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BackgroundRate of nicotine metabolism is an important factor influencing cigarette smoking behavior, dependence, and efficacy of nicotine replacement therapy. The current study examined the hypothesis that chronic alcohol abuse can accelerate the rate of nicotine metabolism. Nicotine metabolite ratio (NMR, a biomarker for rate of nicotine metabolism) and patterns of nicotine metabolites were assessed at three time points after alcohol cessation.MethodsParticipants were 22 Caucasian men randomly selected from a sample of 165 smokers entering a 7-week alcohol dependence treatment program in Poland. Data were collected at three time points: baseline (week 1, after acute alcohol detoxification), week 4, and week 7. Urine was analyzed for nicotine and metabolites and used to determine the nicotine metabolite ratio (NMR, a biomarker for rate of nicotine metabolism), and total nicotine equivalents (TNE, a biomarker for total daily nicotine exposure).Results and conclusionsThere was a significant decrease in urine NMR over the 7 weeks after alcohol abstinence (F(2,42)=18.83, p

SignificanceElectronic cigarettes, also known as e-cigarettes, are devices designed to imitate regular cigarettes and deliver nicotine via inhalation without combusting tobacco. They are purported to deliver nicotine without other toxicants and to be a safer alternative to regular cigarettes. However, little toxicity testing has been performed to evaluate the chemical nature of vapour generated from e-cigarettes. The aim of this study was to screen e-cigarette vapours for content of four groups of potentially toxic and carcinogenic compounds: carbonyls, volatile organic compounds, nitrosamines and heavy metals.Materials and methodsVapours were generated from 12 brands of e-cigarettes and the reference product, the medicinal nicotine inhaler, in controlled conditions using a modified smoking machine. The selected toxic compounds were extracted from vapours into a solid or liquid phase and analysed with chromatographic and spectroscopy methods.ResultsWe found that the e-cigarette vapours contained some toxic substances. The levels of the toxicants were 9-450 times lower than in cigarette smoke and were, in many cases, comparable with trace amounts found in the reference product.ConclusionsOur findings are consistent with the idea that substituting tobacco cigarettes with e-cigarettes may substantially reduce exposure to selected tobacco-specific toxicants. E-cigarettes as a harm reduction strategy among smokers unwilling to quit, warrants further study. (To view this abstract in Polish and German, please see the supplementary files online.).

Aims The amount and pattern of cigarette and alcohol consumption are highly associated with cardiovascular risk. The aim of the present study was the assessment of changes in arterial stiffness and classical risk factors for cardiovascular disease after alcohol withdrawal and detoxification in persons with alcohol use disorder. Methods Two hundred and forty-one individuals (men and women) participated in the investigation. The photoplethysmographic method was applied to assess arterial stiffness in three stages within 6 weeks. Participants were divided into subgroups based on age and sex. Analyses were performed using analysis of variance with repeated measures. Results Different variations in time of stiffness index (SI) and reflection index (RI) values were recorded. Some increases in triglycerides, total cholesterol, low-density lipoprotein and a decrease in high-density lipoproteins were observed in all analyzed groups. Both systolic and diastolic blood pressure (DP) changed significantly during the 3 weeks of the study only in a group of younger men. The SI is correlated with age and gender. No correlation of RI with sex was found; however, RI was strongly correlated with age, pulse and DP. Conclusions The presented study shows that some groups of patients (older women and younger men) after detoxification may be particularly vulnerable to vascular system disorders, i.e. arterial stiffness, making it suggested to include additional observation during therapy. [ABSTRACT FROM AUTHOR]

Byline: Barbara KAapciAska (1), Ewa Sadowska-KrApa (1), SAawomir Jagsz (1), Andrzej Sobczak (2), MaAgorzata A>>endzian-Piotrowska (3), Jan Gorski (3), Jozef Langfort (1,4) Keywords: Left ventricular hypertrophy; Tachycardia; Rat Abstract: Increased oxidative stress resulting from enhanced production of reactive oxygen species and/or inadequate mechanisms of antioxidant defenses has been recognized as an important factor contributing to the initiation and progression of cardiac dysfunction under a wide variety of pathophysiological conditions. The main objective of this study was to examine the effect of electrically induced tachycardia on oxidative stress and the capacity of antioxidant defenses in the normal and hypertrophied left ventricle (LV) in the rat. Left ventricular hypertrophy (LVH) was produced by banding the descending abdominal aorta. The activities of antioxidant enzymes, concentrations of non-enzymatic antioxidants, and biomarkers of oxidative stress were measured in the LV of aortic-banded animals (LVH), untreated or banded rats subjected to short-term (45 min) atrial pacing [(CTR + S) and (LVH + S), respectively], and untreated (CTR) or sham-operated (SHAM) controls. The results indicate that the increase in heart rate in vivo as a result of atrial pacing to a maximum level, independent of sympathetic nerve activity, leads to a substantial increase in oxidative stress and a marked decline in the activities of antioxidant enzymes in both the normal and hypertrophied left ventricle of the rat. The accompanying increase in tissue content of [alpha]- and I3-tocopherols seem to contribute to attenuation of the oxidant stress-related loss of thiol stores in the LV. Stable left ventricular hypertrophy induced by aortic banding for six weeks has a minor impact on the capacity of the endogenous antioxidant defense system in the LV, but significantly and negatively affects the ability of the heart LV to tolerate the stress of tachycardia. Author Affiliation: (1) Department of Physiological and Medical Sciences, Academy of Physical Education, 72A MikoAowska Str, 40-065, Katowice, Poland (2) Department of General and Inorganic Chemistry, School of Pharmacy, The Medical University of Silesia, Sosnowiec, Poland (3) Department of Physiology, Medical University of Bialystok, 2c Mickiewicza Str., BiaAystok, Poland (4) Department of Experimental Pharmacology, Polish Academy of Sciences Medical Research Center, Warsaw, Poland Article History: Registration Date: 02/02/2009 Received Date: 25/11/2008 Accepted Date: 29/01/2009 Online Date: 26/02/2009 Article note: An erratum to this article can be found online at http://dx.doi.org/10.1007/s12576-012-0242-7.