Table 1.

Antioxidant treatments positively evaluated in Drosophila genetic PD models.

Fly PD Model	Associated PD Phenotypes	Antioxidant Molecules/Pathways Tested
α-synuclein (overexpression of the human homologue)	LB-like inclusions, DA degeneration, climbing defects [56], lipid peroxidation and protein carbonylation [69,70]	GstS1 upregulation [71] and overexpression of bovine MSRA [72] or human SOD1 [73] S-methyl-l-cysteine [72], curcumin [74], epicatechin gallate [75], grape extract [76], Decalepis hamiltonii [70], Eucalyptus citriodora [77] and Centella asiatica [69]
parkin (Loss of function)	DA degeneration [78,79,80,81], climbing defects [79,81,82], mitochondrial dysfunctions [79,80,83] and sensitivity to oxidative treatments [83]	GstS1 upregulation [81] and overexpression of fly Sod1 and Sod2 [62] polyphenols (propyl gallate and epigallocatechin gallate) [84] M40403 (SOD-mimetic) [62]
pink1 (Loss of function)	DA degeneration [47,79], climbing defects [47,79], mitochondrial dysfunctions [47,79,85] and sensitivity to oxidative treatments [85]	overexpression of human SOD1 [86] and of fly Sod1 and Sod2 [62] M40403 (SOD-mimetic) [62]
dj-1α and dj-1β (Loss of function, single and double mutants)	Sensitivity to oxidative treatments [49,50], lipid peroxidation and protein carbonylation [87,88]	minocycline and celastrol [89] vitamin C and vitamin E [87,88], Spirulina [90], epigallocatechin-3-gallate [91], pterostilbene, methylene blue, dalfampridine, sodium phenylbutyrate and dexrazoxane [65]

DA: dopaminergic neurons; GstS1: glutathione-S-transferase S1; LBs: Lewy bodies; MSRA: methionine sulfoxide reductase A; SOD1: superoxide dismutase 1.