Ellagic acid mitigates rotenone-induced damage via modulating mitochondria function in Drosophila melanogaster.

Constant, systematic exposure to rotenone has been utilized in animal models to induce Parkinsonism. Ellagic acid is a polyphenol with anti-inflammatory and antioxidative properties which is found in numerous natural fruits. Here, we investigated the therapeutic effects of ellagic acid in rotenone-induced toxicity in Drosophila melanogaster evaluating their antioxidant and mitoprotective properties. Adult flies were treated with rotenone and ellagic acid through their diet for 7 days, thereafter markers of neurotoxicity (acetylcholinesterase, monoamine oxidase, tyrosine hydroxylase), antioxidant and oxidative stress markers (hydrogen peroxide, nitric oxide, lipid peroxidation, protein carbonyl contents, catalase, total thiol, and nonprotein thiol) was measured. Mitochondrial respiration was also evaluated in the flies. Survival assay was carried out with both genders of the flies, and we observed a significant increase in the survival rate of flies exposed to both rotenone and ellagic acid when compared with the increased mortality rate in the groups exposed to rotenone alone. The impaired locomotion, altered redox status, and enzymes of neurotoxicity induced by rotenone were significantly ameliorated by ellagic acid to levels comparable to the control. In addition, rotenone-induced complex 1 inhibition and altered bioenergetic state were restored upon ellagic acid supplementation. These findings show the beneficial properties of ellagic acid against pesticides induced toxicity.

Beneficial actions of esculentin-2CHa(GA30) on high sucrose-induced oxidative stress in Drosophila melanogaster.

Hyperglycaemia-induced oxidative stress plays a critical role in the development of diabetes and its complications. This study investigated actions of esculentin-2CHa(GA30) on high sucrose-induced oxidative stress in adult Drosophila melanogaster. Adult flies were exposed to diets containing graded concentrations of sucrose in the presence or absence of esculentin-2CHa(GA30) (5.0-10 µmol/kg diet) for 7 days. Effects of high sucrose diet and/or esculentin-2CHa(GA30) on survival and longevity of flies, and markers of oxidative stress, antioxidant status and glucose were assessed. High-sucrose diet (15-30%) and esculentin-2CHa(GA30) (5-10 µmol/kg diet) enhanced the percentage of surviving flies by 33.5%-46.2% (P < 0.01) and 7.4%-26.9% (P < 0.01) respectively. Concentration-dependent reduction in total thiol (19.3-51.3%, P < 0.01), reduced glutathione (22.6-54.9%, P < 0.05-0.01), catalase activity (36.8-57.3%, P < 0.05-0.01) and elevated glucose concentration (1.8-2.9-fold, P < 0.001) were observed in high sucrose-fed flies. Esculentin-2CHa(GA30) alone did not affect levels of total thiol, reduced glutathione, glucose and catalase activity. Improved survival (1.2-1.3-fold, P < 0.05-0.01) and longevity (1.3-fold) were observed in flies treated with the peptide (5.0 and 7.5 µmol/kg diet). Feeding on sucrose and esculentin-2CHa(1-30) (5.0 and 7.0 µmol/kg diet) for 7 days increased total thiol (2 - 3-fold, P < 0.001) and reduced glutathione (1.6-1.8-fold, P < 0.05) levels. Reduced catalase activity (21.4-36.4%, P < 0.01) and reduced glucose level (38.6-49.4%, P < 0.01) were observed in peptide-treated flies. Esculentin-2CHa(1-30) inhibited sucrose-induced generation of hydrogen peroxide (7.5-13.7%, P < 0.05) and nitric oxide (22.3-42.9%, P < 0.01) in adult flies. Overall, findings from this study offered further insights into the anti-oxidative properties of esculentin-2CHa(GA30).