engleski

Imidacloprid effects in peripheral sensory neurons in culture

Long-term exposure to environmental chemicals is a predisposing factor for the development of chronic diseases, neurodegeneration, hypersensitisation or ageing. Among pesticides, imidacloprid is a new generation insecticide, belonging to neonicotinoids family, with higher affinity for insects over mammalian nicotinic acetylcholine receptors (AChR). Nicotinic AChR have important role in control tissue physiology of the cardio-vascular system, muscle and sensory neurons. Little is known about potential hazard effects of imidacloprid on human health, especially in terms of potential occupational toxicity. To this aim, discovery of new molecular events evoked by new generation chemicals in mammalian models is interesting to generate more risk assessment data. Sensory neurons have the unique characteristic to sense environmental chemical-physical stimuli, and are highly prone to develop chronic sensorial hypersensitisation. In this work we studied the effects of imidacloprid (0.1 - 4 mM) on sensory neuron-derived cells F11 in vitro. Significant cytotoxicity was observed only at concentrations above 1 mM after 48h exposure, thus confirming overall low toxicity of imidacloprid. Nevertheless, early molecular events such as activation of p38 intracellular pathway, was partly necessary to generate reactive oxygen species and long-lasting lipid peroxidation. While p38 inhibitors were only partially sufficient to block imidacloprid cytotoxicity, anti-oxidants confer significant protection. Differential toxicity of imidacloprid, commercial formulation and its metabolites are also considered.These results contribute to new risk assessment of imidacloprid effects on mammalian tissue and suggest caution for chronic sub-threshold exposure doses of imidacloprid in terms of potential long-term sensitization of peripheral sensory neurons.

Neonicotinoids; Imidacloprid; F11 cells; cytotoxicity

nije evidentirano