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Abstract
In order to identify the properties of nicotine in relation to oxidative stress or
neuroprotection, differentiated PC12 cells were treated with nicotine, beta-amyloid
peptide (Abeta(25-35)), free radical inducer and antioxidant by a separate addition
or a combination way. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide
(MTT) reduction, lipid peroxidation, [3H]epibatidine binding sites for nicotinic receptor
and [3H]quinuclidinyl benzilate (QNB) for muscarinic receptor have been detected.
The significant decrease of MTT reduction and increase of lipid peroxidation in PC12
cells were only observed at treatments with high concentrations of nicotine (1 and
10 mM), while Vitamin E (VitE), an antioxidant, can prevent the neurotoxic effects.
In addition, nicotine in low dosage (10 microM) rescued the decreased rates of cell
viability and inhibited the production of lipid peroxidation resulted from H(2)O(2)
and Abeta in the cultured cells. Significant increases in [3H]epibatidine binding
sites were observed in PC12 cells exposed to nicotine, while no change was detected
in [3H]QNB. The decreased number of nicotinic receptor binding sites due to the toxicity
of Abeta was prevented by the addition of nicotine with low concentration. It is plausible
that nicotine treatment may play dual effects on oxidative stress and neuroprotection,
in which the effects are dependent on the differences in dosage of the drug used and
their mechanisms of action. Generally, high dose of nicotine may induce neurotoxicity
and stimulate oxidative stress, while reasonably low concentration may act as an antioxidant
and play an important role for neuroprotective effect.