Low Doses of Imidacloprid Induce Oxidative Stress and Neural Cell Disruption in Earthworm <i>Eisenia fetida</i>

Abstract

Imidacloprid is a widely used pesticide that belongs to the class of neonicotinoids. There is a piece of rising evidence that neonicotinoids exert cytotoxic effects in non-target organisms including vertebrate species such as mammals. Nevertheless, dose-limiting toxicity and molecular mechanisms of neonicotinoids' deleterious effects are still poorly understood. In accord to imidacloprid fate in the environment, the most of used pesticide is absorbed in the soil. Therefore, earthworms, which are prevailing soil organisms, could be considered as a target of neonicotinoids toxicity. The earthworm’s simple nervous system is a prospective model for neurotoxicological studies. We exposed earthworms to imidacloprid in a paper contact test with a doses range of 0.1‑0.4 µg/cm2 for 14 days. In the present work, we studied the imidacloprid effect on oxidative stress generation and neuronal marker neuron-specific enolase (NSE) expression. The exposure to imidacloprid induced a dose-dependent decrease in NSE. Both reactive oxygen species production and lipid peroxidation level were upregulated as well. Observed NSE decline suggests imidacloprid-caused disturbance in earthworm neuron cells. Obtained data have shown that relatively low doses of imidacloprid are potent to induce cytotoxicity in neurons. Furthermore, neurotoxicity could be recognized as one of an individual scenario of the general imidacloprid toxicity. Thus, presented results suggest the cytotoxicity of imidacloprid low doses in non-target organisms and hypothesize that NSE downregulation could be estimated as a biomarker of neonicotinoid cytotoxicity in a nervous system of non-insect species.

Low doses of imidacloprid induce neurotoxic effects in adult marsh frogs: GFAP, NfL, and angiostatin as biomarkers

“…The functioning of the nervous system depends on the adaptive and regenerative properties of nerve cells (Hall & Tropepe, 2020). Imidacloprid is a neurotoxicant capable of causing molecular changes in animal cells (Abou-Donia et al, 2008;Huslystyi et al, 2021). The study of these phenomena may allow the identification of markers of neurotoxicity that adequately reflect critical disorders, as well as metabolic pathways that are targets for the cytotoxic compounds in a polluted environment (Manzo et al, 2001).…”

Cypermethrin induces neurotoxicity via inhibition of glial cell viability and apoptosis initiation

“…The use of molecular biomarkers in assessing neurotoxicity is considered a promising and adequate tool in ecotoxicology (Nedzvetsky et al, 2018;Iqubal et al, 2020). Cultures of neurons and glial cells are widely used in in vitro studies of neurotoxicity and provide valuation means of the potential risks of environmental pollution (Huslystyi et al, 2021). The initiation of programmed cell death is determined by evaluating the expression of proapoptotic proteins of the caspase family, Bcl family, and the relative content of cytochrome C in the cytosol compared to its mitochondrial pool (Tomiyama et al, 2010;Jemmerson et al, 2005).…”