Sperm Dysfunction in the Testes and Epididymides due to Overweight and Obesity Is Not Caused by Oxidative Stress

Abstract

Obesity is a condition that has been linked to male infertility. The current hypothesis regarding the cause of infertility is that sperm are highly sensitive to reactive oxygen species (ROS) during spermatogenesis in the testes and transit through the epididymides, so the increase in ROS brought on by obesity could cause oxidative stress. The aim of this study was to evaluate whether the activity of the enzymes catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX) is capable of counteracting oxidative stress in sperm. The male Wistar rat was used as an overweight and obesity model, and analysis of fertility in these groups was carried out including the control group. Serum testosterone levels were determined, and the scrotal fat, testes, and epididymides were extracted. The epididymides were separated ini0 3 principal parts (caput, corpus, and cauda) before evaluating sperm viability, sperm morphology, damage to desoxyribonucleic acid of the sperm, and ROS production. The protein content and specific activity of the three enzymes mentioned above were evaluated. Results showed a gain in body weight and scrotal fat in the overweight and obese groups with decreased parameters for serum testosterone levels and sperm viability and morphology. Fertility was not greatly affected and no DNA integrity damage was found, although ROS in the epididymal sperm increased markedly and Raman spectroscopy showed a disulfide bridge collapse associated with DNA. The specific activities of CAT and GPX increased in the overweight and obesity groups, but those of SOD did not change. The amounts of proteins in the testes and epididymides decreased. These findings confirm that overweight and obesity decrease concentrations of free testosterone and seem to decrease protein content, causing poor sperm quality. Implications. An increase in scrotal fat in these conditions fosters an increase of ROS, but the increase of GPX and CAT activity seems to avoid oxidative stress increase in the sperm without damaging your DNA.

Sperm DNA damage: The possible link between obesity and male infertility, an update of the current literature

“…Western-style diet inducing obesity and/or metabolic syndrome consistently find that male obesity increases sperm DNA damage. [70][71][72][73] Comorbidities associated with obesity have also been shown to significantly amplify the effects of obesity on sperm DNA damage.…”

“…Given the large heterogeneity amongst human studies, animal models can be more informative for understanding the true effects obesity has on sperm DNA damage. Rodent models utilising high‐fat diets (commonly high in saturated fats ranging 20%–40%) mimicking a Western‐style diet inducing obesity and/or metabolic syndrome consistently find that male obesity increases sperm DNA damage 70–73 . Comorbidities associated with obesity have also been shown to significantly amplify the effects of obesity on sperm DNA damage.…”