Comparison of Oxidative Effects of Electronic Cigarette and Tobacco Smoke Exposure Performed Experimentally

2021 ◽  
pp. 1-7
Author(s):  
Oktay Aslaner
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Electronic Cigarette ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Exposure Group ◽  
Oxidative Effects

<b><i>Objective:</i></b> Cigarette smoking is a life-threatening habit that has rapidly spread in every socioeconomic part of the public worldwide. There exist mechanisms of nicotine delivery available to use in the hope of halting cigarette smoking, and the electronic cigarette (EC) is one of the common methods used for tobacco smoking replacement. This study aimed to investigate experimentally the oxidative effects of tobacco smoke and EC smoke which contain nicotine. <b><i>Method:</i></b> We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (<i>N</i> = 8); the electronic cigarette group (<i>N</i> = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (<i>N</i> = 8), exposure to traditional cigarette smoke for 2 h per day. After the first and second week of exposure, blood samples were obtained, and serum oxidative stress index (OSI), paraoxonase 1 (PON1) activity, and prolidase levels were evaluated. <b><i>Results:</i></b> Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (<i>p</i> &#x3c; 0.001) when compared with the control group, and partial decrements were observed in the second week. By contrast, elevated PON1 levels were observed in the second week after EC or tobacco smoke exposure. The highest OSI levels were observed in the tobacco smoke group (<i>p</i> &#x3c; 0.001). The lowest values of PON1 levels were detected in the first week of the electronic cigarette smoke group, and this decremental value was statistically different than normal, the second week of the electronic cigarette smoke group, the first week of the traditional cigarette smoke exposure group, and the second week of the traditional cigarette smoke exposure group values (<i>p</i> &#x3c; 0.000). <b><i>Conclusion:</i></b> Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.

Cigarette Smoke Exposure and Acute Respiratory Infection in Children Under Five: A Meta-Analysis

2020 ◽  
Author(s):  
Maya Ayu Riestiyowati ◽  
◽  
Setyo Sri Rahardjo ◽  
Vitri Widyaningsih ◽  
◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Respiratory Infection ◽  
Tobacco Smoke ◽  
Acute Respiratory Infection ◽  
Meta Analysis ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Children Under Five ◽  
Under Five

Background: Acute Respiratory Infections are classified into the upper and lower respiratory tract infections, contributing to the leading cause of death among children under five globally. The estimation showed the deaths of more than 800,000 children under five every year or about 2,200 per day. One of the risk factors for ARI in children under five years of age is secondary exposure to tobacco smoke. This study aimed to examine the effect of cigarette smoke exposure and acute respiratory infection in children under five. Subjects and Method: This was meta analysis and systematic review. The study was conducted by collecting published articles from Google Scholar, Pubmed, and Springer Link databases, from year 2010 to 2019. Keywords used “risk factor” OR “passive smoking” OR “secondhand smoking” AND “ARI due to children under five”. The inclusion criteria were full text, using English language, using cross-sectional study design, and reporting adjusted odds ratio. The collected articles were selected by PRISMA flow chart. The quantitative data were analyzed by fixed effect model using Revman 5.3. Results: 6 studies from Cameroon, Ethiopia, India, Nepal, and Nigeria reported that tobacco smoke exposure increased the risk of acute respiratory infection in children under five (aOR=1.39; 95% CI= 1.22 to 1.58; p<0.001). Conclusion: Tobacco smoke exposure increases the risk of acute respiratory infection in children under five. Keywords: tobacco smoke, acute respiratory infection, children under five Correspondence: Maya Ayu Riestiyowati. Masters Program in Public Health. Universitas Sebelas Maret, Jl. Ir. Sutami 36A, Surakarta 57126, Central Java. Email: [email protected]. Mobile: 081235840067.

Cigarette smoke exposure potentiates bleomycin-induced lung fibrosis in guinea pigs

2003 ◽  
Vol 285 (4) ◽  
pp. L949-L956 ◽  
Author(s):  
José Cisneros-Lira ◽  
Miguel Gaxiola ◽  
Carlos Ramos ◽  
Moisés Selman ◽  
Annie Pardo
Keyword(s):  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Guinea Pigs ◽  
Lung Fibrosis ◽  
Smooth Muscle Actin ◽  
Smoke Exposure ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Fibroblast Proliferation

