Renoprotection of Kolaviron against benzo (A) pyrene-induced renal toxicity in rats

Abstract

Benzo(a)pyrene (B[a]P), a polycyclic aromatic hydrocarbon generally formed from incomplete combustion of organic matter, reportedly causes renal injury and elicits a nephropathic response. The present study investigated the modulatory effect of Kolaviron, an isolated bioflavonoid from the seed of Garcinia kola, on renal toxicity induced by B[a]P in Wistar rats. Benzo[a]pyrene was administered at a dose of 10 mg/kg alone or in combination with Kolaviron at 100 and 200 mg/kg for 15 d. Administration of B[a]P alone resulted in significant increase in plasma levels of urea and creatinine in the treated rats. Moreover, B[a]P exposure significantly decreased the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-s-transferase (GST) as well as glutathione (GSH) level in the kidneys of treated rats. Conversely, myeloperoxidase (MPO) activity, hydrogen peroxide (H₂O₂) and malondialdehyde (MDA) levels were markedly elevated in kidneys of B[a]P-treated rats compared with control. Further, B[a]P exposure significantly decreased the circulatory concentrations of triiodothyronine (T₃) and T₃/T₄ ratio without affecting thyroxine (T₄) in the treated rats. Light microscopy revealed tubular lumen with numerous protein casts in kidneys of rats exposed to B[a]P alone. Kolaviron co-treatment significantly improved the renal antioxidant status, thyroid gland function and restored the renal histology, thus demonstrating the protective effect of Kolaviron in B[a]P-treated rats. Dietary inclusion of Kolaviron could exert protective effects against renal toxicity resulting from B[a]P exposure.

• Benzo[a]pyrene
• Kolaviron
• kidney
• thyroid hormones
• rats

Declaration of interest

The authors report no conflicts of interest. This research was done without specific grant from any funding agency in the public, commercial, or not-for-profit sectors.