Abstract
The Drosophila melanogaster cardinal mutant (cd[1]) is characterized by a deletion in the gene for phenoxazinone synthase (PHS), which converts 3-hydroxykynurenine (3HOK) to the screening eye pigment xanthommatin (XAN). This results in altered locomotor activity and loss of long-term memory, as well as in age-related loss of middle-term memory, distortion of courtship song, and heat-induced apoptosis in the brain. Hence, cd[1] can be considered as a model of senile memory impairment and neurodegeneration. Its behavioral disturbances are believed to be a result of elevated levels of 3HOK, which can induce oxidative stress and neuronal apoptosis. However, 3HOK can also act as an antioxidant. In this study, we measured age-related changes in hydrogen peroxide levels and superoxide dismutase (SOD) activity in cd[1] males. Surprisingly, both young and old cd[1] had lower level of hydrogen peroxide compared to the wild-type strain Canton-S (CS). No interstrain differences in SOD activity were observed, but it was reduced in cd[1] compared to CS after hypomagnetic conditioning (HMC). Mean levels of reactive oxygen species (ROS) in the brain of young and old flies showed no significant interstrain differences. Transcription activity of the catalase (Cat) and Sod1 genes was reduced in young cd[1], whereas Cat expression was increased in old cd[1]. Thus, the PHS dysfunction and the increase in 3HOK in cd[1] do not result in increased hydrogen peroxide levels. Activation of Cat expression in old cd[1] may compensate for the development of oxidative stress.