The role of tobacco smoking in the development and outcome of pulmonary fibrosis is uncertain. To approach the effects of cigarette smoke on bleomycin-induced lung fibrosis, we studied five groups of guinea pigs: 1) controls, 2) instilled with bleomycin (B), 3) exposed to tobacco smoke for 6 wk (TS), 4) bleomycin instillation plus tobacco smoke exposure for 6 wk (B+TS), and 5) tobacco smoke exposure for 6 wk and bleomycin after smoking (TS/B). Guinea pigs receiving bleomycin and tobacco smoke exposure exhibited higher fibrotic lesions including a significant increase in the number of positive α-smooth muscle actin cells compared with bleomycin alone (B+TS, 3.4 ± 1.2%; TS/B, 3.7 ± 1.5%; B, 2.3 ± 1.5%; P < 0.01). However, only the TS/B group reached a significant increase in lung collagen compared with the bleomycin group (TS/B, 3.5 ± 0.7; B ± TS, 2.9 ± 0.4; B, 2.4 ± 0.2 mg hydroxyproline/lung; P < 0.01). Bronchoalveolar lavage (BAL) from TS/B showed an increased number of eosinophils and higher levels of IL-4 and tissue inhibitor of metalloproteinase-2 ( P < 0.01 for all comparisons) and induced a significant increase in fibroblast proliferation ( P < 0.05). Importantly, smoke exposure alone induced an increase in BAL neutrophils, matrix metalloproteinase-9, and fibroblast proliferation compared with controls, suggesting that tobacco smoke creates a profibrotic milieu that may contribute to the increased bleomycin-induced fibrosis.

scholarly journals Prenatal cigarette smoke exposure slightly alters neurobehavioral development in neonatal rats: Implications for developmental origins of health and disease (DoHAD)

2020 ◽  
Vol 107 (1) ◽  
pp. 55-66
Author(s):  
B. Mammel ◽  
T. Kvárik ◽  
Zs. Szabó ◽  
J. Gyarmati ◽  
T. Ertl ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Motor Coordination ◽  
Smoke Exposure ◽  
Whole Body ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Developmental Origins ◽  
Smoking During Pregnancy ◽  
Neurobehavioral Development ◽  
Health And Disease

AbstractNumerous studies indicate that smoking during pregnancy exerts harmful effects on fetal brain development. The aim of this study was to determine the influence of maternal smoking during pregnancy on the early physical and neurobehavioral development of newborn rats. Wistar rats were subjected to whole-body smoke exposure for 2 × 40 min daily from the day of mating until day of delivery. For this treatment, a manual closed-chamber smoking system and 4 research cigarettes per occasion were used. After delivery the offspring were tested daily for somatic growth, maturation of facial characteristics and neurobehavioral development until three weeks of age. Motor coordination tests were performed at 3 and 4 weeks of age. We found that prenatal cigarette smoke exposure did not alter weight gain or motor coordination. Critical physical reflexes indicative of neurobehavioral development (eyelid reflex, ear unfolding) appeared significantly later in pups prenatally exposed to smoke as compared to the control group. Prenatal smoke exposure also resulted in a delayed appearance of reflexes indicating neural maturity, including hind limb grasping and forelimb placing reflexes. In conclusion, clinically relevant prenatal exposure to cigarette smoke results in slightly altered neurobehavioral development in rat pups. These findings suggest that chronic exposure of pregnant mothers to cigarette smoke (including passive smoking) results in persisting alterations in the developing brain, which may have long-lasting consequences supporting the concept of developmental origins of health and disease (DoHAD).

scholarly journals Pengaruh pemberian ubi jalar ungu (Ipomoea batatas L.Poir) terhadap kadar superoksida dismutase (SOD) tikus wistar jantan (Rattus Norvegicus) yang dipapar asap rokok

2020 ◽  
Vol 8 (1) ◽  
pp. 45
Author(s):  
Alfreda Sabrina Widyanti ◽  
Martha Ardiaria ◽  
Nurmasari Widyastuti
Keyword(s):  
Superoxide Dismutase ◽  
Sweet Potato ◽  
Cigarette Smoke ◽  
Ipomoea Batatas ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Standard Diet ◽  
Control Group Design ◽  
Significant Difference

Background: Cigarette smoke exposure is one of the source of free radicals that causes oxidative stress and decreases superoxide dismutase (SOD) level. Purple fleshed sweet potato is a type of food that contains antioxidants to neutralize oxidative stress.Objectives: To study the effect of purple fleshed sweet potato on superoxide dismutase (sod) level on rats exposed to cigarette smoke.Methods: This was a true experimental study with a post-test randomized control group design. The rats were randomized into 4 groups (6 rats in each group). The negative control group (K-) was treated with standard diet; the positive control group (K+) was treated with cigarette smoke exposure and standard diet; the treatment 1 (P1) group was treated with standard diet and purple fleshed sweet potato with the dose of 8 g / 200 g bw/day, and the treatment 2 (P2) group was treated with cigarette smoke exposure and purple fleshed sweet potato with the dose of 8 g /200 g bw/day.Results: There was a significant difference of SOD levels in each group (p=0.00) except between group K- and P1. Giving purple fleshed sweet potatoes increased SOD levels as much as 85.81±4.59 (P1). The K+ group had the lowest SOD level 22.34±3.98. The SOD level for K- group and P2 group was 82.27±4.59 and 67.73±6.68 respectively.Conclusion: The highest SOD level is on the treatment 1 group which is administered with purple fleshed sweet potato.

scholarly journals Tobacco smoking induces cardiovascular mitochondrial oxidative stress, promotes endothelial dysfunction, and enhances hypertension

