Effect of Luteolin on Nickel Chloride–Induced Renal Hyperproliferation and Biotransformation Parameters in Wistar Rats

Abstract

Nickel, a major environmental pollutant, is a known potent nephrotoxic agent. In this communication, we report the chemopreventive effect of luteolin on nickel chloride (NiCl₂)-induced renal oxidative stress, toxicity, and cell proliferation response in male Wistar rats. NiCl₂ (250 µmol/kg b.wt./2 mL) enhances reduced renal glutathione content (GSH), glutathione S.-transferase (GST), glutathione reductase (GR), lipid peroxidation (LPO), H₂O₂ generation, blood urea nitrogen (BUN), and serum creatinine with a concomitant decrease in the activity of glutathione peroxidase (GPx) (p < 0.001). NiCl₂ administration also dose-dependently induced the renal ornithine decarboxylase (ODC) activity several-fold compared with the activity in saline-treated rats. Similarly, renal DNA synthesis, which is measured as [³H]thymidine incorporation in DNA, is also increased after NiCl₂ treatment. Prophylactic treatment of rats with luteolin (10 and 20 µmol/kg b.wt.) daily for 1 week resulted in the diminution of NiCl₂-mediated damage as evident from the downregulation of glutathione content, GST, GR, LPO, H₂O₂ generation, BUN, serum creatinine, DNA synthesis (p < 0.001), and ODC activity (p < 0.01) with concomitant restoration of GPx activity. Thus, the current investigation suggests that luteolin can be used as a chemopreventive agent for cancer prevention as evident from the study where it blocks or suppresses the events associated with chemical carcinogenesis.

Keywords:

• Cell proliferation response
• chemoprevention
• luteolin
• nickel chloride
• oxidative stress