Imidacloprid impedes mitochondrial function and induces oxidative stress in cotton bollworm, Helicoverpa armigera larvae (Hubner: Noctuidae)

• Published in: Journal of bioenergetics and biomembranes Vol. 50; no. 1; pp. 21 - 32
• Main Authors: Nareshkumar, Bharat, Akbar, Shaik Mohammad, Sharma, Hari Chand, Jayalakshmi, Senigala K., Sreeramulu, Kuruba
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.02.2018; Springer Nature B.V
• Subjects: Acetylcholine receptors (nicotinic); Adenosine triphosphatase; Agrochemicals; Animal Anatomy; Animal Biochemistry; Animals; Biochemistry; Bioorganic Chemistry; Catalase; Chemistry; Chemistry and Materials Science; Cotton; Cytochrome c; Electron Transport Complex IV - antagonists & inhibitors; F0F1-ATPase; Histology; Hydrogen peroxide; Imidacloprid; Insecticides; Insecticides - toxicity; Larva - drug effects; Larva - growth & development; Larvae; Lipid peroxidation; Mitochondria; Mitochondria - metabolism; Morphology; Moths - drug effects; Moths - metabolism; Moths - ultrastructure; Neonicotinoids - toxicity; Neurotoxicity; Neurotoxicity Syndromes - etiology; Nitro Compounds - toxicity; Organic Chemistry; Oxidative stress; Oxidative Stress - drug effects; Pests; Proton-Translocating ATPases - antagonists & inhibitors; Receptors; Respiration; Superoxide dismutase; Time dependence; Oxidative stress; Mitochondria; Imidacloprid; Oxidative phosphorylation; H. armigera
• ISSN: 0145-479X; 1573-6881
• DOI: 10.1007/s10863-017-9739-3

Neonicotinoids have high agonistic affinity to insect nicotinic acetylcholine receptors (nAChR) and are frequently used as insecticides against most devastating lepidopteran insect pests. Imidacloprid influenced dose-dependent decline in the state III and IV respiration, respiration control index (RCI), and P/O ratios, in vitro and in vivo. The bioassay indicated its LD 50 value to be 531.24 μM. The insecticide exhibited a dose-dependent inhibition on F 0 F 1 -ATPase and complex IV activity. At 600 μM, the insecticide inhibited 83.62 and 27.13% of F 0 F 1 -ATPase and complex IV activity, respectively, and induced the release of 0.26 nmoles/min/mg protein of cytochrome c. A significant dose- and time-dependent increase in oxidative stress was observed; at 600 μM, the insecticide correspondingly induced lipid peroxidation, LDH activity, and accumulation of H 2 O 2 content by 83.33, 31.51 and 223.66%. The stress was the maximum at 48 h of insecticide treatment (91.58, 35.28, and 189.80%, respectively). In contrast, catalase and superoxide dismutase were reduced in a dose- and time-dependent manner in imidacloprid-fed larvae. The results therefore suggest that imidacloprid impedes mitochondrial function and induces oxidative stress in H. armigera , which contributes to reduced growth of the larvae along with its neurotoxic effect.