Neonicotinoid insecticides are potential substrates of the multixenobiotic resistance (MXR) mechanism in the non-target invertebrate, Dreissena sp.

Abstract

Mussels are among the most frequently used invertebrate animals in aquatic toxicology to detect toxic exposure in the environment. The presence and activity of a cellular defence system, the multixenobiotic resistance (MXR) mechanism, was also established in these organisms.In isolated gill tissues of dreissenid mussels (D. bugensis) the MXR activity was assayed after treatment by commercially available insecticides (formulated products) which contain neonicotinoids as their active ingredients: Actara (thiamethoxam), Apacs (clothianidin), Calypso (thiacloprid) and Kohinor (imidacloprid), respectively. While applying the accumulation assay method, 0.5 μM rhodamine B was used as model substrate and 20 μM verapamil as model inhibitor of the MXR mechanism.In acute (in vitro) experiments when isolated gills were co-incubated in graded concentrations of insecticides and rhodamine B simultaneously, Calypso and Kohinor treatment resulted increasing rhodamine accumulation. Chemical analysis of gills in vitro incubated in insecticides demonstrated higher tissue concentrations of thiamethoxam, clothianidin and thiacloprid in the presence of verapamil suggesting that the active ingredients of Actara, Apacs and Calypso are potential substrates of the MXR mediated cellular efflux. In contrast, verapamil did significantly alter the accumulated imidacloprid concentrations in gills, suggesting that the active component of Kohinor is not transported by the MXR mechanism.Chronic (in vivo) exposures of the intact animals in lower, 1, 10 mg/L concentration of neonicotinoid products, resulted in a decreased level of both rhodamine accumulation and verapamil inhibition by the 12 th -14 th days of treatment. These results suggest an enhancement of MXR activity (chemostimulation), building up gradually in the animals exposed to Actara, Apacs and Kohinor, respectively.Neonicotinoid-type insecticides are generally considered as selective neurotoxins for insects, targeting the nicotinic type acetylcholine receptors (nAChRs) in their central nervous system. Our present results provide the first evidences that neonicotinoid insecticides are also able to alter the transmembrane transport mechanisms related to the MXR system.

Neonicotinoids: Spreading, Translocation and Aquatic Toxicity

“…The sensitivity differences may be due to different toxin-target interactions and heterogeneity of the toxin-induced changes in metabolism or gene expression [85,86,88]. Recent results also suggest contribution of the cellular defense system (the multixenobiotic resistance mechanism, MXR) in the organism's resistance to neonicotinoid insecticides [89].…”

Multi-marker approach for the evaluation of environmental impacts of APACS 50WG on aquatic ecosystems

“…2), it has been proven that APACS 50WG insecticide has an enhancement of MXR activity (chemostimulation). Though just a few literature data are available concerning the effects of neonicotinoids on the MXR system, in case of isolated mussel gill, it was found that the APACS 50WG acted as a substrate of MXR, while long-term treatment functioned as a chemostimulator (Vehovszky et al 2018). We conclude that at a low concentration of neonicotinoid the oxidative damage evoked by the neonicotinoid impairs the intracellular compensatory mechanisms, yielding to increased activity against the neonicotinoid-induced toxicity.…”

“…Treated and untreated animals were frozen following the exposition period (3 h) until further processing. We applied the "accumulation" method of MXR assay (Vehovszky et al 2018, Smital et al 2003 where rhodamine B served as a model P-gp substrate. The samples were homogenized in a tissue layer (Tyssuelyzer LT, Qiagen) and centrifuged at 8000 g for 20 min at 4 °C (Biofuge Fresco, HERAUS).…”

“…Evaluation of locomotor activity as a potential biomarker of exposure of environmental stressors was suggested to monitor freshwater ecosystems (Wallace and Estephan 2004;Felten et al 2008). It has already been proven that the multixenobiotic resistance system (MXR) is activated by the effect of various neonicotinoids in aquatic invertebrates (Vehovszky et al 2018).…”

Alterations in Some Biochemical Responses of Freshwater Mussels in Acute Imidacloprid Exposure

“…Neonicotinoids are highly selective neurotoxins because they act as an agonist of the nicotinic acetylcholine receptor (nAChR) in post-synaptic membrane. Since these insecticides act more systemically, they do not only affect the central nervous system but also cause intracellular alterations in both vertebrates and invertebrates [4,5]. Imidacloprid causes more serious adverse effects on non-target organisms than other neonicotinoid pesticides and is one of the most important potential risks for local freshwater ecosystems in particular [6].…”