No abstract

Electronic cigarettes (ECs) are categorized into generations which differ in terms of design, aerosol production, and customizability. Current and former smokers prefer third-generation devices that satisfy tobacco cravings more effectively than older generations. Recent studies indicate that EC aerosols from firstand second-generation devices contain reactive carbonyls and free radicals and can cause in vitro cytotoxicity. Third-generation ECs have not been adequately studied. Further, previous studies have focused on cells from the respiratory tract, whereas those of the oral cavity, which is exposed to high levels of EC aerosols, have been understudied. We quantified the production of reactive carbonyls and free radicals by a thirdgeneration EC and investigated the induction of cytotoxicity and oxidative stress in normal and cancerous human oral cell lines using a panel of eight commercial EC liquids. We found that EC aerosols produced using a new atomizer contained formaldehyde, acetaldehyde, and acrolein, but did not contain detectable levels of free radicals. We found that EC aerosols generated from only one of the eight liquids tested using a new atomizer induced cytotoxicity against two human oral cells in vitro. Treatment of oral cells with the cytotoxic EC aerosol caused a concomitant increase in intracellular oxidative stress. As atomizer age increased with repeated use of the same atomizer, carbonyl production, radical emissions, and cytotoxicity increased. Overall, our results suggest that thirdgeneration ECs may cause adverse effects in the oral cavity and normal EC use, which involves repeated use of the same atomizer to generate aerosol, may enhance the potential toxic effects of third-generation ECs.

Objectives Soybean fiber (SBF) is an insoluble, but highly fermentable dietary fiber. Previous in vitro fermentation studies with human feces have shown that SBF produces 1.5–8 times more acetate, propionate, and butyrate than oat bran, corn bran, or wheat bran fiber. Short chain fatty acids (SCFA) have been reported to play a key role in maintaining colon health and reducing inflammation. The impact of dietary SBF on colonic inflammation has not previously been examined. Our objective was to determine the anti-inflammatory efficacy of dietary supplementation with SBF in a mouse model of acute colonic inflammation. Methods Male C57BL/6 J mice (5 weeks old) were randomized to AIN93G diet (CTL) or diet where 40% of the fiber was replaced with SBF (SBF-Hi). After 2 weeks of pretreatment, mice were given 2% dextran sulfate sodium (DSS) as the sole source of drinking fluid for 1 week to induce colonic inflammation. During DSS treatment, mice were maintained on their diet treatments. After DSS treatment, mice were euthanized and colonic inflammation was assessed. Results DSS-treated mice had significantly larger spleens and shorter colons than mice treated with water. SBF-Hi mitigated DSS-induced increases in spleen weight (20% lower) and colon shortening (15% longer). Quantitative, reverse transcriptase PCR analysis showed that DSS-treatment increased colonic mRNA expression of interleukin-6 (Il6) and tumor necrosis factor-a (Tnfa) by 3-fold compared to water-treated mice. Dietary supplementation with SBF blunted these increases in Il6 and Tnfa by 87% and 71%, respectively. Conclusions Our results suggest that dietary supplementation with SBF may be a useful approach to mitigate colonic inflammation. On-going studies are focused on determining fecal levels of SCFA and measuring protein markers of inflammation and gut barrier function. Future studies are needed to evaluate whether the protective effects observed in this study are maintained in situations of more chronic colonic inflammation. Funding Sources This work was funded by a grant from the Pennsylvania Soybean Board and by USDA National Institute of Food and Agriculture Appropriations under Project PEN04565.

Electronic cigarettes (ECs) have emerged as a popular alternative to conventional cigarettes. These devices operate by using resistive heating to vaporize a fluid consisting of a propylene glycol‐glycerol base, flavorings, and nicotine. Although considered safer than conventional cigarettes, recent studies have shown that EC vapor contains harmful compounds such as free radicals and carbonyls. A limited number of studies have shown that EC liquid and vapor can cause oxidative stress and cell death in vitro. While the majority of in vitro studies have focused on the toxicity in respiratory tract cell lines, the tissues in the oral cavity, which are exposed to high local concentrations of EC vapor, have been under‐studied. Our objective was to investigate the ability of EC vapor to induce cytotoxicity and oxidative stress in human oral cell lines. HGF‐1 human gingival fibroblasts and SCC‐25 human oral squamous cell carcinoma cells were exposed to a panel of commercially‐available fruit and tobacco‐flavored EC vapors using an air‐liquid interface exposure model, which mimics physiological exposures in vitro. Cytotoxicity and markers of oxidative stress were assessed after ecologically‐relevant exposure protocols. Cytotoxic EC vapors caused a greater than 30% reduction in cell viability. Nicotine was shown to ablate the effects of the cytotoxic EC vapors. There was no difference in the cytotoxic response to EC vapor between the cell lines tested. Treatment of SCC‐25 cells with a cytotoxic EC vapor caused a significant increase in intracellular ROS after a single 15 puff exposure. This increase occurred for both nicotine‐containing and nicotine‐free vapors. The differential effects of nicotine on cytotoxicity and oxidative stress suggest that either (1) cytotoxicity is not driven by ROS or (2) that nicotine protects cells by a mechanism that does not impact intracellular ROS levels. Ongoing studies are investigating the role of nicotine in this aerosolized system and the relationship between EC vapor constituents and cytotoxicity in human oral cells.Support or Funding InformationPenn State Tobacco Center of Regulatory Science; Penn State Department of Food ScienceThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.