Effects of ozone on gene expression and lipid peroxidation in adults and larvae of the red flour beetle (Tribolium castaneum)

Ozone has in recent years been increasingly investigated for its potential use in the control of insect pests of stored cereals. Ozone is a powerful oxidizing agent that can react directly, or via production of reactive oxygen species, with proteins, DNA and double bonds of polyunsaturated fatty acids (PUFA). The aim of the present study was to investigate the mode of action in ozone toxicity using the red flour beetle, Tribolium castaneum (Herbst), as a relevant model. Transcription of focal genes thought to be involved in protection against ozone, and repair of cellular damage caused by ozone exposure, was studied together with the composition of storage lipid fatty acids and membrane phospholipid fatty acids in order to detect lipid peroxidation. Contrary to expectations, transcription of focal genes (Cu/Zn-Superoxide Dismutase, Catalase, Glutathione Peroxidase, Glutathione S-Transferase, Δ-9 Desaturase 1, Δ-12 Desaturase, DNA Ligase IV, Heat Shock Proteins 60, 70, 83) was either decreased or unchanged in larvae and adults exposed to 40 ppm ozone for 6 or 24 h, respectively, as compared to parallel control samples. No, or only little, peroxidation of lipid fractions occurred during exposure to 40 ppm ozone, although it was demonstrated that this concentration is sufficient to kill both larvae and adults of the red flour beetle. Possible explanations for these observations may be that the time-scale of the experimentation was such that any up-regulatory change may have been missed, or that ozone had caused a general depression of metabolism (including transcription of reactive oxygen species detoxifying genes) as the insects had been oxygen-deprived due to longer than normal closure of the spiracles.

► Larvae of Tribolium castaneum were more susceptible to 40 ppm ozone than adults.
► Ozone caused down-regulation of genes protecting against oxidative stress.
► Ozone induced little or no lipid peroxidation.