The effect of low-level maternal lead (Pb) exposure on the reproductive maturation of their female offspring /
Recent human and animal studies have shown that in utero and postnatal lead (Pb) exposure causes a decrease in key reproductive hormones and a subsequent delay in the onset of puberty. However, two critical unanswered questions are when does the insult occur and what is/are the specific mechanism(s...
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| Format: | Thesis Book |
| Language: | English |
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[Place of publication not identified] :
[publisher not identified] ;
2003.
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| Subjects: | |
| Online Access: | http://proxy.library.tamu.edu/login?url=http://proquest.umi.com/pqdweb?did=764884681&sid=1&Fmt=2&clientId=2945&RQT=309&VName=PQD |
| Summary: | Recent human and animal studies have shown that in utero and postnatal lead (Pb) exposure causes a decrease in key reproductive hormones and a subsequent delay in the onset of puberty. However, two critical unanswered questions are when does the insult occur and what is/are the specific mechanism(s) of action? Therefore, this study correlated maternal Pb levels during gestational and/or lactational exposure, as well as blood and tissue levels of Pb in their developing offspring, with the subsequent detrimental effects of Pb on puberty related hormones and the timing of female puberty. Adult Fisher 344 female rats were gavaged daily with either a 1.0 ml solution of lead acetate (PbAc) containing 12 mg of Pb/ml, or sodium acetate (NaAc) for the controls, from 30 days prior to breeding and throughout gestation and lactation. Pb caused depressed circulating levels of insulin-like growth factor-1 (IGF-1), luteinizing hormone (LH) and estradiol (E₂), and delayed the timing of female puberty. This occurred regardless of the developmental time of exposure and at levels that equate to those considered to be a risk for human populations. To investigate potential mechanisms of action, we utilized in vivo and in vitro physiological techniques and molecular biology to assess hypothalamic, pituitary and ovarian functions. Pb was incapable of centrally blocking IGF-1 induced LH-releasing hormone (LHRH) secretion in vitro and LH secretion in vivo. IGF-1 replacement in the presence of E₂ reversed the Pb-induced delay in puberty. Pb decreased basal ovarian steroidogenic acute regulatory protein (StAR) gene and protein expression, and suppressed serum E₂ levels. Pb failed to block PMSG-stimulated ovarian StAR protein expression and subsequent E₂ release. These results suggest Pb causes suppressed peripheral IGF-1 synthesis or release, causing decreased IGF-1 availability to facilitate the increased release of LHRH from the hypothalamus, resulting in suppressed LH followed by E₂ secretion and delayed female puberty. Comparing the effects of maternal Pb exposure on developing Fisher 344 and Sprague-Dawley offspring, revealed Fisher rats were more sensitive to maternal Pb exposure and thus, serve as a better rodent model to study the effects of low level Pb toxicity and delayed female puberty. |
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| Item Description: | Vita. "Major Subject: Veterinary Anatomy". |
| Physical Description: | xi, 96 leaves : illustrations ; 28 cm. Issued also on microfiche from University Microfilm Inc. |
| Bibliography: | Includes bibliographical references (leaves 80-93). |