Mechanism underlying transient gestational-onset hypothyroidism–induced impairment of posttesticular sperm maturation in adult rats  

Oleh:

Anbalagan, Jaganathan ; Sashi, Arokya Mary ; Vengatesh, Ganapathy

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Fertility and Sterility (keterangan: ada di ClinicalKey) vol. 93 no. 08 (Jun. 2010), page 2491-2497.
Topik: Androgen receptor; dihydrotestoterone; epididymis; male fertility; sperm forward motility; testosterone; thyroid hormone

Ketersediaan

Perpustakaan FK Nomor Panggil: F02.K.2010.03 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Objective To understand the mechanism underlying gestational-onset hypothyroidism–induced male infertility. Design Controlled laboratory study. Setting Research laboratory in a university department of endocrinology. Animal(s) Wistar rat. Intervention(s) Pregnant rats were exposed to methimazole from embryonic days 9 to 14, 18, and 21, covering specific fetal periods of differentiation and development of male reproductive tract organs. Main Outcome Measure(s) Fertility of male rats was assessed by testing sperm count, forward motility, and in vivo fertilizing ability. Secretory activity of the epididymis was evaluated by quantifying sialic acid, carnitine, and glycerylphosphorylcholine. Bioavailability of androgens was assessed by quantifying testosterone in serum and testicular interstitial fluid and epididymal 5a-reductase activity/mRNA expression. Androgen receptor (AR) status in the epididymis was tested by detecting the expression levels of its mRNA and protein, as well as ligand binding activity. Data were analyzed statistically by one-way analysis of variance. Result(s) Gestational exposure to methimazole decreased sperm forward motility, in vivo fertilizing ability, bioavailability of androgens, AR status, and secretory activity of the epididymis in adult rats. Conclusion(s) Transient gestational-onset hypothyroidism affects male fertility by impairing posttesticular sperm maturation process in the epididymis, owing to subnormal androgen(s) bioavailability, AR expression, and AR functional activity.

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