Background: Parkinson's disease (PD) is a multifactorial neurodegenerative disease with pathogenic mechanisms traceable to oxidative damage and mitochondrial dysfunction. Rotenone, a chemical compound commonly found in pesticides, has been found to inhibit mitochondrial complex-I and initiate PD-like symptoms in mammals and several invertebrates. Virgin Coconut Oil (VCNO) obtained from the coconut fruit has been found to possess anti-oxidative and anti-inflammatory properties. Objectives: The present study evaluated the effect of VCNO on rotenone-induced Parkinsonism in fruit flies- Drosophila melanogaster (D. melanogaster). Methods: Canton special (CS) strains of D. melanogaster, aged between 1 to 3 days were orally exposed for 7 days to 0, 250, 500 and 750 μM rotenone diet for toxicity assay, and 0, 2.5, 5 and 10 % w/w VCNO diet for longevity assay. Thereafter, 5 % VCNO diet was selected for evaluation against 500 μM rotenone. Subsequently, behavioural test (negative geotaxis), markers for redox status and enzyme activities were evaluated. Results: The results showed that rotenone induced toxicity in the flies, while VCNO increased the lifespan of D. melanogaster in a dose-dependent manner. In addition, VCNO ameliorated rotenone-induced locomotor deficits, elevated MDA, as well as the depleted GSH levels. It also mitigated the inhibited activities of SOD, CAT and ATPase in the flies. Conclusions: VCNO protected D. melanogaster against rotenone-induced toxicity by extending longevity, preventing locomotor deficits and reducing oxidative stress.
Fasting, but Not Aging, Dramatically Alters the Redox Status of Cysteine Residues on Proteins in Drosophila melanogaster
