A preclinical study on effect of betanin on sodium fluoride induced hepatorenal toxicity in Wistar rats.

Abstract

Background: Excessive fluoride exposure leads to increased oxidative stress and lipid peroxidation, causing harmful effects on the metabolic organs in the human body. Betanin, a pigment obtained from beetroot, is seen to have powerful anti-inflammatory and antioxidant. The study was conducted to determine the role of betanin in fluoride induced hepato-renal toxicity in Wistar rats.

Methods: Twenty four rats were divided into four groups. Group Ⅰ (control) rats received 1 mL distilled water; group Ⅱ rats were administered 10 mg/kg of sodium fluoride (NaF); group Ⅲ received 10 mg/kg NaF and 50 mg/kg (low dose) betanin; group Ⅳ received 10 mg/kg NaF and 200 mg/kg (high dose) betanin. Animals were dosed orally for 90 days. Various markers of liver and kidney function as well as oxidative stress were measured. Liver and kidney samples were examined for histopathology.

Results: Animals in group Ⅱ had significantly increased levels of serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, creatinine, and blood urea nitrogen compared to the NaF + betanin treated animals (group Ⅲ & Ⅳ). Malondialdehyde, nitric oxide levels were significantly lower in rats treated with NaF + betanin (low and high dose). Histologically, in group II rats, signs of interstitial nephritis were seen in the kidneys while liver sections showed clear indication of features of fatty liver and inflammatory cell infiltration. Treatment with betanin alleviated the severity of histopathological changes induced by NaF.

Conclusions: Betanin significantly ameliorated NaF-induced oxidative stress and inflammation, therefore, has potential to be used as protective agent against fluoride induced hepato-renal toxicity.