
Toxics, Год журнала: 2024, Номер 12(12), С. 878 - 878
Опубликована: Дек. 1, 2024
As one of the most common air pollutants, fine particulate matter (PM2.5) increases risk diseases in various systems, including urinary system. In present study, we exposed male and female C57BL/6J mice to PM2.5 for 8 weeks. Examination renal function indices, creatinine (CRE), blood urea nitrogen (BUN), uric acid (UA), microalbumin, indicated that kidneys mice, not underwent early injury, exhibiting glomerular hyperfiltration. Meanwhile, pathological staining showed exhibited enlarged glomerulus filled entire Bowman’s capsule mice. Afterward, explored potential causes mechanisms Variations mRNA levels key genes involved renin–angiotensin system (RAS) kallikrein–kinin (KKS) demonstrated led elevated capillary hydrostatic pressure by disturbing balance between RAS KKS, which turn increased filtration rate (GFR). addition, found glucose females, enhanced tubular reabsorption glucose, attenuated macular dense sensory signaling, induced hypoxia, affected adenosine triphosphate (ATP) synthesis, thus attenuating tubuloglomerular feedback (TGF)-induced afferent arteriolar constriction leading conclusion, this study hyperfiltration affecting RAS/KKS imbalances, as well regulation TGF; innovatively unveiled association subchronic exposure kidney injury its gender dependence; enriched toxicological evidence confirmed importance reducing ambient concentrations.
Язык: Английский