Морфологія (Jun 2019)
Immunohistochemical investigation of testicular morphogenesis in offspring rats, developing under the influence of maternal hypothyroidism.
Abstract
Background. Thyroid disorders are currently among the most widespread endocrine pathologies, influencing morphogenesis and histophysiology of multiple organs. Objective. The aim of present investigation was to study the impact of maternal hypothyroidism on the testicular development of rats progeny using immunohistochemical detection of cell proliferation marker Ki-67 and vascular endothelium growth factor VEGF. Methods. Hypothyroidism was induced by daily food supplementation of experimental group rats with 10 mg/kg of anti-thyroid drug Merkazolil during two weeks before pregnancy, throughout the whole gestation and lactation periods. Testes of their progeny on postnatal days 1st, 10th, 20th and 40th were removed after euthanasia, fixed in Bouin’s fluid, embedded in paraffin and subjected to immunohistochemical investigation. Results. On postnatal day 1st in control group rats Ki-67 labeling was restricted to cytoplasmic granularity of gonocytes – fetal germ cells, located centrally in within the seminiferous cords. Under hypothyroid conditions additionally to gonocytes Ki-67 binding was detected in macrophages and Leydig cells, number of both significantly elevated. On postnatal day 10th control group animals demonstrated moderate labeling of Sertoli cells, spermatogonia and gonocytes being completely non-reactive. In hypothyroidism affected testes was revealed disperse distribution of Ki-67 marker with predominant accumulation on the periphery of seminiferous cords and in Leydig cells. On postnatal day 20th Ki-67 reactivity was detected in spermatogenic cells of seminiferous tubules. In hypothyroidism affected animals cytoplasmic granularity labeling of maturating spermatogenic cells was higher compared to control, though seminiferous tubules were smaller in diameter and lacking luminae. On postnatal day 40th Ki-67 labeled predominantly spermatogonia, immunoreactivity of which enhanced under hypothyroid conditions. Distribution of VEGF label was generally similar to that of Ki-67, indicating a direct correlation of cell proliferation intensity on saturation of tissues with oxygen. Unlike Ki-67, VEGF exposed strong reactivity with acrosomal granules of early spermatids on postnatal day 20th, as well as more intense spermatogenic cells labeling compared to Ki-67. Conclusion. Testicular morphogenesis in offspring rats, developing under maternal hypothyroidism, was accompanied by the increased immunoreactivity of spermatogenic cell cytoplasm on postnatal days 20th and 40th with Ki-67 and VEGF, as well as acrosomal granules labeling with VEGF. This trend was supplemented with the increased count of macrophages and Leydig cells in testicular interstitium, decreased count and size of spermatogenic cells, damage of their syncytial complexes, all these signs encompassing degenerative changes in seminiferous tubules.
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