2019 ◽  
Vol 316 (3) ◽  
pp. H639-H646 ◽  
Author(s):  
Sergey Dikalov ◽  
Hana Itani ◽  
Bradley Richmond ◽  
Liaison Arslanbaeva ◽  
Aurelia Vergeade ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Tobacco Smoking ◽  
Smoke Exposure ◽  
Metabolic Reprogramming ◽  
Wild Type ◽  
Mitochondrial Oxidative Stress

Tobacco smoking is a major risk factor for cardiovascular disease and hypertension. It is associated with the oxidative stress and induces metabolic reprogramming, altering mitochondrial function. We hypothesized that cigarette smoke induces cardiovascular mitochondrial oxidative stress, which contributes to endothelial dysfunction and hypertension. To test this hypothesis, we studied whether the scavenging of mitochondrial H2O2 in transgenic mice expressing mitochondria-targeted catalase (mCAT) attenuates the development of cigarette smoke/angiotensin II-induced mitochondrial oxidative stress and hypertension compared with wild-type mice. Two weeks of exposure of wild-type mice with cigarette smoke increased systolic blood pressure by 17 mmHg, which was similar to the effect of a subpresssor dose of angiotensin II (0.2 mg·kg−1·day−1), leading to a moderate increase to the prehypertensive level. Cigarette smoke exposure and a low dose of angiotensin II cooperatively induced severe hypertension in wild-type mice, but the scavenging of mitochondrial H2O2 in mCAT mice completely prevented the development of hypertension. Cigarette smoke and angiotensin II cooperatively induced oxidation of cardiolipin (a specific biomarker of mitochondrial oxidative stress) in wild-type mice, which was abolished in mCAT mice. Cigarette smoke and angiotensin II impaired endothelium-dependent relaxation and induced superoxide overproduction, which was diminished in mCAT mice. To mimic the tobacco smoke exposure, we used cigarette smoke condensate, which induced mitochondrial superoxide overproduction and reduced endothelial nitric oxide (a hallmark of endothelial dysfunction in hypertension). Western blot experiments indicated that tobacco smoke and angiotensin II reduce the mitochondrial deacetylase sirtuin-3 level and cause hyperacetylation of a key mitochondrial antioxidant, SOD2, which promotes mitochondrial oxidative stress. NEW & NOTEWORTHY This work demonstrates tobacco smoking-induced mitochondrial oxidative stress, which contributes to endothelial dysfunction and development of hypertension. We suggest that the targeting of mitochondrial oxidative stress can be beneficial for treatment of pathological conditions associated with tobacco smoking, such as endothelial dysfunction, hypertension, and cardiovascular diseases. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/mitochondrial-oxidative-stress-in-smoking-and-hypertension/ .

Differential induction of apoptosis by cigarette smoke extract in primary human lung fibroblast strains: implications for emphysema

2006 ◽  
Vol 291 (1) ◽  
pp. L19-L29 ◽  
Author(s):  
Carolyn J. Baglole ◽  
Seth M. Bushinsky ◽  
Tatiana M. Garcia ◽  
Aruna Kode ◽  
Irfan Rahman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Mitochondrial Membrane ◽  
Human Lung ◽  
Cigarette Smoke Extract ◽  
Lung Fibroblast ◽  
Cigarette Smoke Exposure ◽  
Human Lung Fibroblast

Cigarette smoke is the principal cause of emphysema. Recent attention has focused on the loss of alveolar fibroblasts in the development of emphysema. Fibroblasts may become damaged by oxidative stress and undergo apoptosis as a result of cigarette smoke exposure. Not all smokers develop lung diseases associated with tobacco smoke, a fact that may reflect individual variation among human fibroblast strains. We hypothesize that fibroblasts from different human beings vary in their ability to undergo apoptosis after cigarette smoke exposure. This could account for emphysematous changes that occur in the lungs of some but not all smokers. Primary human lung fibroblast strains were exposed to cigarette smoke extract (CSE) and assessed for viability, morphological changes, and mitochondrial transmembrane potential as indicators of apoptosis. We also examined the generation of intracellular reactive oxygen species (ROS), 4-hydroxy-2-nonenal, and changes in glutathione (GSH) and glutathione disulfide (GSSG) levels. Each human lung fibroblast strain exhibited a differential sensitivity to CSE as judged by changes in mitochondrial membrane potential, viability, ROS generation, and glutathione production. Interestingly, the thiol antioxidants N-acetyl-l-cysteine and GSH eliminated CSE-induced changes in fibroblast morphology such as membrane blebbing, nuclear condensation, and cell size and prevented alterations in mitochondrial membrane potential and the generation of ROS. These findings support the concept that oxidative stress and apoptosis are responsible for fibroblast death associated with exposure to tobacco smoke. Variations in the sensitivity of fibroblasts to cigarette smoke may account for the fact that only some smokers develop emphysema.

Sign in / Sign up

Export Citation Format

Share Document