Nephroprotective action of tocotrienol-rich fraction (TRF) from palm oil against potassium dichromate (K2Cr2O7)-induced acute renal injury in rats

Industrial and occupational exposure to chromium compounds, particularly hexavalent chromium (Cr(VI))-containing compounds are often known to cause acute renal injury (ARI) in humans and animals. Its nephrotoxicity is associated with an increased formation of reactive oxygen species and lipid peroxidation in renal tissue. Recent studies suggest that antioxidants of the vitamin E family have protective effects against metal toxicity. Tocotrienols are known to have greater antioxidant activity than tocopherols and protect more efficiently against some free radical-related diseases than does tocopherols. In the present study, ARI induced by potassium dichromate (K2Cr2O7) has been used as a model to investigate the possible nephroprotective effect of tocotrienol-rich fraction (TRF) from palm oil. Wistar male rats having an average body weight (bw) of 210 g were divided into four groups. The first group was taken as control and injected with vehicle alone while the second group was drug control and ingested with TRF (200 mg/kg, bw, orally, once daily for 21 days); the third group served as toxicant and was pre-treated with saline, followed by a single subcutaneous (SC) injection of K2Cr2O7 (15 mg/kg bw). The fourth group was pre-treated with TRF and subsequently injected with K2Cr2O7 (same dose as for the third group). Renal functions, oxidative and nitrosative stress were evaluated on days 0, 1, 2, 4, 7, 11 and 14 after treatment with K2Cr2O7. The results revealed altered proximal tubular function; decreased glomerular filtration accompanied by oxidative damage 48 h after exposure to dichromate; while in the TRF-treated group proximal reabsorptive function, glomerular function and the cellular redox status were sustained. These results were further supported and confirmed by histological findings. The study suggests that TRF is effective in preventing K2Cr2O7-induced acute renal injury, but more studies are needed to confirm the effects of TRF as a nephroprotective agent.