Abstract

Nicotine, a component of tobacco smoke, is a neurotoxin. It exerts its effects by stimulating nicotine-containing acetylcholine receptors. Nicotine, one of over 4,700 components in tobacco smoke, was previously used as an insecticide in agriculture. Although the use of nicotine in agriculture has been banned in many countries, nicotine poisoning due to accidental or intentional ingestion of nicotine products remains a problem for smoking workers as well as children and adults. Understanding the mechanisms of nicotine poisoning is important for both prevention and treatment, as well as for appropriate regulatory approaches. We study the pharmacological properties of nicotine and the cellular mechanisms underlying acute and persistent nicotine addiction that appear to be related to the central and peripheral nervous systems. The electrochemical properties of nicotine were studied using a glassy carbon-chitosan/multiwalled carbon nanotubes-COOH electrode. Nicotine-COOH via chitosan/multiwalled carbon nanotubes was irreversibly reduced in the presence of oxygen and nitrogen gas. Oxidation signals at lower potentials and higher currents were obtained for nicotine via the modified electrode compared to the glassy carbon electrode. This condition proliferated in the presence of oxygen gas, suggesting that nanotubes, including carbon nanotubes, facilitate electron transfer and form the basis for electrocatalytic nicotine applications. Under optimal conditions, cyclic voltammetry (CV) shows oxidation of nicotine in the presence of oxygen at 0.74 V and nitrogen at 0.81 V in phosphate buffer solution at pH = 7.4. Linear calibration curves range from 0.1 to 200 μM for oxygen and 0.05 to 200 μM for nitrogen conditions, both with R2 = 0.99, and detection limits of 7.1 for oxygen and 9.2 nM for nitrogen.

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