article · Archives of Razi Institute
Lead toxicity has been identified in soft tissues, whereas retinoid facilitates embryonic development during the intrauterine phase and supports tissue regeneration. The present study investigated the histological changes associated with the testes of animals exposed to lead II oxide during intrauterine period and the protective role of retinol. Twenty gestational animals were utilized in the study. These animals were exposed to lead (II) oxide for a period of three weeks, which corresponds to their gestational period. The subjects received daily administration of 60 mg/kg/body weight of lead (II) oxide alongside 25,000 IU/kg body weight of retinol, respectively. Subsequent to parturition, offspring from each designated group were procured and subsequently allocated into distinct cages for duration of three weeks, comprising a neonatal period of 21 days. The progeny were euthanized via cervical dislocation twelve hours after the completion of the neonatal period of 21 days. This was followed by the excision of the testes, which were then fixed in Bouin's fluid for histopathological examination and immunohistochemical analysis using Ki-67 protein expression. The study demonstrated the teratogenic effects of lead (II) oxide, which resulted in degenerative alterations in the seminiferous tubules, vascular congestion, and alterations in spermatogonia lineage across the seminiferous tubules. The intra-uterine lead (II) oxide exposed group exhibited widening of interstitial spaces and degeneration of leydig cells. Retinol treatment has been demonstrated to result in enhancements in testicular histological features and Ki-67 migration molecule expression in neonatal testes. The embryogenic influence of retinol was established through the examination of testicular histological features in animals subjected to intrauterine exposure and the corresponding testicular expression of Ki-67. Consequently, retinol demonstrated protective and fertility-enhancing properties against the detrimental effects induced by exposure to lead (II) oxide.
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DOI: 10.32592/ari.2025.80.2.361
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