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

Area of Science:

• Environmental Health
• Reproductive Biology
• Cellular Metabolism

Background:

• Particulate matter (PM2.5) is a widespread environmental pollutant.
• Male reproductive health is susceptible to environmental toxicant exposure.
• NAD+ metabolism plays a critical role in cellular function and survival.

Purpose of the Study:

• To investigate the mechanism by which PM2.5 induces damage in male mouse reproductive cells.
• To explore the role of NAD+ depletion in PM2.5-induced testicular toxicity.
• To evaluate the potential protective effect of nicotinamide (NAM) against PM2.5 toxicity.

Main Methods:

• Primary mouse testis Sertoli TM4 cells were cultured in vitro.
• Cells were exposed to PM2.5 (100 μg/mL) with or without nicotinamide (5 mM).
• Apoptosis rates, intracellular NAD+/NADH levels, and protein expression of SIRT1 and PARP1 were analyzed.

Main Results:

• PM2.5 exposure significantly increased TM4 cell apoptosis and PARP1 expression.
• PM2.5 exposure decreased intracellular NAD+ and NADH levels and SIRT1 expression.
• Co-treatment with nicotinamide reversed the PM2.5-induced changes, reducing apoptosis and restoring NAD+ levels.

Conclusions:

• PM2.5 exposure causes damage to Sertoli TM4 cells, a key component of the male reproductive system.
• This damage is mediated, at least in part, by the depletion of intracellular NAD+ levels.
• Nicotinamide demonstrates a protective effect against PM2.5-induced testicular cell damage, highlighting NAD+ metabolism as a therapeutic target.