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

Autor: Ouma PA; Department of Biochemistry and Biotechnology, Technical University of Kenya, P. O. Box 52428, 00200, Nairobi, Kenya., Mwaeni VK; Department of Biochemistry and Biotechnology, Technical University of Kenya, P. O. Box 52428, 00200, Nairobi, Kenya., Amwayi PW; Department of Biochemistry and Biotechnology, Technical University of Kenya, P. O. Box 52428, 00200, Nairobi, Kenya., Isaac AO; Department of Pharmaceutical Sciences and Technology, School of Health Sciences and Technology, Technical University of Kenya, P. O. Box 52428, 00200, Nairobi, Kenya., Nyariki JN; Department of Biochemistry and Biotechnology, Technical University of Kenya, P. O. Box 52428, 00200, Nairobi, Kenya. nyabukaj@tukenya.ac.ke.
Jazyk: angličtina
Zdroj: Laboratory animal research [Lab Anim Res] 2022 Aug 12; Vol. 38 (1), pp. 26. Date of Electronic Publication: 2022 Aug 12.
DOI: 10.1186/s42826-022-00136-1
Abstrakt: 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.
(© 2022. The Author(s).)
Databáze: MEDLINE
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