Calcium Carbide Ripened Musa sapientum-Induced Reduction in White Blood Cell Count in Challenged Albino Wistar Rats

Osakue, J.O.; Okungbowa, Michael

doi:10.26538/tjnpr/v2i3.2

Cited by 2 publications

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“…Similar findings have been noted in rat fed with CaC 2 -ripened mango [1]. Moreover, elevated creatinine levels is associated with reduced glomerular filtration, impaired elimination of waste products with potential kidney swelling, inflammation, and necrotic cell damage [16]. Once again, oral administration of vitamin B 12 abrogated CaC 2-induced rise in serum creatinine levels is linked to its anti-inflammatory properties.…”

Section: Discussionsupporting

confidence: 78%

“…A similar study in which mice were fed on fruits ripened by CaC 2 showed reduced PCV levels [11]. Indeed, a decline in PCV is one of the key features of exposure to toxic chemicals that is associated with generation of ROS and lipid peroxidation [16]. Notably, administration of vitamin B 12 significantly stabilized the PCV levels which may be attributed to its anti-inflammatory properties.…”

Section: Discussionmentioning

confidence: 84%

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

et al. 2022

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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 CaC2, 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.

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 84%

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

et al. 2022

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Effect of subacute oral exposure to calcium carbide (CaC2) on some haematobiochemical parameters in male Wistar rats

2021

Savannah Vet J

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Introduction: One of the most common methods of forced ripening of fruits involves the use of calcium carbide (CaC2). Commercial grade CaC2 contains impurities with the potential to cause harmful effects to exposed individuals. This study was conducted to determine the effect of exposure to CaC2 on some haematological and biochemical parameters in rats. Methods: Adult male Wistar rats (n=20) were divided into four equal groups. Animals in Groups I (control), II, III and IV were respectively administered distilled water (2 mL/kg), 125, 250 and 500 mg/kg calcium carbide, orally, by gavage, before feeding, daily for 28 days. The erythrogram, leucogram and plasma total protein were determined, while changes in serum and brain biomarkers of oxidative stress (superoxide dismutase (SOD) activity and malondialdehyde (MDA) concentration) were assessed. Weight changes at the beginning and at the end of the exposure period (28 days) and signs of toxicity daily, were recorded. Results: The findings revealed significantly (p<0.05) lowered levels of red blood cells count (RBC count), haemoglobin and total white blood cells count (TWBC) in the rats exposed to CaC2. How-ever, the packed cell volume (PCV) was not significantly (p>0.05) lowered. Furthermore, there was an increase in MDA concentration but a decrease in SOD activity in the brain and serum of the experimental animals. Significance: Exposure to CaC2 induced adverse heamatobiochemical changes in rats which could signal danger to humans using this agent for fruit ripening.

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Calcium Carbide Ripened Musa sapientum-Induced Reduction in White Blood Cell Count in Challenged Albino Wistar Rats

Cited by 2 publications

References 0 publications

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

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

Effect of subacute oral exposure to calcium carbide (CaC2) on some haematobiochemical parameters in male Wistar rats

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