Abstract
Damage from reactive oxygen species (ROS) is thought to be a cause of organismal aging. Reactive oxygen species have also been proposed to be responsible for several age-associated phenotypes, including age-related memory impairment (AMI). However, it has not previously been tested whether increasing ROS affects AMI onset. Here we examined the effects of feeding hydrogen peroxide, and the ROS-generating agent, paraquat, on olfactory aversive memory in Drosophila at young ages and during AMI onset. Reactive oxygen species feeding greatly reduced fly survival, and increased oxidized proteins and transcripts of an antioxidant enzyme, catalase (Cat) and a stress-responsive chaperone, heat-shock protein 22 (Hsp22) in fly heads. However, feeding did not impair memory in young wild-type flies, nor did it exacerbate the memory deficits in flies at the onset of AMI. Strikingly ROS feeding did disrupt memory at young ages and accelerated AMI onset was observed when expression of genes involved in the defense system to ROS, including antioxidant enzymes and Hsp22, was reduced in the mushroom bodies, neural centers required for olfactory memory. These results implicate that although ROS production increases upon aging, neuronal functions required for memory processes are sufficiently protected by the defense system to ROS even at the age of AMI onset. Thus we propose that ROS production does not affect AMI onset in Drosophila.
