Neurotoxic and behavioral deficit in Drosophila melanogaster co-exposed to rotenone and iron.

Exposure to environmental toxicants has been linked with the onset of different neurodegenerative diseases in animals and humans. Here, we evaluated the toxic effects of co-exposure to iron and rotenone at low concentrations in Drosophila melanogaster. Adult wild-type flies were orally exposed to rotenone (50.0 µM) and ferrous sulfate (FeSO 4 ; 1.0 and 10.0 µM) through the diet for 10 days. Thereafter, we evaluated markers of oxidative damage (Hydrogen Peroxide (H 2 O 2 ), Nitric Oxide (NO), Protein Carbonyl, and malondialdehyde (MDA)), antioxidant status (catalase, Glutathione S-Transferase (GST), Total Thiol (T-SH) and Non-protein Thiol (NPSH), neurotransmission (monoamine oxidase; MAO and acetylcholinesterase, AChE) and mitochondrial respiration. The results indicated that flies fed rotenone and FeSO 4 had impaired locomotion, reduced survival rate, and AChE activity with a corresponding increase in MAO activity when compared with the control (p < 0.05). Furthermore, rotenone and FeSO 4 significantly decreased the antioxidant status with a concurrent accumulation of NO, MDA, and H 2 O 2 . Additionally, the activity of complex 1 and mitochondria bioenergetic capacity was compromised in the flies. These findings suggest that the combination of rotenone and FeSO 4 elicited a possible synergistic toxic response in the flies and therefore provided further insights on the use of D. melanogaster in toxicological studies.