The influence of tobacco smoke exposure on selected markers of oxidative stress, kidneys and liver function in the serum of rats with streptozotocin-induced diabetes

Objective: 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. Method: We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (N = 8); the electronic cigarette group (N = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (N = 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. Results: Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (p < 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 (p < 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 (p < 0.000). Conclusion: Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.

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Secondhand tobacco smoke, arterial stiffness, and altered circadian blood pressure patterns are associated with lung inflammation and oxidative stress in rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00852.2011 ◽

2012 ◽

Vol 302 (3) ◽

pp. H818-H825 ◽

Cited By ~ 19

Author(s):

Nicole J. Gentner ◽

Lynn P. Weber

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Blood Pressure ◽

Arterial Stiffness ◽

Tobacco Smoke ◽

Pulse Wave ◽

Smoke Exposure ◽

Tobacco Smoke Exposure ◽

Secondhand Tobacco Smoke ◽

Blood Pressure Patterns

Chronic smoking and secondhand tobacco smoke exposure are major risk factors for cardiovascular disease that are known to adversely alter the structural and mechanical properties of arteries. The objective of this study was to determine the effects of subchronic secondhand tobacco smoke exposure on circadian blood pressure patterns, arterial stiffness, and possible sources of oxidative stress in conscious, unsedated radiotelemetry-implanted rats. Pulse wave change in pressure over time (dP/d t) was used an indicator of arterial stiffness and was compared with both structural (wall thickness) and functional (nitric oxide production and bioactivity and endothelin-1 levels) features of the arterial wall. In addition, histology of lung, heart, and liver was examined as well as pulmonary and hepatic detoxifying enzyme activity (cytochrome P450, specifically CYP1A1). Subchronic secondhand tobacco smoke exposure altered the circadian pattern of heart rate and blood pressure, with a loss in the normal dipping pattern of blood pressure during sleep. Secondhand tobacco smoke exposure also increased pulse wave dP/d t in the absence of any structural modifications in the arterial wall. Furthermore, although nitric oxide production and endothelin-1 levels were not altered by secondhand tobacco smoke, there was increased inactivation of nitric oxide as indicated by peroxynitrite production. Increased lung neutrophils or pulmonary CYP1A1 may be responsible for the increase in oxidative stress in rats exposed to secondhand tobacco smoke. In turn, this may be related to the observed failure of blood pressure to dip during periods of sleep and a possible increase in arterial stiffness.

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The role of oxidative stress and lipid peroxidation in ventricular remodeling induced by tobacco smoke exposure after myocardial infarction

Clinics ◽

10.1590/s1807-59322009000700014 ◽

2009 ◽

Vol 64 (7) ◽

Cited By ~ 10

Author(s):

Daniella R. Duarte ◽

Marcos F. Minicucci ◽

Paula S. Azevedo ◽

Beatriz B. Matsubara ◽

Luiz S. Matsubara ◽

...

Keyword(s):

Oxidative Stress ◽

Myocardial Infarction ◽

Lipid Peroxidation ◽

Tobacco Smoke ◽

Ventricular Remodeling ◽

Smoke Exposure ◽

Tobacco Smoke Exposure

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Effect of waterpipe tobacco smoke exposure during lactation on learning and memory of offspring rats: Role of oxidative stress

Life Sciences ◽

10.1016/j.lfs.2019.04.049 ◽

2019 ◽

Vol 227 ◽

pp. 58-63 ◽

Cited By ~ 7

Author(s):

Nour A. Al-Sawalha ◽

Karem H. Alzoubi ◽

Omar F. Khabour ◽

Weam Alyacoub ◽

Yehya Almahmood

Keyword(s):

Oxidative Stress ◽

Learning And Memory ◽

Tobacco Smoke ◽

Smoke Exposure ◽

Tobacco Smoke Exposure

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Children are particularly vulnerable to environmental tobacco smoke exposure: Evidence from biomarkers of tobacco-specific nitrosamines, and oxidative stress

Environment International ◽

10.1016/j.envint.2018.08.006 ◽

2018 ◽

Vol 120 ◽

pp. 238-245 ◽

Cited By ~ 15

Author(s):

Mu-Rong Chao ◽

Marcus S. Cooke ◽

Chung-Yih Kuo ◽

Chih-Hong Pan ◽

Hung-Hsin Liu ◽

...

