Chlorine dioxide enhances lipid peroxidation through inhibiting calcium-independent cellular PLA2 in larvae of the Indianmeal moth, Plodia interpunctella.

Polyunsaturated fatty acids usually undergo lipid peroxidation induced by reactive oxygen species (ROS). Calcium-independent cellular phospholipase A2 (iPLA2) can maintain fatty acid compositions in phospholipids depending on physiological conditions. An insect iPLA2 (Pi-iPLA2) was predicted from the transciptome of the Indianmeal moth, Plodia interpunctella. It encodes 835 amino acids. It possesses five ankyrin repeats in the N terminal and patatin lipase domain in the C terminal. Pi-iPLA2 was expressed in all developmental stages of the Indianmeal moth. In the larval stage, it was expressed in all tissues tested. RNA interference (RNAi) specific to Pi-iPLA2 was performed using specific double-stranded RNA (dsRNA). It resulted in almost 70% of reduction in gene expression. Under such RNAi condition, P. interpunctella exhibited significant accumulation of lipid peroxidation based on the amount of malondialdehyde. RNAi of Pi-PLA2 expression also impaired cellular immune response of P. interpunctella. Chlorine dioxide (ClO2), an insecticidal agent by generating ROS, increased lipid peroxidation in a dose-dependent manner. However, the addition of vitamin E (an antioxidant) reduced the formation of lipid peroxidation. ClO2 treatment significantly reduced expression of Pi-iPLA2 but increased lipid peroxidation in larval fat body of P. interpunctella. Furthermore, larvae treated with dsRNA specific to Pi-iPLA2 were significantly susceptible to ClO2 treatment. These results suggest that Pi-iPLA2 plays a crucial role in repairing damaged fatty acids from phospholipids. Our results also suggest that ClO2 can elevate lipid peroxidation through inhibiting Pi-iPLA2 expression in addition to direct ROS production.