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.
Key words
nicotine -
Nicotiana tabacum
- Solanaceae - dopaminergic neurones - neuroblastoma - rotenone