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.

The pig has been used as an important animal model for human studies because of its similarity in size, physiology and disease development. However, in contrast to the extensive data available on the cytochrome P450 (CYP) system for humans and rodents, the data related to pig are limited because of, among others, the presence of intra-species differences (domestic pigs and minipigs). The knowledge of the CYP superfamily in a given experimental animal is crucial for pharmacological and toxicological tests in developing drugs and for understanding the metabolic pathways of toxicants and carcinogens. In addition, information on the CYP system in pigs is important since it plays a dominant role in the metabolism of veterinary drugs, whose residues remain in the porcine tissues which are food for humans. The aim of the present review is to examine - in the liver and extrahepatic tissues of pig - our current knowledge of the xenobioticmetabolizing CYPs belonging to families 1-4, in terms of drug metabolism, substrate specificity, inhibition, gene expression and receptor- driven regulation, in comparison with human data. It is hoped, furthermore, that this review may stimulate research on the porcine drug – metabolizing enzymes in order to evaluate the hypothesis whereby pig data may better reflect human drug metabolism and toxicity than those obtained from the traditional non-rodent models.

The aim of this study was to verify the activation details and products of human lymphomonocytes, stimulated by different β‐glucans, that is Euglena paramylon, MacroGard^®, and lipopolysaccharide. We investigated the gene expression of inflammation‐related cytokines and mediators, transactivation of relevant transcription factors, and phagocytosis role in cell‐glucan interactions, by means of RT‐PCR, immunocytochemistry, and colorimetric assay. Our results show that sonicated and alkalized paramylon upregulates pro‐inflammatory factors (NO, TNF‐α, IL‐6, and COX‐2) in lymphomonocytes. A clear demonstration of this upregulation is the increased transactivation of NF‐kB visualized by immunofluorescence microscopy. Phagocytosis assay showed that internalization is not a mandatory step for signaling cascade to be triggered, since immune activity is not present in the lymphomonocytes that have internalized paramylon granules and particulate MacroGard^®. Moreover, the response of Euglena β‐glucan‐activated lymphomonocytes is much greater than that induced by commercially used β‐glucans such as MacroGard^®. Our in vitro results indicate that linear fibrous Euglena β‐glucan, obtained by sonication and alkaline treatment can act as safe and effective coadjutant of the innate immune system response.