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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. [ABSTRACT FROM AUTHOR]

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. 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. 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. Sodium arsenite-induced reduction in survival and emergence rates of flies occurred via the disruption of oxidative stress-antioxidant homeostasis in D. melanogaster. [ABSTRACT FROM AUTHOR]

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 (H 2 O 2 ) 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 ., (© 2021 Walter de Gruyter GmbH, Berlin/Boston.)