Alteration in thiols homeostasis, protein and lipid peroxidation in renal tissue following subacute oral exposure of imidacloprid and arsenic in Wistar rats

Abstract

The aim of present study was to assess whether No Observed Effect Level (NOEL) of imidacloprid (IMI) potentiates the arsenic induced renal toxicity at its maximum contaminant level in drinking water in Wistar rats. Significant elevation of lipid and protein oxidation with reduced level of total thiols and antioxidant enzymes (catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase and glutathione-s-transferase) in renal tissue may have contributed to increased renal plasma biomarkers (creatinine and blood urea nitrogen) following repeated exposure of IMI and arsenic alone and in-combination. The altered renal biomarkers in co-exposed groups corroborated with histopathological alterations in renal tissue. The observations indicated that altered thiol homeostasis in renal tissue may be associated with increased lipid and protein oxidation in IMI and arsenic administered rats. It is concluded that administration of IMI potentiate the arsenic induced renal damage in Wistar rats.

Keywords: Arsenic; Imidacloprid; Malondialdehyde; Nephrotoxicity; Thiols.

Graphical abstract

Fig. 1

Photomicrograph of Hematoxylin and Eosin (10X) stained sections of formalin fixed kidney (a) control animals showing normal renal parenchyma (b & c) group II and III showing alterations in histological appearance of renal parenchyma with slight degenerative changes (d) group VI: hemorrhages and congestion in renal interstitial tissues (e) group VII: vacuolar degeneration of tubular epithelium and presence of hyaline casts in tubular lumen of rats (f) and group VIII: necrosis of tubular epithelium in Wistar rats.