Effects Of Tobacco Cigarette Smoking Research Articles

Inhibition of miR‐155 Attenuates Detrimental Vascular Effects of Tobacco Cigarette Smoking

BackgroundThe role of microRNAs dysregulation in tobacco cigarette smoking–induced vascular damage still needs to be clarified. We assessed the acute effects of tobacco cigarette smoking on endothelial cell‐related circulating microRNAs in healthy subjects. In addition, we investigated the potential role of microRNAs in smoking‐dependent endothelial cell damage.Methods and ResultsA panel of endothelial‐related microRNAs was quantified in healthy subjects before and after smoking 1 tobacco cigarette. Serum levels of miR‐155 were found to be significantly increased shortly after smoking. We also observed a progressive and significant miR‐155 accumulation in culture media of human endothelial cells after 30 minutes and up to 4 hours of cigarette smoke condensate treatment in vitro without evidence of cell death, indicating that miR‐155 can be released by endothelial cells in response to smoking stress. Cigarette smoke condensate appeared to enhance oxidative stress and impair cell survival, angiogenesis, and NO metabolism in human endothelial cells. Notably, these effects were abrogated by miR‐155 inhibition. We also observed that miR‐155 inhibition rescued the deleterious effects of cigarette smoke condensate on endothelial‐mediated vascular relaxation and oxidative stress in isolated mouse mesenteric arteries. Finally, we found that exogenous miR‐155 overexpression mimics the effects of smoking stress by inducing the upregulation of inflammatory markers, impairing angiogenesis and reducing cell survival. These deleterious effects were associated with downregulation of vascular endothelial growth factor and endothelial NO synthetase.ConclusionsOur results suggest that miR‐155 dysregulation may contribute to the deleterious vascular effects of tobacco smoking.

Electronic Cigarettes Impair Human Coronary Endothelial Function

Electronic (e‐) cigarettes are claimed—but unproven—to be less harmful than standard tobacco cigarettes, which are well known to impair coronary endothelial function and constitute a major cardiovascular risk factor. To determine whether e‐cigarettes cause impairment in human coronary endothelial function, we compared effects of tobacco cigarette smoking and e‐cigarette use to blunt the normal increase in myocardial blood flow (MBF) quantified by contrast enhanced echocardiography perfusion imaging, induced by the exercise pressor reflex (post‐handgrip forearm vascular occlusion). The exercise pressor reflex is a reproducible stimulus to endothelial‐dependent coronary vasodilation while also increasing coronary sympathetic vasoconstrictor drive. The coronary endothelial function testing was performed in healthy young adult cigarette smokers (n=5) and age‐matched e‐cigarette users (n=8), ages 21–38 years: a) after overnight smoking/vaping abstinence; and b) immediately after smoking one Camel‐filtered cigarette or one standard use (15 puffs in 7 minutes) of a popular tank‐style e‐cigarette (Evod: battery 3.7 volts, nicotine content 18 mg). During tobacco abstinence in the young cigarette smokers, the exercise pressor reflex increased mean arterial pressure (MAP) by 21.6 ± 4 mmHg (mean ± SE) and increased MBF by 66 ± 20% over baseline (p<0.05), the latter indicating endothelial‐dependent vasodilation in the human coronary microcirculation. As expected, the MBF failed to increase when the exercise pressor reflex was elicited immediately after cigarette smoking (Δ MBF −2 ± 24%, p=n.s.), indicating acute impairment in coronary endothelial function. The surprising new findings of this study are that MBF also failed to increase and tended to decrease by −45 ± 20% (p=n.s.) when the exercise pressor reflex was elicited immediately after acute e‐cigarette use and by −16 ± 10% (p=n.s.) even when elicited during vaping abstinence (despite comparable mean reflex increases in MAP of 21.1 and 21.6 mm Hg, respectively). Thus, our data to date suggest that, in contrast to what has been widely assumed, e‐cigarette use in young adults causes an impairment in coronary endothelial function that appears to be more persistent than with traditional tobacco cigarettes. Further research is warranted to determine if specific oxidant nanoparticles in e‐cigarette vapor mediate the impaired coronary endothelial function.Support or Funding InformationFunded by Tobacco Related Disease Research Program; ClinicalTrials.gov NCT02612701This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Effects of Tobacco Cigarette Smoking on Some Hematological Parameters of Male Cigarette Smokers in Southern Nigeria

Effects of Tobacco Cigarette Smoking on Some Hematological Parameters of Male Cigarette Smokers in Southern Nigeria

Effects of Tobacco Smoking on the Kinetics of the Pupillary Light Reflex: A Comparison between Smokers and Non-Smokers

Background: The time course of the pupillary light reflex (PLR) is determined by the successive activation of parasympathetic and sympathetic innervations of the iris, latency and amplitude reflecting parasympathetic activity and recovery time showing mainly sympathetic activity. Objective: To determine the effects of tobacco cigarette smoking on the PLR in smokers after an abstinence period of at least 12 h. Methods: Ten smokers (mean 15.7 cigarettes/day) and 10 non-smokers participated in a randomised, non-intervention controlled, cross-over study that included a parallel control group. Smokers underwent two sessions with a time interval between 3 and 8 days; two recordings were taken at each session, separated by 20 min: session 1, without smoking, and session 2, smoking 3 cigarettes within a 30-min period. Non-smokers underwent one session; two recordings were taken separated by 20 min. At each recording, in both groups, PLR was elicited with four light flashes of increasing luminance. Results: The relationship between PLR parameters and light intensity was linear in each subject. The slope of the regression line for relative amplitude increase versus intensity was significantly flatter in abstinent smokers than in non-smokers (p = 0.033); the slope returned significantly after smoking (p = 0.043). No other significant effects were obtained. Conclusions: Kinetic parameters of PLR provide a sensitive pharmacological test to detect cholinergic neurotransmission manipulation effects, as they seem to detect changes in moderate smokers after 12 h of abstinence, and their reversal on return to smoking. These results suggest an enhancement in the suppression of the parasympathetic oculomotor reflex arc rather than a facilitation of the sympathetic drive to the iris.

