Treatment with folic acid ameliorated the histopathological alterations caused by propylthiouracil-induced hypothyroid rat testes

Journal article


Tousson, E., Ali, E.M.M., Ibrahim, W. and Mansour, M.A. (2012). Treatment with folic acid ameliorated the histopathological alterations caused by propylthiouracil-induced hypothyroid rat testes. Toxicology and industrial health. 28 (6), pp. 566-576. https://doi.org/10.1177/0748233711420469
AuthorsTousson, E., Ali, E.M.M., Ibrahim, W. and Mansour, M.A.
Abstract

Hypothyroidism is an underactive thyroid gland that cannot make enough thyroid hormone to keep the body running normally. Here we studied the histopathological, immunohistochemical, and ultrastructural changes in the hypothyroid rat testes at the postpubertal stage, in addition to the ameliorating role of folic acid in enhancing spermatogenesis, boosting sperm concentration and building up the antioxidant status against the oxidants. A total of 50 male albino rats were equally divided into 5 groups; the first and second groups comprised the control and folic acid groups, respectively; while the third group comprised the hypothyroid group in which rats received 6-n-propyl-2-thiouracil in drinking water for 6 weeks to induce hypothyroidism. The fourth and fifth groups comprised hypothyroid rats treated with folic acid for 4 weeks and dissected after 6 and 10 weeks, respectively. Testes in the hypothyroid rats showed marked morphological and histological changes in the seminiferous tubules with a reduction in sperm count. Our results indicate that hypothyroidism adversely affects spermatogenesis, suggesting that thyroid hormone might play an important role not only in controlling normal testicular development but also in maintaining normal testicular function and spermatogenesis. Further, we suggested an ameliorating role of folic acid in the relief of testicular tissue from changes due to hypothyroidism. However, we found that the best results were found in cases where folic acid was used as an adjuvant therapy for returning to the euthyroid state.

Year2012
JournalToxicology and industrial health
Journal citation28 (6), pp. 566-576
PublisherSage Publications Sage UK: London, England
Digital Object Identifier (DOI)https://doi.org/10.1177/0748233711420469
Publication dates
Print31 Oct 2011
Publication process dates
Deposited10 Aug 2020
Accepted author manuscript
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Open
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