Advances in immunology of male reproductive toxicity induced by common environmental pollutants.
Environ Int
; 190: 108898, 2024 Jul 19.
Article
em En
| MEDLINE
| ID: mdl-39047547
ABSTRACT
Humans are exposed to an ever-increasing number of environmental toxicants, some of which have gradually been identified as major risk factors for male reproductive health, even associated with male infertility. Male infertility is usually due to the reproductive system damage, which may be influenced by the exposure to contaminants such as heavy metals, plasticizers, along with genetics and lifestyle. Testicular immune microenvironment (TIM) is important in maintaining normal physiological functions of the testis, whether disturbed TIM after exposure to environmental toxicants could induce reproductive toxicity remains to be explored. Therefore, the current review aims to contribute to the further understanding of exposure and male infertility by characterizing environmental exposures and the effect on TIM. We first summarized the male reproductive toxicity phenotypes induced by common environmental pollutants. Contaminants including heavy metals and plastic additives and fine particulate matter (PM2.5), have been repetitively associated with male infertility, whereas emerging contaminants such as perfluoroalkyl substances and micro(nano)plastics have also been found to disrupt TIM and lead to male reproductive toxicity. We further reviewed the importance of TIM and its homeostasis in maintaining the normal physiological functions of the testis. Most importantly, we discussed the advances in immunology of male reproductive toxicity induced by metals and metalloids, plastic additives, persistent organic pollutants (POPs), micro(nano)plastic and PM2.5 to suggest the importance of reproductive immunotoxicology in the future study of environmental toxicants, but also contribute to the development of effective prevention and treatment strategies for mitigating adverse effects of environmental pollutants on human health.
Texto completo:
1
Base de dados:
MEDLINE
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article