1-Nitropyrene exposure induces oxido-inflammatory stress in the renal tissues of Wistar rats

Abstract

Background: The mechanism underlying 1-nitropyrene (1-NP)- induced kidney damage remains largely unclear.

Methods: This study examined renal oxido-inflammatory stress in 32 adult male Wistar rats (8 per group) administered graded oral doses of 62.5, 125, or 250 mg/kg body weight 1-NP daily for seven consecutive days. A vehicle control group received corn oil (2 mL/kg body weight).

Results: 1-NP administration induced a marked, dose-dependent reduction in body weight gain, with a significant increase in kidney weight at the highest dose (250 mg/kg body weight). Renal function was impaired, as evidenced by significant dose-dependent elevations in serum urea and creatinine levels. Furthermore, 1-NP exposure significantly reduced the activities of catalase, superoxide dismutase, glutathione-S-transferase, and glutathione peroxidase, and depleted reduced glutathione levels, while concurrently increasing lipid peroxidation and reactive oxygen and nitrogen species. Significant increases in nitric oxide concentration and myeloperoxidase activity confirmed the induction of renal inflammation. These biochemical findings were corroborated by histopathological evidence of glomerular degeneration, focal inflammatory infiltration, and vascular congestion in the renal cortex.

Conclusion: These findings provide experimental evidence that 1-NP induces dose-dependent renal injury through an oxido-inflammatory mechanism in male Wistar rats, with implications for the nephrotoxic risks of environmental nitropyrene exposure.