| Autor: |
Hernández-Montiel HL; Facultad de Medicina, Universidad Autónoma de Querétaro, México. hebert@uaq.mx., Vásquez López CM; Facultad de Medicina, Universidad Autónoma de Querétaro, México., González-Loyola JG; Facultad de Medicina, Universidad Autónoma de Querétaro, México., Vega-Anaya GC; Facultad de Medicina, Universidad Autónoma de Querétaro, México., Villagrán-Herrera ME; Facultad de Medicina, Universidad Autónoma de Querétaro, México., Gallegos-Corona MA; Facultad de Medicina, Universidad Autónoma de Querétaro, México., Saldaña C; Facultad de Medicina, Universidad Autónoma de Querétaro, México., Ramos Gómez M; Facultad de Química, Universidad Autónoma de Querétaro, México., García Horshman P; Instituto de Neurobiología, UNAM, Querétaro, México., García Solís P; Facultad de Medicina, Universidad Autónoma de Querétaro, México., Solís-S JC; Facultad de Medicina, Universidad Autónoma de Querétaro, México., Robles-Osorio ML; Facultad de Medicina, Universidad Autónoma de Querétaro, México., Ávila Morales J; Facultad de Medicina, Universidad Autónoma de Querétaro, México., Varela-Echavarría A; Instituto de Neurobiología, UNAM, Querétaro, México., Paredes Guerrero R; Instituto de Neurobiología, UNAM, Querétaro, México. |
| Abstrakt: |
Aging is a multifactorial universal process and constitutes the most important risk factor for chronic-degenerative diseases. Although it is a natural process, pathological aging arises when these changes occur quickly and the body is not able to adapt. This is often associated with the generation of reactive oxygen species (ROS), inflammation, and a decrease in the endogenous antioxidant systems, constituting a physiopathological state commonly found in chronic-degenerative diseases. At the testicular level, aging is associated with tissue atrophy, decreased steroidogenesis and spermatogenesis, and sexual behavior disorders. This situation, in addition to the elevated generation of ROS in the testicular steroidogenesis, provides a critical cellular environment causing oxidative damage at diverse cellular levels. To assess the effects of a reduction in the levels of ROS, thiamine pyrophosphate (TPP) was chronically administered in senile Wistar rats. TPP causes an activation of intermediate metabolism routes, enhancing cellular respiration and decreasing the generation of ROS. Our results show an overall decrease of atrophic histological changes linked to aging, with higher levels of serum testosterone, sexual activity, and an increase in the levels of endogenous antioxidant enzymes in TPP-treated animals. These results suggest that TPP chronic administration decreases the progression of age-related atrophic changes by improving the intermediate metabolism, and by increasing the levels of antioxidant enzymes. |
