Efecto del hipertiroidismo inducido por L–tiroxina sobre el estrés del retículo endoplásmico testicular y el eje de señalización Nrf2/HO–1 mediado por beneficios de ratas

  • Gözde Arkalı Firat University, Faculty of Veterinary Medicine, Department of Physiology. Elazığ, Türkiye
  • Şeyma Özer Kaya Firat University, Faculty of Veterinary Medicine, Department of Reproduction and Artificial Insemination. Elazığ, Türkiye
  • Songül Çeribaşı Firat University, Faculty of Veterinary Medicine, Department of Pathology. Elazığ, Türkiye
  • Edanur Güler Ekmen Firat University, Faculty of Veterinary Medicine, Department of Physiology. Elazığ, Türkiye
  • Mesut Aksakal Firat University, Faculty of Veterinary Medicine, Department of Physiology. Elazığ, Türkiye
  • Mehmet Çay Firat University, Faculty of Veterinary Medicine, Department of Physiology. Elazığ, Türkiye
Palabras clave: Hipertiroidismo, estrés del retículo endoplásmico, Nrf2, HO–1, infertilidad

Resumen

El efecto de la glándula tiroides en el sistema reproductor masculino (períodos neonatal, prepuberal y adulto) se ha investigado durante muchos años. El hipertiroidismo puede causar infertilidad masculina al afectar parámetros espermatológicos como la pérdida de motilidad y la disminución de la concentración de espermatozoides. Sin embargo, los mecanismos de la infertilidad masculina causada por el hipertiroidismo aún no están completamente explicados. El objetivo de este estudio fue investigar el efecto del hipertiroidismo sobre el estrés del retículo endoplásmico testicular y la vía antioxidante mediada por PERK en ratas macho adultas. Se utilizaron 24 ratas macho adultas Sprague Dawley. Las ratas se dividieron en dos grupos: grupo control (recibió inyecciones intraperitoneales de solución salina 1 mL·día-1 durante 8 semanas) y grupo de hipertiroidismo (recibió inyecciones intraperitoneales de l–tiroxina 0,3 mg·kg-1·mL-1·día-1 durante 8 semanas). Los niveles séricos de fT3 (P<0,01) y fT4 (P<0,05) aumentaron, el nivel de TSH (P<0,01) y el peso corporal final (P<0,001) disminuyeron en los grupos de hipertiroidismo. Se determinó que los diámetros del túbulo seminífero contortus, el espesor de las células germinales y los valores de la puntuación testicular de Johnsen disminuyeron significativamente en el grupo de hipertiroidismo (P<0,001). Se determinó que tenía un efecto negativo sobre el peso de los órganos reproductivos y los parámetros espermatológicos. Según nuestros resultados, el hipertiroidismo aumentó significativamente el nivel de malondialdehído (P<0,01), el nivel de glutatión (P<0,001), la actividad de la enzima glutatión peroxidasa (P<0,001), PERK, GRP78 (P<0,01), ATF4 (P<0,05), Niveles de expresión de proteínas Nrf2, HO–1 (P<0,05) y actividad catalasa significativamente disminuida (P<0,05). Estos resultados mostraron que el aumento de los niveles de hormonas tiroideas puede ser un factor negativo en términos de fisiología testicular, ya que causa estrés en el RE en los testículos, y la respuesta antioxidante mediada por PERK puede desempeñar un papel importante en el tejido testicular en el hipertiroidismo.

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Publicado
2024-11-07
Cómo citar
1.
Arkalı G, Özer Kaya Şeyma, Çeribaşı S, Güler Ekmen E, Aksakal M, Çay M. Efecto del hipertiroidismo inducido por L–tiroxina sobre el estrés del retículo endoplásmico testicular y el eje de señalización Nrf2/HO–1 mediado por beneficios de ratas. Rev. Cient. FCV-LUZ [Internet]. 7 de noviembre de 2024 [citado 9 de diciembre de 2024];34(3):8. Disponible en: https://produccioncientificaluz.org/index.php/cientifica/article/view/42927
Sección
Medicina Veterinaria