The Reassessed Impact of Nicotine against Neurotoxicity in Mesencephalic Dopaminergic Cell Cultures and Neuroblastoma N18TG2 Cells

Abstract

Neuroprotective effects of nicotine are still under debate, so further studies on its effectiveness against Parkinsonʼs disease are required. In our present study, we used primary dopaminergic cell cultures and N18TG2 neuroblastoma cells to investigate the effect of nicotine and its neuroprotective potential against rotenone toxicity. Nicotine protected dopaminergic (tyrosine hydroxylase immunoreactive) neurons against rotenone. This effect was not nAChR receptor-dependent. Moreover, the alkaloid at a concentration of 5 µM caused an increase in neurite length, and at a concentration of 500 µM, it caused an increase in neurite count in dopaminergic cells exposed to rotenone. Nicotine alone was not toxic in either cell culture model, while the highest tested concentration of nicotine (500 µM) caused growth inhibition of N18TG2 neuroblastoma cells. Nicotine alone increased the level of glutathione in both cell cultures and also in rotenone-treated neuroblastoma cells. The obtained results may be helpful to explain the potential neuroprotective action of nicotine on neural cell cultures.

From the tyrosine hydroxylase hypothesis of Parkinson’s disease to modern strategies: a short historical overview

“…Nicotine, the alkaloid derived from tobacco, which was studied more intensely is suggested as a neuroprotective compound in PD based on the negative correlation between tobacco consumption and PD (Barreto et al 2015 ). In rotenone-treated primary dopaminergic cell culture, Delijewski et al ( 2021 ) showed that nicotine protected dopaminergic neurons through an antioxidant mechanism.…”

Research Progress in the Pharmacological Effects and Synthesis of Nicotine

“…To explore nicotine's effectiveness against PD, Delijewski and co‐workers used primary dopaminergic cell cultures and N18TG2 neuroblastoma cells to investigate the effect of nicotine and its neuroprotective potential against rotenone toxicity [47] . The neuroprotective effect to protect dopaminergic neurons, which increased the neurite length and inhibited the growth of neuroblastoma cells, was not nAChR receptor‐dependent.…”