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

Abstract

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 value to be 531.24 μM. The insecticide exhibited a dose-dependent inhibition on FF-ATPase and complex IV activity. At 600 μM, the insecticide inhibited 83.62 and 27.13% of FF-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 HO 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.

Gene expression in bumble bee larvae differs qualitatively between high and low concentration imidacloprid exposure levels

“…Other elements of the mitochondrial cell respiration pathway in addition to cyt c were also down-regulated by both concentrations of imidacloprid, such as NADH dehydrogenase [ubiquinone] 1 beta subcomplex subunit 3. This is consistent with the literature showing that imidacloprid disrupts mitochondrial activity in insects [69][70][71] . The inference from this is that no matter the imidacloprid concentration with the range used here, larvae exposed to this pesticide not only face additional energy investments producing CYPs and investing in costly detoxi cation processes 72,73 , but also experience constrains on their ability to produce energy.…”

Improved mitochondrial function corrects immunodeficiency and impaired respiration in neonicotinoid exposed bumblebees

“…Neonicotinoids produce a sustained influx of Ca 2+ ions into neurons that is associated with increased reactive oxygen species production by mitochondria [ 24 ]. Mitochondrial changes also occur because neonicotinoids inhibit complex III and IV respiration [ 25 ]. They also alter gene expression [ 26 ] and affect thermoregulation [ 21 , 27 ].…”

Neuroprotective potential of berberine against acetamiprid induced toxicity in rats: Implication of oxidative stress, mitochondrial alterations, and structural changes in brain regions

“…Earlier, other neonicotinoids have been reported to cause mitochondrial oxidative stress by inhibiting complexes activities in insects. [ 61 ] Meanwhile, BBR treatment significantly restored the complexes activities, upregulated mRNA expression of complexes subunits and maintained the MnSOD expression in mitochondria against ACMP exposure in rat brain regions. An earlier study has also depicted that BBR improves the mitochondrial complex I, II, and IV activities in the cerebral ischemia rat model.…”