PM2.5 mediates mouse testis Sertoli TM4 cell damage by reducing cellular NAD⁺

Abstract

Objective

This study aims to explore the mechanism of PM2.5 damage to the reproductive system of male mice.

Methods

Mouse testis Sertoli TM4 cells were divided into four groups: a control group (no additional ingredients except for medium), PM2.5 group (medium containing 100 μg/mL PM2.5), PM2.5 + NAM group (medium containing 100 μg/mL PM2.5 and 5 mM NAM), and NAM group (medium containing 5 mM nicotinamide) and cultured in vitro for 24 or 48 h. The apoptosis rate of TM4 cells was measured using flow cytometry, the intracellular levels of NAD⁺ and NADH were detected using an NAD⁺/NADH assay kit, and the protein expression levels of SIRT1 and PARP1 were determined by western blotting.

Results

Mouse testis Sertoli TM4 cells exposed to PM2.5 demonstrated an increase in the apoptosis rate and PARP1 protein expression, albeit a decrease in NAD⁺, NADH, and SIRT1 protein levels (p = 0.05). These changes were reversed in the group treated with a combination of PM2.5 and nicotinamide (p = 0.05).

Conclusion

PM2.5 can cause Sertoli TM4 cell damage in mouse testes by decreasing intracellular NAD⁺ levels.

Keywords:

• PM2.5
• testis Sertoli TM4 cell
• NAD
• +nicotinamide
• reproductive damage

Acknowledgments

Our sincere thanks to the R&D Laboratory of Henan Gene Hospital, Assistant Researcher Zhang Yize for providing experimental supplies, Assistant Researcher Dong Zihui for training experimental techniques, and Dr. Cui Yushan and Dr. Bai Shengjie for their guidance. We thank Home for Researchers editorial team (www.home-for-researchers.com) for the language editing service.

Author contributions

P.X.: conceptualization, methodology, software, formal analysis, investigation, data curation, writing: original draft preparation. Y.Y.: conceptualization, methodology, resources, writing: review and editing, supervision, project administration, funding acquisition. TT.R.: validation, writing: review and editing, visualization. All authors have read and agreed to the published version of the manuscript.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

All data generated or analyzed during this study are included in this published article, or are available on request from the corresponding author upon reasonable request.

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article.