Lab Anim Res.  2022 Sep;38(3):193-208. 10.1186/s42826-022-00136-1.

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

• Ouma PA
• Mwaeni VK
• Amwayi PW
• Isaac AO
• Nyariki JN

• KMID: 2534146
• DOI: http://doi.org/10.1186/s42826-022-00136-1

Abstract

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 v . 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 v-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 upregulated 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.

Keyword

Calcium carbide; Vitamin B12; Hematopoiesis; Toxicity