Suchergebnisse

Abstract
With the rapid expansion of industrial scale, an increasing number of fine particulate matter (PM2.5) has bringing health concerns. Although exposure to PM2.5 has been clearly associated with male reproductive toxicity, the exact mechanisms are still unclear. Recent studies demonstrated that exposure to PM2.5 can disturb spermatogenesis through destroying the blood-testis barrier (BTB), consisting of different junction types, containing tight junctions (TJs), gap junctions (GJs), ectoplasmic specialization (ES) and desmosomes. The BTB is one of the tightest blood-tissue barriers among mammals, which isolating germ cells from hazardous substances and immune cell infiltration during spermatogenesis. Therefore, once the BTB is destroyed, hazardous substances and immune cells will enter seminiferous tubule and cause adversely reproductive effects. In addition, PM2.5 also has shown to cause cells and tissues injury via inducing autophagy, inflammation, sex hormones disorder, and oxidative stress. However, the exact mechanisms of the disruption of the BTB, induced by PM2.5, are still unclear. It is suggested that more research is required to identify the potential mechanisms. In this review, we aim to understand the adverse effects on the BTB after exposure to PM2.5 and explore its potential mechanisms, which provides novel insight into accounting for PM2.5-induced BTB injury.

Abstract
Exposure to PM2.5 is the most significant air pollutant for health risk. The testosterone level in male is vulnerable to environmental toxicants. In the past, researchers focused more attention on the impacts of PM2.5 on respiratory system, cardiovascular system, and nervous system, and few researchers focused attention on the reproductive system. Recent studies have reported that PM2.5 involved in male testosterone biosynthesis disruption, which is closely associated with male reproductive health. However, the underlying mechanisms by which PM2.5 causes testosterone biosynthesis disruption are still not clear. To better understand its potential mechanisms, we based on the existing scientific publications to critically and comprehensively reviewed the role and potential mechanisms of PM2.5 that are participated in testosterone biosynthesis in male. In this review, we summarized the potential mechanisms of PM2.5 triggering the change of testosterone level in male, which involve in oxidative stress, inflammatory response, ferroptosis, pyroptosis, autophagy and mitophagy, microRNAs (miRNAs), endoplasmic reticulum (ER) stress, and N6-methyladenosine (m6A) modification. It will provide new suggestions and ideas for prevention and treatment of testosterone biosynthesis disruption caused by PM2.5 for future research.