Inhibition of eicosanoid signaling leads to increased lipid peroxidation in a host/parasitoid system.

We posed the hypothesis that inhibition of eicosanoid biosynthesis leads to increased lipid peroxidation in insects. Here we report that rearing the greater wax moth, Galleria mellonella, on media supplemented with selected inhibitors of eicosanoid biosynthesis throughout the larval, pupal and adult life led to major alterations in selected oxidative and antioxidative parameters of wax moth and its ectoparasitoid, Bracon hebetor. The highest dietary dexamethasone (Dex), esculetin (Esc) and phenidone (Phe) led to increased malondialdehyde (MDA) levels and to elevated catalase (CAT) and glutathione-S-transferase (GST) activities in all developmental stages of host larvae. Dietary Phe resulted in increased MDA levels, and CAT activity in G. mellonella adults by about 4-fold and about 2-fold, respectively. The Phe effect on GST activity in all stages of the wax moth was expressed in a dose-dependent manner, increased to 140nmol/mg protein/min in larvae. MDA levels were increased by over 30-fold in adult wasps reared on Dex- and Esc-treated hosts. CAT and GST activities were increased in adult parasitoids reared on Esc-and Phe-treated hosts. GST activity of Dex-treated parasitoid larvae increased from about 4 to over 30nmol/mg protein/min. Dietary Phe led to increased GST activity, by about 25-fold, in adult wasps. These data indicate that chronic inhibition of eicosanoid biosynthesis leads to increased oxidative stress, strongly supporting our hypothesis. The significance of this work lies in understanding the roles of eicosanoids in insect biology. Aside from other well-known eicosanoids actions, we propose that eicosanoids mediate reductions in oxidative stress.