No abstract

Electronic cigarettes (e-cigs) are devices designed to deliver nicotine in a vaping solution rather than smoke and without tobacco combustion. Perceived as a safer alternative to conventional cigarettes, e-cigs are aggressively marketed as lifestyle-choice consumables, thanks to few restrictions and a lack of regulatory guidelines. E-cigs have also gained popularity among never-smokers and teenagers, becoming an emergent public health issue. Despite the burgeoning worldwide consumption of e-cigs, their safety remains largely unproven and it is unknown whether these devices cause in vivo toxicological effects that could contribute to cancer. Here we demonstrate the co-mutagenic and cancer-initiating effects of e-cig vapour in a rat lung model. We found that e-cigs have a powerful booster effect on phase-I carcinogen-bioactivating enzymes, including activators of polycyclic aromatic hydrocarbons (PAHs), and increase oxygen free radical production and DNA oxidation to 8-hydroxy-2′-deoxyguanosine. Furthermore, we found that e-cigs damage DNA not only at chromosomal level in peripheral blood, such as strand breaks in leucocytes and micronuclei formation in reticulocytes, but also at gene level such as point mutations in urine. Our results demonstrate that exposure to e-cigs could endanger human health, particularly among younger more vulnerable consumers.

No abstract

The prooxidant role of free fatty acids was studied in soybean oil-in-water emulsions. Addition of oleic acid (0-5.0% of oil) to the emulsions increased lipid hydroperoxides and headspace hexanal formation and increased the negative charge of the emulsion droplet with increasing oleic acid concentration. Methyl oleate (1.0% of oil) did not increase oxidation rates. The ability of oleic acid to promote lipid oxidation in oil-in-water emulsions decreased with decreasing pH with dramatic reduction in oxidation observed when the pH was low enough so that the oleic acid was not able to increase the negative charge of the emulsion droplet. Ethylenediaminetetraacetic acid (EDTA, 200 microm) strongly inhibited lipid oxidation in emulsions with oleic acid, indicating that transition metals were responsible for accelerating oxidation. Oleic acid hydroperoxides did not increase oxidation rates, suggesting that hydroperoxides on free fatty acids are not strong prooxidants in oil-in-water emulsion. These results suggest that the prooxidant activity of free fatty acids in oil-in-water emulsions is due to their ability to attact prooxidant metals to the emulsion droplet surface.

No abstract