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Mark E. Hurtt

Researcher at DuPont

Publications -  19
Citations -  855

Mark E. Hurtt is an academic researcher from DuPont. The author has contributed to research in topics: Developmental toxicity & Leydig cell. The author has an hindex of 11, co-authored 19 publications receiving 817 citations.

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Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro, in vivo, and ex vivo studies.

TL;DR: The hypothesis that C8 produces an increase in estradiol by inducing cytochrome P450 XIX (aromatase), which converts testosterone to Estradiol, and that the elevated estradio levels ultimately produce Leydig cell hyperplasia and adenoma formation is investigated.
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Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism.

TL;DR: The data suggest that the decrease in serum testosterone following hCG challenge may be due to a decrease in the conversion of 17 alpha-hydroxyprogesterone to androstenedione, which is attributed to the elevated serum estradiol levels.
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90-day feeding and one-generation reproduction study in Crl:CD BR rats with 17β-estradiol

TL;DR: This 90-day/one-generation reproduction study with 17 beta-estradiol was designed to set dose levels for future multigenerational reproduction and combined chronic toxicity/oncogenicity studies, and to provide benchmark data for a risk assessment for chemicals with estrogen-like activities.
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Effects of Dietary 17β-Estradiol Exposure on Serum Hormone Concentrations and Testicular Parameters in Male Crl:CD BR Rats

TL;DR: The data demonstrate that in utero and postnatal dietary administration of 17 beta-estradiol at levels which increased serum estradiol levels to approximately 400% of control and decreased testosterone levels to 33% ofControl did not reduce the number of Sertoli cell nuclei per testis.
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Effect of the Peroxisome Proliferator, Ammonium Perfluorooctanoate (C8), on Hepatic Aromatase Activity in Adult Male Crl:CD BR (CD) Rats

TL;DR: The results of this study suggest that the increased serum concentration of estradiol produced by C8 in rats is at least partly due to a direct effect on the liver to increase synthesis ofEstradiol through induction of aromatase cytochrome P450 in the endoplasmic reticulum.