Objective To investigate the influence of chronic manganese (Mn) exposure on renal oxidative injury and the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway in Sprague-Dawley (SD) rats.

Methods A total of 48 healthy male specific pathogen-free(SPF) SD rats were randomly divided into high-dose group (50 mg/kg), low-dose group (10 mg/kg) and control group (sterilized distilled water), with 16 rats in each group, and the rats were sacrificed after Mn exposure(intragastric administration) for 12 months. Renal histopathological changes were observed, and the activity of glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA) in the kidney and the serum levels of creatinine (Cre) and blood urea nitrogen (BUN) were measured, as well as the protein expression levels of Nrf2, heme oxygenase-1 (HO-1), and NAD(P)H: quinone oxidoreductase 1 (NQO1).

Results The high-dose group had a significantly higher kidney organ coefficient than the low-dose group and the control group (P < 0.05). The high-dose group had dilated glomerular capillaries and a significant increase in the number of red blood cells in glomeruli, renal tubules, and renal corpuscles. Compared with the low-dose group and the control group, the high-dose group had significant increases in the serum levels of Cre, BUN and MDA, and a significant reduction in the activity of GSH-Px (P < 0.05). Compared with the control group, the low- and high-dose groups had significant reductions in the protein expression levels of Nrf2, HO-1 and NQO1 (P < 0.05).

Conclusion Chronic high-dose Mn exposure can lead to increase renal parenchymal permeability, renal edema, and abnormal renal function, which may be associated with oxidative injury caused by Mn, and inhibition of the Nrf2 signaling pathway may be one of the important mechanisms of renal oxidative injury caused by chronic Mn exposure in SD rats.