Presentation Title

Menthol Increases Reactive Oxygen Species in Human Lung Epithelial Cells Exposed at the Air-Liquid Interface

Start Date

November 2016

End Date

November 2016

Location

HUB 269

Type of Presentation

Oral Talk

Abstract

Menthol is a popular flavoring in cigarettes and electronic cigarettes. However, it not only is a flavor additive, menthol overrides the harsh taste of tobacco and alleviates nicotine’s irritating effects. This benefits the tobacco industry by making it easier to expose smokers to the addictive powers of nicotine. Because menthol is not regulated by the FDA, tobacco products can be sold with high menthol concentrations without knowing the health risks. Transient receptor potential subfamily M member 8 (TRPM8) is a calcium ion channel that is activated by menthol. We hypothesized that activation of these receptors in the human lung results in excess calcium influx leading to an increase in reactive oxygen species (ROS) and cell damage. Human lung epithelial cells (Beas2B) were exposed to aerosolized menthol generated by a nebulizer in an air-liquid interface system (Vitrocell) to determine its cytotoxic effects. The TRPM8 receptor was demonstrated in Beas2B cells by immunofluorescence and western blotting. To demonstrate increased calcium influx, cells were transfected using a genetically encoded calcium indicator plasmid and treated with menthol. The expression of superoxide, a form of ROS, was analyzed using MitoSOX dye, and the enzyme responsible for counteracting superoxide, superoxide dismutase (SOD-2), was analyzed using western blotting. Menthol exposure significantly increased calcium influx and induced an increase in the expression of superoxide and SOD-2. Data showed that menthol exposure at the air-liquid interface caused oxidative stress in human lung epithelial cells through activation of the TRPM8 receptor, suggesting that inhalation of menthol at doses found in electronic cigarettes could adversely affect lung health.

This document is currently not available here.

Share

COinS
 
Nov 12th, 10:15 AM Nov 12th, 10:30 AM

Menthol Increases Reactive Oxygen Species in Human Lung Epithelial Cells Exposed at the Air-Liquid Interface

HUB 269

Menthol is a popular flavoring in cigarettes and electronic cigarettes. However, it not only is a flavor additive, menthol overrides the harsh taste of tobacco and alleviates nicotine’s irritating effects. This benefits the tobacco industry by making it easier to expose smokers to the addictive powers of nicotine. Because menthol is not regulated by the FDA, tobacco products can be sold with high menthol concentrations without knowing the health risks. Transient receptor potential subfamily M member 8 (TRPM8) is a calcium ion channel that is activated by menthol. We hypothesized that activation of these receptors in the human lung results in excess calcium influx leading to an increase in reactive oxygen species (ROS) and cell damage. Human lung epithelial cells (Beas2B) were exposed to aerosolized menthol generated by a nebulizer in an air-liquid interface system (Vitrocell) to determine its cytotoxic effects. The TRPM8 receptor was demonstrated in Beas2B cells by immunofluorescence and western blotting. To demonstrate increased calcium influx, cells were transfected using a genetically encoded calcium indicator plasmid and treated with menthol. The expression of superoxide, a form of ROS, was analyzed using MitoSOX dye, and the enzyme responsible for counteracting superoxide, superoxide dismutase (SOD-2), was analyzed using western blotting. Menthol exposure significantly increased calcium influx and induced an increase in the expression of superoxide and SOD-2. Data showed that menthol exposure at the air-liquid interface caused oxidative stress in human lung epithelial cells through activation of the TRPM8 receptor, suggesting that inhalation of menthol at doses found in electronic cigarettes could adversely affect lung health.