2-Phenylethylamine is an endogenous constituent of human brain and is implicated in cerebral transmission. It is also found in certain foodstuffs and may cause toxic side-effects in susceptible individuals. Metabolism of 2-phenylethylamine to phenylacetaldehyde is catalyzed by monoamine oxidase and the oxidation of the reactive aldehyde to its acid derivative is catalyzed mainly by aldehyde dehydrogenase and perhaps aldehyde oxidase, with xanthine oxidase having minimal transformation. The present investigation examines the metabolism of 2-phenylethylamine to phenylacetaldehyde in liver slices and compares the relative contribution of aldehyde oxidase, xanthine oxidase and aldehyde dehydrogenase activity in the oxidation of phenylacetaldehyde with precision-cut fresh liver slices in the presence/absence of specific inhibitors of each enzyme. In liver slices, phenylacetaldehyde was rapidly converted to phenylacetic acid. Phenylacetic acid was the main metabolite of 2-phenylethylamine, via the intermediate phenylacetaldehyde. Phenylacetic acid formation was completely inhibited by disulfiram (specific inhibitor of aldehyde dehydrogenase), whereas isovanillin (specific inhibitor of aldehyde oxidase) inhibited acid formation to a lesser extent and allopurinol (specific inhibitor of xanthine oxidase) had little or no effect. Therefore, in liver slices, phenylacetaldehyde is rapidly oxidized by aldehyde dehydrogenase and aldehyde oxidase with little or no contribution from xanthine oxidase.

Aims During the COVID-19 era, the use of surgical face mask hampers the spread of COVID infection. The impact of smoking while wearing a surgical face mask on exhaled CO and vascular function in smokers has not been investigated. Methods We studied 40 smokers of conventional cigarettes (ConCig), 40 exclusive heat-non-burn cigarettes (HNBC) users and 40 non-smokers with similar age and sex (p>0.05 [45.1±10.8 years, 34 (28.3%) male]. We measured exhaled CO (parts per million [ppm]), pulse wave velocity (PWV) and central systolic blood pressure (cSBP). Results A significant interaction was found between CO at baseline and at the end of an 8h period with and without wearing a mask and the use of tobacco products vs no-smoking (F=46.58, p for interaction<0.001). Exhaled CO was higher in ConCig smokers compared to HNBC and nonsmokers throughout the study (p<0.05). Compared to baseline, the percent increase of CO was greater after smoking ConCig with than without wearing a mask for 8h (141.79% [95% confidence interval (CI): 116.16–167.42] vs 56.99% [95% CI: 44.80–69.18], p<0.001). Similarly, the percent increase of CO was greater after smoking HNBC with than without wearing a mask for 8h (103.84% [95% CI: 70.50–137.18] vs 30.76% [95% CI: 15.61–45.92], p<0.001). Among non-smokers, the use of mask did not alter exhaled CO (p>0.05). In both ConCig and HNBC users, all vascular markers were increased at the end of each one of two study assessments, compared to baseline (p<0.05). In non-smokers, the use of a mask had a neutral effect on vascular markers (p>0.05). Compared to baseline, the percent increase of PWV was greater after smoking ConCig with than without wearing a mask for 8h (16.54% [95% CI: 9.13–23.95] vs 4.36% [95% CI: 1.41–7.31], p=0.001). Compared to baseline, the percent increase of PWV was greater after smoking HNBC with than without wearing a mask for 8h (9.71% [95% CI: 4.57–14.84] vs 2.73% [95% CI: 0.12–5.35], p=0.003). Conclusion Ssmoking of any tobacco product (conventional tobacco or HNBC) during a prolonged use of a surgical face mask may further compromise vascular function. Thus, quitting both conventional and HNBC cigarettes is imperative for a better health in the COVID-19 pandemic. Funding Acknowledgement Type of funding sources: None.