Impairment of renal mitochondria by nanoparticles

Abstract

This study investigates the toxicological impact of nickel dioxide nanoparticles (NiO2 NPs) on renal mitochondrial function and oxidative stress biomarkers in Wistar rats. Animals were administered NiO2 NPs orally at two doses (5 and 15 mg/kg/day) over a defined treatment period (20 days). Biochemical evaluations revealed dose-dependent disruptions. Total protein levels increased at 5 mg but decreased at 15 mg, while lipid levels consistently declined at both doses, suggesting membrane damage. Malondialdehyde (MDA) levels increased significantly, while reduced glutathione (GSH) levels decreased at both doses, reflecting elevated oxidative stress. Antioxidant enzyme activities (GST, GPx, CAT) were upregulated at 5 mg but markedly suppressed at 15 mg, indicating enzymatic exhaustion at higher exposure.

Mitochondrial assessments revealed increased swelling at both doses and a dose- dependent decline in mitochondrial respiration, highlighting mitochondrial

dysfunction. In conclusion, NiO2 nanoparticles induce oxidative stress, impair mitochondrial bioenergetics, and trigger nephrotoxic effects in a dose-dependent manner in Wistar rats.