The effect of nicotine and lead on neuron morphology, function, and ɑ-Synuclein levels in a C. elegans model

Abstract

An electronic cigarette (e-cigarette) is a device that simulates cigarette-tobacco smoking by atomizing a liquid into an inhalable vapor. It is often billed as a smoking cessation device that is safer than cigarette smoking, however, these devices are feared to work as a gateway to cigarette smoking through nicotine addiction. In addition to e-cigarette injury and death, there are also neurological implications to using an e-cigarette. Our research aimed to determine the effect of chemicals commonly found in e-cigarette aerosol, specifically nicotine and lead, on dopaminergic neuron morphology and ɑ-synuclein levels using the model organism Caenorhabditis elegans. Our hypothesis stated that should exposure to these chemicals have an effect, then we would observe negative neurological implications such as changes in dopamine neuron morphology and possible neurodegeneration. We used transgenic C. elegans to assess the effects of nicotine and lead on ɑ-synuclein levels and neuron morphology. C. elegans were treated with different doses of lead, nicotine, or a mixture of to simulate the neurological effects of e-cigarette use. We determined dopamine and acetylcholine-dependent behavior using a 1-nonanol assay and an aldicarb assay, respectively. We observed a significant dopaminergic deterioration upon the treatment of lead and nicotine. At higher concentration of each treatment (lead, nicotine, and the combination), we observed C. elegans(NL5901 and BZ555) strains were smaller with an increase in protein aggregation. Our findings indicate that using e-cigarettes may induce morphological changes that are not favorable for normal brain function and could lead to a decrease in individuals’ e-cigarette use.