with depressed steroid production as a result of chemical exposure. Although the chemicals acted on the HPG axis through different mechanisms, reproductive effects appeared to be expressed through a common pathway, depression of vitellogenin production in females. Plasma concentrations of E2 or T in the females were significantly, positively correlated with fecundity. Linear regression models describing the relationship between E2 or T concentrations and relative fecundity were linked to a population model to predict population trajectories of fathead minnows exposed to chemicals that inhibit steroid production. For example, a population existing at carrying capacity and exposed to a chemical stressor(s) that causes a 50% decrease in E2 production was predicted to exhibit a 92% decrease in population size over a 5-year period. Results of our analysis illustrate a conceptual framework whereby a commonly measured biomarker, sex steroid status, could be linked to individual- and population-level effects in fish.
在涉及内分泌活性化学物质的野外研究中,通常会测量鱼类体内17β-雌二醇(E2)和睾酮(T)等性类固醇的浓度和/或产量。将E2或T用作生物标志物有合理的机制基础,因为化学物质可通过对下丘脑-垂体-性腺(HPG)轴的直接和间接作用来改变类固醇的产生。然而,类固醇状态的变化相对于直接影响种群状况的顶端终点(如繁殖)可能意味着什么,仍存在不确定性。在本研究中,我们分析了黑头呆鱼(Pimephales promelas)繁殖研究的数据,在这些研究中,由于化学物质暴露,繁殖力下降与类固醇产量降低有关。尽管这些化学物质通过不同机制作用于HPG轴,但生殖效应似乎通过一条共同途径表现出来,即雌性卵黄蛋白原产量降低。雌性体内E2或T的血浆浓度与繁殖力显著正相关。描述E2或T浓度与相对繁殖力之间关系的线性回归模型与种群模型相联系,以预测暴露于抑制类固醇产生的化学物质的黑头呆鱼的种群轨迹。例如,一个处于承载能力的种群暴露于导致E2产量降低50%的化学应激源下,预计在5年内种群数量将减少92%。我们的分析结果说明了一个概念框架,即一种常用的生物标志物——性类固醇状态,可以与鱼类个体和种群水平的效应联系起来。