Exposure Duration-Dependent Ovarian Recovery in Methoxychlor-Treated Mice

Lawrence V. Tannenbaum, Jodi A. Flaws
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引用次数: 4

Abstract

The pesticide methoxychlor (MXC) is known to target ovarian antral follicles in the mouse. In previous in vivo studies, MXC administration for 20 days increased atresia, but did not affect female fertility immediately after dosing. Thus, we hypothesized that perhaps not enough time had elapsed between the onset of MXC-induced atresia and actual follicle loss to result in reduced fertility. The current study was undertaken to determine whether MXC treatment for 20 days results in reduced antral follicle numbers and fertility at 30 and 60 days after dosing. To test this hypothesis, adult CD-1 female mice were dosed with vehicle control or MXC (64 mg/kg/day) for 20 days. At 30 and 60 days postdosing, the mice were either subjected to fertility tests or their ovaries were collected and subjected to histological evaluation of follicle numbers and atresia. The results indicate that at 30 days after the completion of dosing, MXC significantly increased atresia and reduced primordial and total follicle numbers, but did not affect fertility compared to controls. At 60 days after completion of dosing, MXC did not significantly affect fertility, follicle numbers, or atresia compared to controls. Collectively, these data indicate that the ovary may be able to recover from MXC treatment for 20 days

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甲氧基氯处理小鼠暴露时间依赖性卵巢恢复
农药甲氧基氯(MXC)是已知的目标卵巢窦卵泡在小鼠。在之前的体内研究中,服用MXC 20天会增加闭锁,但在给药后不会立即影响女性的生育能力。因此,我们假设,从mxc诱导的闭锁开始到实际卵泡丢失之间的时间可能不足以导致生育能力降低。目前的研究是为了确定MXC治疗20天是否会在给药后30天和60天减少窦卵泡数量和生育能力。为了验证这一假设,将成年CD-1雌性小鼠分别给予对照或MXC (64 mg/kg/天)20天。在给药后30和60天,对小鼠进行生育试验或收集其卵巢,对卵泡数量和闭锁进行组织学评估。结果表明,在给药完成后30天,MXC显著增加闭锁,减少原始和总卵泡数量,但与对照组相比,不影响生育能力。在给药后60天,与对照组相比,MXC对生育能力、卵泡数量或闭锁没有显著影响。总的来说,这些数据表明卵巢可能能够从MXC治疗中恢复20天
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来源期刊
CiteScore
1.65
自引率
0.00%
发文量
0
审稿时长
>12 weeks
期刊介绍: The purpose of this journal is to publish original contributions describing the toxicity of chemicals to developing organisms and the process of reproduction. The scope of the journal will inlcude: • toxicity of new chemical entities and biotechnology derived products to developing organismal systems; • toxicity of these and other xenobiotic agents to reproductive function; • multi-generation studies; • endocrine-mediated toxicity, particularly for endpoints that are relevant to development and reproduction; • novel protocols for evaluating developmental and reproductive toxicity; Part B: Developmental and Reproductive Toxicology , formerly published as Teratogenesis, Carcinogenesis and Mutagenesis
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