Glyphosate-based herbicides (GBH) are widely used worldwide. Their negative impact on human health is a matter of debate by regulatory bodies and the public. The present study sought to determine the impact of a GBH on the vital organs; and the potential protective effects of vitamin B12 (cyanocobalamin) supplementation. Sixty white Swiss mice were randomly assigned to five treatment groups, each containing twelve mice. Group one represented the normal control; Group two mice were treated with 375 mg/kg of GBH for 56 days; Group three mice received 10 mg/kg of cyanocobalamin for 56 days; Group four mice were administered with 375 mg/kg of GBH and 10 mg/kg cyanocobalamin for 56 days and Group five received 10 mg/kg cyanocobalamin first for 7 days, then continued thereafter co-administered together with 375 mg/kg of GBH for 56 days). Oral administration of GBH induced severe anemia in mice, which was attenuated by cyanocobalamin. Moreover, GBH resulted in a very significant alteration of platelets, WBCs, and its sub-types. Once again, cyanocobalamin stabilized the levels of platelets and WBCs in the presence of GBH. GBH-induced elevation of triglycerides and HDL was nullified by the administration of cyanocobalamin. Further studies showed evidence for GBH-induced inflammation represented by an imbalance in serum levels of the TNF-α: IL-10 and IFN-γ ratios. The GBH severely depleted GSH levels in the liver. A GBH-induced rise in GSH in the kidney, lungs and brain was noted; and is an indicator of antioxidant capacity enhancement in response to a GBH-induced oxidant challenge. Moreover, cyanocobalamin supplementation abrogated GBH-induced oxidative stress as depicted by stabilized GSH levels in the liver, kidney, lungs, and brain. In the presence of cyanocobalamin, the GBH-induced liver injury depicted by elevation of AST, ALT, and bilirubin, was attenuated. From the results, we conclude that the capacity of cyanocobalamin to assuage GBH-induced inflammatory responses, hepatotoxicity, and hematological alteration as well as oxidative stress may be attributable to its antioxidant and anti-inflammatory properties. The current findings provide a solid foundation for further scrutiny of this phenomenon, with vital implications in GBH exposure and the role of potent antioxidant supplementation in the management of GBH-induced toxicity.

Background: Calcium carbide (CaC₂) is a chemical primarily used in the production of acetylene gas. The misuse of CaC₂ to induce fruit ripening is a global challenge with a potential adverse effects to human health. Additionally, CaC₂ is known to contain some reasonable amount of arsenic and phosphorous compounds that are toxic and pose a danger to human health when ingested. The current study sought to characterize CaC₂ toxicity and elucidate any protective effects by cyanocobalamin (vitamin B₁₂), a well-established antioxidant and anti-inflammatory bio-molecule. Female Swiss white mice were randomly assigned into three groups; the first group was the control, while the second group was administered with CaC₂. The third group received CaC₂ followed by administration of vitamin B12. The mice were sacrificed at 60 days post treatment, hematological, biochemical, glutathione assay, cytokine ELISA and standard histopathology was performed. Results: CaC₂ administration did not significantly alter the mice body weight. CaC₂ administration resulted in a significant decrease in packed cell volume (PCV), hemoglobin (Hb), red blood cells (RBCs) and RBC indices; indicative of CaC₂-driven normochromic microcytic anaemia. Further analysis showed CaC₂-driven leukopenia. Evidently, vitamin B₁₂ blocked CaC₂-driven suppression of PCV, Hb, RBCs and WBCs. Monocytes and neutrophils were significantly up-regulated by CaC₂. CaC₂-induced elevation of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and bilirubin signaled significant liver damage. Notably, vitamin B₁₂ stabilized AST, ALT and bilirubin in the presence of CaC_2, an indication of a protective effect. Histopathological analysis depicted that vitamin B₁₂ ameliorated CaC₂-driven liver and kidney injury. CaC₂ resulted in the depletion of glutathione (GSH) levels in the liver; while in the brain, kidney and lungs, the GSH levels were elevated. CaC₂ administration resulted in elevation of pro-inflammatory cytokines TNF-α and IFN-γ. Vitamin B₁₂ assuaged the CaC₂-induced elevation of these pro-inflammatory cytokines. Conclusions: These findings demonstrate for the first time that oral supplementation with vitamin B₁₂ can protect mice against CaC₂-mediated toxicity, inflammation and oxidative stress. The findings provide vital tools for forensic and diagnostic indicators for harmful CaC₂ exposure; while providing useful insights into how vitamin B₁₂ can be explored further as an adjunct therapy for CaC₂ toxicity.

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 (100mg/kg/day) and SMB (98mg/kg/day) were administered by gastric gavage for 40days. 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.