Particulate matter inhalation induces male reproductive dysfunction comparable to renal failure: insights from a rat model
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Byeong Jo Jeon1, Bum Sik Tae1, Jin Joo Cha2
1Department of Urology, Korea University Ansan Hospital, Korea University College of Medicine, Ansan, Korea.
Background:
Particulate matter (PM), particularly PM2.5, is a pervasive environmental pollutant capable of penetrating alveolar tissues and causing systemic effects. Although its detrimental impact on the respiratory and cardiovascular systems is well documented, its effects on male reproductive function remain incompletely understood. This study aimed to investigate whether inhalation exposure to PM2.5 induces male reproductive dysfunction and to compare these alterations with those observed in renal insufficiency (RI), a systemic condition known to impair reproductive health.
Methods:
Male rats were divided into three groups: control, PM2.5 exposure (30 mg/kg/day, 3 h/day for 10 days), and RI induced by unilateral ureteral obstruction. Sperm parameters, including count, motility, and morphology, were evaluated. Testicular tissues were examined using angiotensin-converting enzyme 2 (ACE2) immunohistochemical (IHC) staining to assess alterations in the testicular renin-angiotensin system and quantitative real-time polymerase chain reaction (PCR) to measure inflammatory and endothelial-related gene expression.
Results:
Exposure to PM2.5 resulted in a significant increase in sperm abnormalities, whereas sperm count and motility did not reach statistical significance. IHC analysis revealed altered ACE2 expression patterns in PM2.5 group, which partially overlapped with those observed in the RI group. Gene expression analyses indicated upregulation of inflammatory and endothelial activation markers in both the PM2.5 and RI groups.
Conclusions:
PM inhalation induces measurable male reproductive dysfunction characterized by increased sperm abnormalities and molecular alterations in testicular tissues. The partially overlapping injury patterns between PM exposure and RI suggest shared oxidative and inflammatory stress-related mechanisms. These findings highlight the vulnerability of the male reproductive system to environmental toxicants and support consideration of PM exposure as a potential contributor to male reproductive impairment.
