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

Abstract

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.