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The electronic cigarette (e-cigarette), which is accepted as a new market by the tobacco industry, is highly dependent on health and is addictive due to its nicotine content. Informing and raising awareness is extremely valuable to protect the identified risks of e-cigarette in society. The aim of this study was to determine the socio-demographic characteristics of volunteer e-cigarette users, to determine the causes of e-cigarette smoking, to identify some risks (nicotine, carbon monoxide). In this descriptive study, volunteer electronic cigarette smokers participated in the questionnaire, carbon monoxide was measured, urine sample was taken and directed to the toxicology laboratory for measurement of cotinine, and cotinine was measured in urine. Twenty volunteer e-cigarette smokers participated in the survey. Eighty five percent of the participants were male, 60% were married, 75% were college / university graduates, 80% were working, 65% of them were economical, 35% were good, 40% and 35% regularly use medicines. The median age of participants was 38.5 years, the youngest participant was 22, the oldest was 69 years old. Fifteen (75%) of the respondents stated that they were passively affected by tobacco smoke. Eight of these 15 (73%) were exposed to friends, eight (54%) were at home, eight (54%) were at cafes, etc., and four were exposed at work. The participants' main reasons for starting to smoke are friend influence and curiosity. Thirty percent of participants had tried e-cigarette before using e-cigarette, 90% used e-cigarette every day, e-cigarette was most frequently obtained from internet and friends / relatives, 79% did not use cigarette e-cigarette and all use nicotine. Participants' median e-cigarette smoking duration was 5.5 months; monthly e-cigarette expenditures are median 60 TL. Participants main reasons to smoke e-cigarette are to quit smoking, reduce smoking cigarettes and for reasons of cheapness. Eleven of the respondents (55%) stated that they never smoked together with e-cigarette but 9 (45%) smoked together with e-cigarette, but e-cigarette smoking significantly reduced the cigarette. Only 15% of the participants (three people) knew that smoking was harmful to health; only 45% of e-cigarette users knew that e-cigarette is addictive although they all use nicotine in their e-cigarettes. Of the 19 people who responded to the question 15 (79%) do not consider leaving e-cigarettes. Participants' carbon monoxide levels were measured as median 3, lowest 1, highest 22. Carbon monoxide level in 25% of participants was found to be above 7 ppm, which is used as threshold value in determining smokers. The levels of cotinine detected in urine samples are 709.9, lowest 318.6, highest 825.3 ng / ml. A moderate and statistically significant correlation was found between the amount of fluids used by the participants in one day (ml) and cotinine levels in urine specimens (Pearson correlation test, r = 0.511, p = 0.025). As a result, this study, in which nicotine exposure and increase in carbon monoxide and urine cotinine levels due to the use of e-cigarettes is documented, is an important proof of the country's scientific work on e-cigarettes. Preventive strategies should be strictly used for any tobacco products including e-cigarettes. Funding Statement: This project was funded by Hacettepe University, Scientific Research Projects Coordination Unit (Project nb. TAY-2016-9469).

In vitro and in vivo interactions which are commonly met during drug therapy and their toxicological outcomes are important. In order to increase effect of certain drugs, interactions, which are called as beneficial interactions, are intentionally applied. However, examples of these interactions are in limited number. On the other hand, untoward and hazardous interactions that cause very important outcomes in toxicological point of view are common. These types of interactions develop more easily during therapy with drugs have a narrow therapeutic window. Theophylline which is used in the treatment of asthma and chronic obstructive pulmonary disease (COPD) has also a narrow therapeutic window. Therefore, in the present review, some important examples resulted from interactions of theophylline with drug, diet, xenobiotic, herbal product, habits and their toxicological outcomes have been given.

… European Soc Toxicol

To investigate the possibility of the involvement of an oxidative stress induction in the mechanism of the cytotoxic effect of quinolone antibiotics, we examined the viability of human fibroblast cells exposed to ciprofloxacin (CPFX), and measured the levels of lipid peroxidation (LP), glutathione (GSH), and the activities of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX). The data showed that the effect of CPFX on the viability of cells, as determined by neutral red uptake assay, was time-dependent, and the dose-response relation was biphasic. Cytotoxicity was not observed in the concentration range 5–150 mg/l CPFX when the cells were incubated for 24 h. In contrast, lower concentrations (5 and 12.5 mg/l) of CPFX increased the cell growth in all incubation periods tested. Marked decreases in the viability of fibroblasts were observed at concentrations 50 and 75 mg/l, and ⩾50 mg/l, following 48 and 72 h exposure, respectively ( p < 0.05). However, when the cells were exposed to >75 mg/l CPFX for 48 h, no cytotoxicity was observed. By exposing fibroblast cultures to 75 mg/l CPFX for 48 h, an induction of LP enhancement and a marked decrease in intracellular GSH were observed. Vitamin E pretreatment of the cells lowered the level of LP, increased the total GSH content, and provided significant protection against CPFX-induced cytotoxicity. The biphasic effect of CPFX possibly resulted from the complex dose-dependent relationships between reactive oxygen species (ROS), cell proliferation, and cell viability. It was previously reported, in fact, for several cell models that ROS exert a biphasic effect on cell growth. Furthermore, cultured fibroblasts release their own free radicals, and the inhibition of endogenous ROS inhibits the fibroblast cell proliferation, whereas the effect of exogenous ROS is biphasic.