Prenatal exposure to hexavalent chromium disrupts testicular steroidogenic pathway in peripubertal F 1 rats.

Autor: Navin AK; Department of Endocrinology, Dr. A.L.M. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Taramani-Velachery Link Road, Chennai, 600113, Tamil Nadu, India; Department of Veterinary Integrative Biosciences, College of Veterinary Medicine & Biomedical Sciences, TAMU-4458, Texas A&M University, College Station, TX, 77843, USA., Aruldhas MM; Department of Endocrinology, Dr. A.L.M. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Taramani-Velachery Link Road, Chennai, 600113, Tamil Nadu, India. Electronic address: aruldhasmm@gmail.com., Navaneethabalakrishnan S; Department of Endocrinology, Dr. A.L.M. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Taramani-Velachery Link Road, Chennai, 600113, Tamil Nadu, India., Mani K; Department of Endocrinology, Dr. A.L.M. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Taramani-Velachery Link Road, Chennai, 600113, Tamil Nadu, India., Michael FM; Department of Anatomy, Dr. A.L.M. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Taramani-Velachery Link Road, Chennai, 600113, Tamil Nadu, India., Srinivasan N; Department of Tissue Engineering and Regenerative Medicine, Chettinad Academy of Research and Education, Chettinad Health City, Kelambakkam, 603103, Tamil Nadu, India., Banu SK; Department of Veterinary Integrative Biosciences, College of Veterinary Medicine & Biomedical Sciences, TAMU-4458, Texas A&M University, College Station, TX, 77843, USA.
Jazyk: angličtina
Zdroj: Reproductive toxicology (Elmsford, N.Y.) [Reprod Toxicol] 2021 Apr; Vol. 101, pp. 63-73. Date of Electronic Publication: 2021 Mar 03.
DOI: 10.1016/j.reprotox.2021.01.014
Abstrakt: We have reported sub-fertility in F 1 progeny rats with gestational exposure to hexavalent chromium [Cr(VI)], which had disrupted Sertoli cell (SC) structure and function, and decreased testosterone (T). However, the underlying mechanism for reduced T remains to be understood. We tested the hypothesis "transient prenatal exposure to Cr(VI) affects testicular steroidogenesis by altering hormone receptors and steroidogenic enzyme proteins in Leydig cells (LCs)." Pregnant Wistar rats were given drinking water containing 50, 100, and 200 mg/L potassium dichromate during gestational days 9-14, encompassing fetal differentiation window of the testis from the bipotential gonad. F 1 male rats were euthanized on postnatal day 60 (peripubertal rats with adult-type LCs alone). Results showed that prenatal exposure to Cr(VI): (i) increased accumulation of Cr(III) in the testis of F 1 rats; (ii) increased serum levels of luteinizing and follicle stimulating hormones (LH and FSH), and 17β estradiol, and decreased prolactin and T; (iii) decreased steroidogenic acute regulatory protein, cytochrome P450 11A1, cytochrome P450 17A1, 3β- and 17β-hydroxysteroid dehydrogenases, cytochrome P450 aromatase and 5α reductase proteins, (iv) decreased specific activities of 3β and 17β hydroxysteroid dehydrogenases; (v) decreased receptors of LH, androgen and estrogen in LCs; (vi) decreased 5α reductase and receptor proteins of FSH, androgen, and estrogen in SCs. The current study concludes that prenatal exposure to Cr(VI) disrupts testicular steroidogenesis in F 1 progeny by repressing hormone receptors and key proteins of the steroidogenic pathway in LCs and SCs.
(Copyright © 2021 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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