Calcium carbide–induced derangement of hematopoiesis and organ toxicity ameliorated by cyanocobalamin in a mouse model

BACKGROUND: Calcium carbide (CaC(2)) is a chemical primarily used in the production of acetylene gas. The misuse of CaC(2) to induce fruit ripening is a global challenge with a potential adverse effects to human health. Additionally, CaC(2) 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 CaC(2) toxicity and elucidate any protective effects by cyanocobalamin (vitamin B(12)), 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 CaC(2). The third group received CaC(2) 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: CaC(2) administration did not significantly alter the mice body weight. CaC(2) administration resulted in a significant decrease in packed cell volume (PCV), hemoglobin (Hb), red blood cells (RBCs) and RBC indices; indicative of CaC(2)-driven normochromic microcytic anaemia. Further analysis showed CaC(2)-driven leukopenia. Evidently, vitamin B(12) blocked CaC(2)-driven suppression of PCV, Hb, RBCs and WBCs. Monocytes and neutrophils were significantly up-regulated by CaC(2). CaC(2)-induced elevation of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and bilirubin signaled significant liver damage. Notably, vitamin B(12) stabilized AST, ALT and bilirubin in the presence of CaC(2,) an indication of a protective effect. Histopathological analysis depicted that vitamin B(12) ameliorated CaC(2)-driven liver and kidney injury. CaC(2) resulted in the depletion of glutathione (GSH) levels in the liver; while in the brain, kidney and lungs, the GSH levels were elevated. CaC(2) administration resulted in elevation of pro-inflammatory cytokines TNF-α and IFN-γ. Vitamin B(12) assuaged the CaC(2)-induced elevation of these pro-inflammatory cytokines. CONCLUSIONS: These findings demonstrate for the first time that oral supplementation with vitamin B(12) can protect mice against CaC(2)-mediated toxicity, inflammation and oxidative stress. The findings provide vital tools for forensic and diagnostic indicators for harmful CaC(2) exposure; while providing useful insights into how vitamin B(12) can be explored further as an adjunct therapy for CaC(2) toxicity.