Pre-treatment with Beta Carotene Gives Protection Against Nephrotoxicity Induced by Bromobenzene via Modulation of Antioxidant System, Pro-inflammatory Cytokines and Pro-apoptotic Factors.

Bromobenzene is an environmental toxin which causes hepatotoxicity, and the secondary metabolites on biotransformation cause nephrotoxicity. The objective of this study was to assess the alleviation of the nephrotoxic effect of bromobenzene by beta carotene in female Wistar albino rats. Beta carotene (10 mg/kg b.w.p.o.) was delivered orally to the rats for 9 days before bromobenzene (10 mM/kg b.w.p.o.) was intragastrically intubated. Kidney markers, antioxidant status and lipid peroxidation were evaluated. In addition, the levels of TNF-α, IL-6 and IL-1β were measured in serum and in kidney tissue homogenate using ELISA. Caspase, COX-2 and NF-κB were measured with the help of Western blotting. Histopathological analysis of the kidney was done for the control and experimental rats. Bromobenzene induction caused elevation in levels of creatinine, urea, uric acid, cytokines and lipid per oxidation along with deterioration in histological observations and antioxidant status. Pre-treatment with beta carotene significantly (*p < 0.05) normalised the levels of kidney markers and pro-inflammatory cytokines. It also reduced oxidative stress and lipid peroxidation, as shown by improved antioxidant status. The anti-apoptotic activity was evidenced by inhibition of protein expression of caspase, COX-2 and NF-κB. This significant reversal (*p < 0.05) of the above variations in comparison with the control group as noticed in the bromobenzene-administered rats demonstrates that beta carotene possesses promising nephroprotective effect through its antioxidant, anti-inflammatory and anti-apoptotic activity and therefore suggests its use as a potential therapeutic agent for protection from bromobenzene and hence environmental pollutant toxicity.