D-ribose-L-cysteine protects against rotenone-induced neurotoxicity in Drosophila via redox, neurotransmitter, and DDC gene regulation

through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms, possibly via enhanced GSH synthesis and dopamine regulation. Although we cannot fully rule out the possibility that DRLC affected rotenone ingestion or feeding behavior, the fact that ROT-dependent phenotypes persisted in the absence of DRLC and were only selectively reversed by DRLC suggests a neuroprotective effect.