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Adipokinetic hormone counteracts oxidative stress elicited in insects by hydrogen peroxide: in vivo and in vitro study

Authors

  • ANDREA BEDNÁŘOVÁ,

    1. Institute of Entomology, Biology Centre, Academy of Science, České Budějovice, Czech Republic
    2. Faculty of Science, South Bohemian University, České Budějovice, Czech Republic
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  • NATRAJ KRISHNAN,

    1. Department of Biochemistry, Molecular Biology, Entomology and Plant Pathology, Mississippi State University, Mississippi State, Mississippi, U.S.A.
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  • I-CHENG CHENG,

    1. Institute of Entomology, Biology Centre, Academy of Science, České Budějovice, Czech Republic
    2. Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan
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  • JOSEF VEČEŘA,

    1. Institute of Entomology, Biology Centre, Academy of Science, České Budějovice, Czech Republic
    2. Faculty of Science, South Bohemian University, České Budějovice, Czech Republic
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  • HOW-JING LEE,

    1. Department of Entomology, National Taiwan University, Taipei, Taiwan
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  • DALIBOR KODRÍK

    Corresponding author
    1. Faculty of Science, South Bohemian University, České Budějovice, Czech Republic
    • Institute of Entomology, Biology Centre, Academy of Science, České Budějovice, Czech Republic
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Correspondence: Dr Dalibor Kodrík, Institute of Entomology, Biology Centre, Academy of Science, Branišovská 31, České Budějovice 370 05-CZ, Czech Republic. Tel.: +420 387 775 271; e-mail: kodrik@entu.cas.cz

Abstract

The role of adipokinetic hormone (AKH) in counteracting oxidative stress elicited in the insect body is studied in response to exogenously applied hydrogen peroxide, an important metabolite of oxidative processes. In vivo experiments reveal that the injection of hydrogen peroxide (8 µmol) into the haemocoel of the firebug, Pyrrhocoris apterus L. (Heteroptera: Pyrrhocoridae) increases the level of AKH by 2.8-fold in the central nervous system (CNS) and by 3.8-fold in the haemolymph. The injection of hydrogen peroxide also increases the mortality of experimental insects, whereas co-injection of hydrogen peroxide with Pyrap-AKH (40 pmol) reduces mortality to almost control levels. Importantly, an increase in haemolymph protein carbonyl levels (i.e. an oxidative stress biomarker) elicited by hydrogen peroxide is decreased by 3.6-fold to control levels when hydrogen peroxide is co-injected with Pyrap-AKH. Similar results are obtained using in vitro experiments. Oxidative stress biomarkers such as malondialdehyde and protein carbonyls are significantly enhanced upon exposure of the isolated CNS to hydrogen peroxide in vitro, whereas co-treatment of the CNS with hydrogen peroxide and Pyrap-AKH reduces levels significantly. Moreover, a marked decrease in catalase activity compared with controls is recorded when the CNS is incubated with hydrogen peroxide. Incubation of the CNS with hydrogen peroxide and Pyrap-AKH together curbs the negative effect on catalase activity. Taken together, the results of the present study provide strong support for the recently published data on the feedback regulation between oxidative stressors and AKH action, and implicate AKH in counteracting oxidative stress. The in vitro experiments should facilitate research on the mode of action of AKH in relation to oxidative stress, and could help clarify the key pathways involved in this process.

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