Formation of 8-nitroguanine in tobacco cigarette smokers and in tobacco smoke-exposed Wistar rats

Our previous studies have shown that 8-nitroguanine (8-NO 2-G) could serve as a specific biomarker of DNA damage induced by gaseous nitrogen oxides (NO x ) exposure. To evaluate the effect of tobacco cigarette smoking on the DNA damage in peripheral lymphocytes of cigarette smoke ones, we randomly collected and determined the level of 8-NO 2-G in DNA extracted from peripheral lymphocyte of 15 each of light-smoking healthy volunteer (L-S, less than one pack per day), moderate-smoking healthy volunteers (M-S, one to two pack per day for 5–10 years), heavy-smoking healthy volunteers (H-S, over two packs per day for 10 years), lung cancer patients with heavy smoking (cancer H-S) and non-smoking healthy controls. Both of the mean level of the 8-NO 2-G levels in peripheral lymphocyte (0.90±1.0, 1.23±1.14, 1.43±0.79, 3.62±1.38 ng per μg DNA) and serum nitrite (38.99±9.58, 46.70±9.38, 55.46±10.45, 70.1±18.54 μM) of L-S, M-S, H-S and cancer H-S groups were higher than that of non-smoking healthy controls (0.02±0.04 and 18.96±4.31 for 8-NO 2-G level and serum nitrite, respectively). Furthermore, in animal experiment, a dose-dependent increase in 8-NO 2-G was observed in rat lung and peripheral lymphocyte DNA of Wistar rats after tobacco cigarette smoke exposure twice a day, for 1 month. The level of 8-NO 2-G is 0.17±0.41, 1.65±3.15, 23.50±20.75 and 37.58±17.55 ng per μg lung DNA for rat exposed with tobacco cigarette smoke from 0, 5, 10, 15 cigarettes per day, respectively. It was also found that count of peripheral lymphocytes and nitrite concentration in serum of rat increased after the tobacco smoke exposure. It is postulated that tobacco cigarette smoking could induce DNA damage (8-NO 2-G formation) by exo- and endogenous NO x .

Respiratory effects of non-tobacco cigarettes.

Data from the Tucson epidemiological study of airways obstructive disease on smoking of non-tobacco cigarettes such as marijuana were analysed to determine the effect of such smoking on respiratory symptoms and pulmonary function. Among adults aged under 40, 14% had smoked non-tobacco cigarettes at some time and 9% were current users. The prevalence of respiratory symptoms was increased in smokers of non-tobacco cigarettes. After tobacco smoking had been controlled for men who smoked non-tobacco cigarettes showed significant decreases in expiratory flow rates at low lung volumes and in the ratio of the forced expiratory volume in one second to the vital capacity. This effect on pulmonary function in male non-tobacco cigarette smokers was greater than the effect of tobacco cigarette smoking. These data suggest that non-tobacco cigarette smoking may be an important risk factor in young adults with respiratory symptoms or evidence of airways obstruction.

Effect of smoking on plasma and platelet fatty acid composition in middle-aged men

The effect of tobacco cigarette smoking on plasma and platelet fatty acid composition was studied in 219 male subjects. The effect of tobacco on plasma malondialdehyde-like material (MDA-LM) was also evaluated. In the total fatty acid percentage composition in plasma, an increase in the saturated fatty acids at the expense of polyunsaturated fatty acids was observed in those subjects who smoked more than 20 cigarettes/day. In the total fatty acid composition of platelets, an increase in myristic acid (14:0) and palmytoleic acid (16:1) was found. Additionally, when the fatty acid composition of the different platelet lipid fractions was evaluated, an increase in 14:0 and 16:0 + 16:1 was observed in phospholipids. Finally, the plasma MDA-LM level was significantly higher in those subjects who smoked more than 10 cigarettes/day. The biochemical variations found in this study may be compatible with the greater incidence of CHD observed in smokers.

Acute effect of tobacco cigarette smoking on the platelet aggregate ratio

Acute effect of tobacco cigarette smoking on the platelet aggregate ratio

Acute effect of tobacco cigarette smoking on the platelet aggregate ratio.

The purpose of this study was to determine whether cigarette smoking acutely increased circulating platelet aggregates as detected by lowering of the platelet aggregate ratio. Eighteen (11 male and 7 female) volunteers ranging from 16 to 47 years of age rested during a 20-minute control period and smoked two unfiltered tobacco cigarettes during another 20-minute period. Platelet aggregate ratios (mean +/- SD) before and after the control period were 0.86 +/- 13 and 0.82 +/- 0.12 respectively (p greater than 0.05) and before and after smoking were 0.84 +/- 0.14 and 0.66 +/- 0.18 respectively (p less than 0.01). The mean plasma nonesterified fatty acid concentration was not significantly different before and after smoking suggesting that the decrease in platelet aggregate ratio was not mediated through elevation of the plasma nonesterified fatty acid concentration. Our results are consistent with the theory that platelet aggregates contribute to the increased incidence of myocardial infarction and sudden death from coronary artery disease observed among cigarette smokers.