Sodium Metabisulfite-Induced Hematotoxicity, Oxidative Stress, and Organ Damage Ameliorated by Standardized Ginkgo biloba in Mice

Abstract

Sodium metabisulfte (SMB) is a biocide and antioxidant agent generally used as a preservative in food and beverage industries but can oxidize to harmful sulfte radicals. A standardized Ginkgo biloba (EGb-761) has demonstrated potent antioxidant and antiinfammatory activities, which is benefcial for the treatment of diseases that exhibit oxidative stress and infammation. Te present study sought to investigate the putative ameliorative efects of EGb-761 against SMB-induced toxicity in mice. Tirty-twomale Swiss white mice were randomized into control, SMB-treated, SMB + EGb-761-treated, and EGb-761-treated groups. EGb761 (100 mg/kg/day) and SMB (98 mg/kg/day) were administered by gastric gavage for 40 days. Oral administration of EGb-761restored SMB-induced decrease in body weight and prevented SMB-induced thrombocytopenia, leukocytosis, and anemia.Furthermore, EGb-761-treatment protected against SMB-induced liver and kidney injury depicted by decreased serum levels ofaspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, bilirubin, creatinine, urea, uric acid, and albumin. Furthermore, EGb-761 treatment attenuated SMB-driven dyslipidemia and metabolic acidosis. Besides, EGb-76 supplementation abrogated SMB-driven oxidative stress as depicted by stabilized reduced glutathione (GSH) levels in the brain, liver, kidney, spleen, heart, and lungs. SMB induced a signifcant increase of tissue levels of malondialdehyde (MDA), serum nitric oxide (NO), interferon-gamma (IFN-c) and tumor necrosis factor-α (TNF-α) which were abrogated by EGb-761 treatment. In conclusion, these results deepen our understanding of EGb-761 in light of various detrimental efects of SMB-driven toxicities.These findings provide a novel approach that can be optimized for preventing or treating exposure due to SMB toxicity