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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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Development of cerebral malaria (CM) is driven by parasitemia levels, harmful inflammatory response, oxidative stress and consequent breach of the blood brain barrier. Use of adjunct therapy that utilizes an antioxidant and anti-inflammatory agent alongside chloroquine (CQ), may improve treatment outcome and shorten recovery from post-infection sequelae. Though withdrawn in some countries, CQ is still in use for prophylaxis and treatment of malaria in many countries. Current study investigated whether oral co-administration of 50 mg/kg CQ and 200 mg/kg of coenzyme Q10 (CoQ10) would improve treatment outcome against experimental cerebral malaria (ECM) and assuage the deleterious effects of oxidative stress and inflammation upon infection by Plasmodium berghei ANKA (PbA) in a C57BL/6 J mouse model. Treatment with CQ + CoQ10 resulted in an improved parasite elimination; clearing the parasite one day early, when compared to mice on CQ alone. Remarkably, treatment with CQ and CoQ10 separately or in combination, assuaged PbA induced elevation of serum levels of TNF-α and IFN-γ an indication of protection from ECM progression. Furthermore, CQ and CoQ10-administration, blocked parasite-driven elevation of aspartate transaminase (AST), alanine transaminase (ALT) and bilirubin. In the presence of CQ and CoQ10, severe PbA-induced systemic induction of oxidative stress and resultant GSH depletion was reduced in the brain, liver, spleen, and kidney. Overall, these findings demonstrate that administration of CQ and CoQ10 ameliorates harmful parasite-driven oxidative stress and inflammation, while slowing the progression to full blown ECM and may improve treatment outcome in CM.

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Pumpkins (Cucurbita spp.) are among most neglected and underutilized crops cultivated for food and medicine. The major constraint to pumpkin production is lack of genetically improved seeds. The current study was aimed at evaluating the genetic diversity of pumpkins from eight counties in western Kenya using five SSR markers. Seeds were extracted from pumpkin fruits, dried and planted on plastic trays for 4 weeks. DNA was isolated from young leaves using CTAB method and amplified. The samples were genotyped using an ABI 3730 genetic analyzer and the allelic data analyzed using Power Marker V 3.25, DARwin V 6.0.12 and GenAIEx V 6.41software. The five SSR loci were polymorphic with a total of 33 alleles and a mean PIC value of 0.534. The gene diversity and observed heterozygosity was 0.796-0.329 and 0.967-0.164, respectively. Most of genetic variations were found within and among individual samples rather than among counties, with samples of some counties having private alleles. Based on the inbreeding coefficient (F), there was outbreeding in pumpkins from Kakamega county (F = - 0.282) and inbreeding in pumpkins from Kisii, Bungoma and Nyamira counties (F = 0.500, 0.409 and 0.286 respectively). The findings of this study suggest that genetic variation and distribution of pumpkins in western Kenya was due to monocropping and intercropping farming systems, trading of pumpkins in markets and exchange of seeds among local farmers rather than geographical and climatic differences.

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Wings and legs of the gregarious desert locust, Schistocerca gregaria have been shown to be release sites of phenylacetonitrile (PAN), the major adult male-produced pheromone. However, there is limited information on the distribution of PAN within the locust. Here we show, using gas chromatography-mass spectrometry (GC-MS), that PAN occurs in nearly all body parts of both adult males and females of the locust in varying amounts. PAN was 20-fold more concentrated in males than in females. In females, PAN was concentrated more in the tarsal segments. The greatest amounts of PAN were in 2- and 3-week old female and male body parts, respectively. No trace of PAN was found in similar ages and sexes of the solitarious phase desert locust. Our results show that PAN is distributed in the body matrix of both sexes of gregarious phase locusts and suggest that no specific tissue is responsible for biosynthesis of the pheromone.

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