A ripple effect? The impact of obesity on sperm quality and function.

Infertility affects approximately 15% of couples trying to conceive. Male-related causes account for roughly 50% of cases, with obesity emerging as a possible significant factor. Obesity, defined as a body mass index of 30.0 or higher, has become a widespread epidemic associated with numerous health issues, including a decrease of fertility. This review discusses the relationship between obesity and male infertility, particularly focusing on sperm quality and function. An overview of the literature suggests that obesity may influence the male reproductive system via disruptions in hormonal profiles, oxidative stress, and inflammation, leading to changes in sperm parameters. Several studies have discussed if obesity causes a decrease in sperm concentration, motility, and normal morphology, so far without a consensus being reached. However, available evidence suggests an impairment of sperm function in obese men, due to an increase in DNA damage and oxidative stress, impaired mitochondrial function and acrosome reaction in response to progesterone. Finally, the relationship between obesity and assisted reproductive technologies outcomes remains debatable, with conflicting evidence regarding the influence on fertilisation, pregnancy, and live birth rates. Therefore, the actual impact of obesity on human spermatozoa still needs to be clarified, due to the multiple factors potentially in play.

Comparative in vitro study on the local tolerance and efficacy of benzalkonium chloride, myristalkonium chloride and nonoxynol-9 as active principles in vaginal contraceptives.

BACKGROUND: Spermicides have been identified as a potentially attractive alternative to hormonal contraceptives and/or intrauterine devices. Thus, this study aimed evaluating the efficacy and local tolerance of benzalkonium chloride (BKC) and myristalkonium chloride (MKC) contained in Pharmatex® vaginal formulations and compare them with nonoxynol-9 (N-9), the most common active ingredient in topical vaginal contraceptives. METHODS: Human normozoospermic samples were assessed for motility, viability, acrosome status and penetration ability after exposure to control, N-9 or different BKC and MKC doses for 0 and 10 minutes. Local tolerance on HeLa cells was evaluated by the Trypan-blue and MTT assays. RESULTS: Exposure to BKC and MKC reduced acrosome integrity while promoting total immobilisation and complete loss of sperm viability (p < .001, n = 15). Both compounds also compromised sperm penetration ability upon exposure (p < .001, n = 15). N-9 induced the same outcomes (p < .001, n = 15); nevertheless, it was more toxic to HeLa cells than BKC and MKC (p < .05, n = 14). CONCLUSIONS: BKC and MKC present strong in vitro spermicidal activity at lower doses than N-9 and were better tolerated after immediate exposure than N-9. Available Pharmatex® galenic formulations were as effective as products based on N-9.