Abstract

In an integrated series of experiments, we assessed effects of translactational exposure to Aroclor 1254 at three different ages: as young adults (2-4.5 months), as mature adults (5-8 months), and as older adults (8.5-13 months). Developing female rats were exposed postnatally to polychlorinated biphenyls (PCBs) via oral treatment of the dams on Days 1, 3, 5, 7, and 9 of lactation at the following doses: 8 μg/g (PCBI), 32 μg/g (PCBII), and 64 μg/g (PCBIII) in peanut oil. Normal controls (CI) and underfed nutritional controls (CII) received peanut oil. Puberty, both vaginal opening and first estrus, was delayed in PCBII and PCBIII offspring. PCB exposure at all doses had a pronounced and consistent effect on uterine response. In mature PCBII and PCBIII adults, uterine wet weights were reduced at all stages of the estrous cycle and in light-induced persistent vaginal estrus (PVE). PCBI offspring exhibited a decreased uterine weight in proestrus and in light-induced PVE. Exogenous estradiol-17β (0.2 μg) given to ovariectomized offspring was less effective in causing a uterotrophic and vaginal response in all PCB-exposed offspring. Analysis of estrous cycles for 40 days at all ages indicated increases in diestrus. Fertility in young adults and mature adults was affected, with PCBIII young adults exhibiting less success with preimplantation stages, and PCBII and PCBIII mature adults showing an effect at pre- and/or postimplantation stages. As determined by patterns in estrous cycling and rate of development of PVE in 64 days of constant light, exposure to PCBs did not hasten reproductive aging at any of the ages examined. Instead, PCBIII young adults and PCBII and PCBIII older adults exhibited a delay in onset of light-induced PVE. This study demonstrates that translactational exposure to a PCB mixture that has little notable effect on the dams, not only delays puberty in the female offspring, but also several months later results in decreased uterine response, impairment of fertility, and irregular cycle patterns. Reproductive aging, however, is not hastened, and even may be delayed. Many of these effects could be explained, in part, by interference with estrogen.

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