Toxicological assessment of sodium benzoate in Drosophila melanogaster.

Sodium benzoate (SB), the sodium salt of benzoic acid, is a food preservative with wide applications in the food, cosmetic and pharmaceutical industries due to its ability to kill many microorganisms effectively. Experimental evidence however suggests that excessive intake of SB poses detrimental health risks among consumers in the population. The present study investigated the toxic effects of various concentrations of SB using Drosophila melanogaster as a model. Adult wild-type flies of Canton S strain (1- to 3-days old) was orally exposed to SB (0, 0.5, 1.0, 2.0 and 5.0 mg/5 g diet) to evaluate survival rates for 21 days. Thereafter, we evaluated markers of oxidative stress, antioxidant status and behavioral activity in D. melanogaster exposed to SB for seven (7) days. We observed that SB (2.0 and 5.0 mg/5 g diet) decreased the survival of D. melanogaster. Also, SB inhibited glutathione-S-transferase activity and depleted total thiols and nonprotein thiols contents. Moreover, SB (5 mg/5 g diet) increased nitric oxide (nitrite/nitrate) level and reduced flies' emergence rate. Conclusively, findings from this study revealed that exposure to high concentrations of SB reduced survival rate and induced toxicity via the induction of oxidative stress and inhibition of antioxidant enzymes in D. melanogaster.

Carcinogen sodium arsenite disrupts antioxidant and redox homeostasis in Drosophila melanogaster.

OBJECTIVES: The inadvertent exposure to environmental contaminants has been reported to induce cancer in different animal models. Here, we investigated the toxicity of Sodium Arsenite (SA), a Class I Carcinogen in Drosophila melanogaster. METHODS: Harwich fly strain (1-3 days old) of both sexes were orally exposed to SA (0, 0.0312, 0.0625 and 0.125 mM) for 14 days for survival study. Thereafter, 5 days exposure period was selected to assess the toxic effects of SA on oxidative stress and antioxidant markers. RESULTS: The results indicated that SA induced significant reduction in survival and emergence rate of flies. Furthermore, SA significantly increased Nitric Oxide (NO, nitrite and nitrate) and Hydrogen Peroxide (H2O2) levels in flies compared with control (p<0.05). In addition, SA inhibited catalase and glutathione-S-transferase (GST) activities, and depleted total thiol and glutathione (GSH) contents. Moreover, acetylcholinesterase activity significantly increased in flies treated with SA when compared with control. CONCLUSIONS: Sodium arsenite-induced reduction in survival and emergence rates of flies occurred via the disruption of oxidative stress-antioxidant homeostasis in D. melanogaster.

Vitellaria paradoxa inhibits arsenic-induced toxicity in Drosophila melanogaster via the augmentation of antioxidant system.

The Ethyl Acetate Fraction (EACF) of Ethanol Leaf Extract of Vitellaria paradoxa (ELVp) was assessed against Sodium Arsenite (SA)-induced toxicity in Drosophila melanogaster. The Gas Chromatography-Mass Spectrometry (GC-MS) analysis of EACF was carried out. The molecular docking of the compounds obtained from GC-MS was performed against D. melanogaster glutathione-S-transferase-2 (GST-2). Firstly, D. melanogaster (Harwich strain) was treated with EACF to determine its effect on longevity. Secondly, D. melanogaster was fed with EACF (1.0 and 3.0 mg/5 g diet) and/or SA (0.0625 mM) for 5 days. Thereafter, the ameliorative role of EACF in SA-induced toxicity was evaluated using the fly's emergence rate, locomotor activity, oxidative stress and antioxidant biomarkers. The in-silico study revealed varying degrees of binding affinity of the twelve active compounds of EACF against GST-2 which was comparable with the co-crystalized ligand (glutathione). The EACF increased the longevity of D. melanogaster by 20.0 % compared with control and ameliorated SA-induced reduction of emergence rate and locomotor performance by 178.2 and 20.5 %, respectively. Additionally, EACF ameliorated SA-induced reduction of total thiol and non-protein thiols and inhibition of catalase and GST activities (p < 0.05). These results corroborated with histological data obtained in the fat body of D. melanogaster. Overall, EACF augmented the antioxidant system of D. melanogaster and prevented sodium arsenite-induced oxidative stress due to its high antioxidant property.

Ethanol extract of Vitellaria paradoxa (Gaertn, F) leaves protects against sodium arsenite - induced toxicity in male wistar rats.

The inadvertent exposure to arsenic has been associated with diverse diseases such as cancers. Vitellaria paradoxa is a medicinal plant with antidiabetic and antiproliferative properties. Here, we assessed the ameliorative role of Ethanol Leaf extract of Vitellaria paradoxa (ELVp) in Sodium Arsenite (SA) - induced toxicity in rats after oral treatment for two weeks as follows: Group 1 (Control, distilled water), Group 2 (Vitamin E, 100 mg/kg), Groups 3 and 4 (ELVp, 100 & 200 mg/kg respectively), Group 5 (SA, 2.5 mg/kg), Group 6 (SA + Vit E) and Group 7 (SA + ELVp (100 mg/kg) and Group 8 (SA + ELVp (200 mg/kg). The results indicated that SA significantly increased liver and kidney function markers and elevated platelet, white blood cell (WBC) count and malondialdehyde levels in rats. Additionally, SA decreased Red Blood Cell (RBC), Hemoglobin (HGB) and Hematocrit (HCT) levels in rats (p < 0.05). Sodium arsenite caused mild expression of BCL-2 protein> NF-Kb = p53 in the kidney of rats. However, ELVp ameliorated SA-induced toxicity in the liver and kidney of rats with respect to these markers. Overall, ELVp has hepatoprotective, nephroprotective and apoptotic properties against sodium arsenite-induced toxicity.