INFLUENCE OF MATERNAL HYPERTYROIDISM ON POSTNATAL MORPHOGENESIS OF PROGENY TESTES AS DETECTED BY MORPHOMETRIC AND LECTIN HISTOCHEMISTRY METHODS
DOI:
https://doi.org/10.11603/1811-2471.2019.v.i3.10393Keywords:
rats, maternal hyperthyroidism, progeny testes morphogenesis, morphometry, lectin histochemistryAbstract
SUMMARY. By means of morphometric and lectin histochemistry methods the impact of maternal hyperthyroidism on the structural components of progeny testes on the successive stages of postnatal ontogeny was investigated.
The aim of the study – to invesigate the impact of maternal hyperthyroidism on the micromorphology and glycan profile of progeny testes.
Material and Methods. Hyperthyroidism was induced by feeding experimental group of animals with 100 mkg/kg of L-thyroxine for two weeks before pregnancy, throughout the gestational and lactation period. The lectin panel included GNA, PNA, SBA, WGA, SNA, and LABA.
Results. On the 20th prenatal and 1st postnatal days within the progeny testes maternal hyperthyroidism induced significant decrease of interstitial connective tissue content, which was accompanied by the enhanced proliferative activity of Sertoli cells of seminiferous cords. On postnatal day 20th increased proliferative rate of the spermatogenic epithelium was combined with reduction of lectin receptors sites in spermatocytes located within seminiferous tubules adulmenal compartment. On postnatal day 40th experimental group animals demonstrated acceleration of acrosomal biogenesis, destructive changes in cellular components of seminiferous tubules with diminution of their diameter and compensatory interstitial space expansion. Differences in morphometric parameters and lectin labeling of testicular components of control and experimental group rats were maximally expressed on the prenatal day 20th with subsequent deminishing in sexually mature animals, indicating a transient impact of maternal hyperthyroidism on the histophysiology of progeny testes. A trend for reduction of lectin receptor sites in progeny testes under the influence of maternal hyperthyroidism has been noted, but no significant qualitative differences in their carbohydrate determinants were detected so far. In the present study it was documented intense labeling of fetal Leydig cells with GNA and LABA, of acrosomal granules and caps of early spermatids – with PNA, SBA, and SNA, of interstitial macrophages – with WGA and PNA lectins, which therefore can be recommended as selective histochemical markers of these cell populations.
Conclusions. The data presented expands the existing knowledge on the negative impact of maternal hyperthyroidism on morphogenesis and histophysiology of progeny testes, and demonstrate new possibilities of lectins application as selective histochemical markers of rat testicular components.
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