Reproductive cytotoxic and genotoxic impact of polystyrene microplastic on spermatozoa.

In recent decades, industrialization, intensive agriculture, and urban development have severely impacted marine environments, compromising the health of aquatic and terrestrial organisms. Inadequate disposal results in hundreds of tons of plastic products released annually into the environment, which degrade into microplastics (MPs), posing health risks due to their ability to biomagnify and bioaccumulate. Among these, polystyrene MPs (PS-MPs) are significant pollutants in marine ecosystems, widely studied for their reproductive toxicological effects.

Oxidative Stress Biomarkers in Male Infertility: Established Methodologies and Future Perspectives.

Male fertility can be affected by oxidative stress (OS), which occurs when an imbalance between the production of reactive oxygen species (ROS) and the body's ability to neutralize them arises. OS can damage cells and influence sperm production. High levels of lipid peroxidation have been linked to reduced sperm motility and decreased fertilization ability.

Genotoxicity Assessment of Quinoin, a Ribosome Inactivating Protein from Quinoa Seeds, in the Teleost .

Background: Ribosome inactivating proteins (RIPs) are N-glycosylases found in various plants that are able to specifically and irreversibly inhibit protein translation, thereby leading to cell death. Their cytotoxic properties have attracted attention in the medical field in the context of developing new anticancer therapies. Quinoin is a novel toxic enzyme obtained from quinoa seeds and classified as a type 1 RIP ( Willd.

In Vitro Combination of Ascorbic and Ellagic Acids in Sperm Oxidative Damage Inhibition.

It is known that an altered redox balance interferes with normal spermatic functions. Exposure to genotoxic substances capable of producing oxidative stress (OS) can cause infertility in humans. The use of antioxidants to reduce oxidative stress contributes to the improvement in reproductive function.

The Future Evolution of the Mortality Acceleration Due to the COVID-19: The Charlson Comorbidity Index in Stochastic Setting.

The empirical evidence from different countries point out many of those who die from coronavirus would have died anyway in the relatively near future due to their existing frailties or co-morbidities. The of the mortality conceives the underlying insight according to deaths are "accelerated" ahead of schedule due to COVID-19. Starting from this idea, we forecast the future mortality acceleration, based on the deterioration due to the presence of the comorbidities at COVID-19 diagnosis.