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

Nancy Wambui Wairimu; Peninah Wairagu; Kennedy W Chepukosi; George F Obiero; Patrick W Okanya; Alfred Orina Isaac; James Nyabuga Nyariki

doi:10.1155/2023/7058016

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

J Toxicol. 2023 Oct 10:2023:7058016. doi: 10.1155/2023/7058016. eCollection 2023.

Authors

Nancy Wambui Wairimu¹, Peninah Wairagu¹, Kennedy W Chepukosi¹, George F Obiero¹, Patrick W Okanya¹, Alfred Orina Isaac², James Nyabuga Nyariki¹

Affiliations

¹ Department of Biochemistry and Biotechnology, Technical University of Kenya, P. O. Box 52428, Nairobi 00200, Kenya.
² Department of Pharmaceutical Technology, School of Health Sciences and Technology, Technical University of Kenya, P. O. Box 52428, Nairobi 00200, Kenya.

Abstract

Sodium metabisulfite (SMB) is a biocide and antioxidant agent generally used as a preservative in food and beverage industries but can oxidize to harmful sulfite radicals. A standardized Ginkgo biloba (EGb-761) has demonstrated potent antioxidant and anti-inflammatory activities, which is beneficial for the treatment of diseases that exhibit oxidative stress and inflammation. The present study sought to investigate the putative ameliorative effects of EGb-761 against SMB-induced toxicity in mice. Thirty-two male Swiss white mice were randomized into control, SMB-treated, SMB + EGb-761-treated, and EGb-761-treated groups. EGb-761 (100 mg/kg/day) and SMB (98 mg/kg/day) were administered by gastric gavage for 40 days. Oral administration of EGb-761 restored 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 of aspartate 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-761 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 significant increase of tissue levels of malondialdehyde (MDA), serum nitric oxide (NO), interferon-gamma (IFN-γ) 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 effects of SMB-driven toxicities. These findings provide a novel approach that can be optimized for preventing or treating exposure due to SMB toxicity.