Keyword(s):

Oxidative Stress ◽

Environmental Tobacco Smoke ◽

Tobacco Smoke ◽

Environmental Tobacco Smoke Exposure ◽

Smoke Exposure ◽

Tobacco Smoke Exposure ◽

Tobacco Specific Nitrosamines ◽

And Oxidative Stress

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Racial Differences In Traffic And Environmental Tobacco Smoke Exposure-Induced Systemic Oxidative Stress In Children

10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5440 ◽

2011 ◽

Cited By ~ 1

Author(s):

Melinda Butsch Kovacic ◽

Sara Stigler ◽

Sharon Sauter ◽

Tianying Wu ◽

Patrick H. Ryan ◽

...

Keyword(s):

Oxidative Stress ◽

Racial Differences ◽

Environmental Tobacco Smoke ◽

Tobacco Smoke ◽

Environmental Tobacco Smoke Exposure ◽

Smoke Exposure ◽

Tobacco Smoke Exposure ◽

Systemic Oxidative Stress

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The effect of tobacco smoke on oxytocin concentrations and selected oxidative stress parameters in plasma during pregnancy and post-partum – an experimental model

Human & Experimental Toxicology ◽

10.1177/0960327116639363 ◽

2016 ◽

Vol 36 (2) ◽

pp. 135-145 ◽

Cited By ~ 9

Author(s):

M Napierala ◽

TA Merritt ◽

J Mazela ◽

K Jablecka ◽

I Miechowicz ◽

...

Keyword(s):

Oxidative Stress ◽

Experimental Model ◽

Tobacco Smoke ◽

Smoke Exposure ◽

Tobacco Smoke Exposure ◽

Trolox Equivalent Antioxidant Capacity ◽

Enzyme Linked Immunosorbent Assay ◽

Lactation Period ◽

Oxidative Stress Parameters ◽

Stress Parameters

Background: Tobacco smoking is a serious threat to life and health of society. Among the most vulnerable to the toxic effects of tobacco smoke are foetuses and newborns. The objective of the research was to assess the impact of tobacco smoke exposure on oxytocin levels and biochemical oxidative stress parameters during pregnancy and after birth in an experimental model. Methods: In the experiment, exposure to tobacco smoke of gravid and non-gravid rats was monitored. A reliable biomarker of exposure – cotinine – was used in the process and it was determined by means of high-performance liquid chromatography with diode array detection, which ensured high analytical accuracy and precision. Determination of oxytocin was performed by means of enzyme-linked immunosorbent assay. The levels of selected oxidative stress parameters: total protein concentration, uric acid, trolox equivalent antioxidant capacity, protein S-nitrosylation and lipid peroxidation (thiobarbituric acid reactive substances) were measured by spectrophotometric methods. Results and conclusions: The effect of prenatal and postnatal exposure to tobacco smoke was a lower medium body mass of rat foetuses and pups. Oxidative stress during pregnancy, additionally intensified by tobacco smoke exposure, led to adaptive changes in properties of plasmatic antioxidant barriers. Moreover, the disturbance of oxidoreductive balance by tobacco smoke affects oxytocin fluctuations, what was observed in this study during lactation period. Therefore, women who smoke may breastfeed their children less frequently and for a shorter period.

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Molecular Basis of Tobacco-Induced Bacterial Biofilms

Otolaryngology ◽

10.1177/0194599812447263 ◽

2012 ◽

Vol 147 (5) ◽

pp. 876-884 ◽

Cited By ~ 12

Author(s):

Marcelo B. Antunes ◽

John J. Chi ◽

Zhi Liu ◽

Natalia Goldstein-Daruech ◽

James N. Palmer ◽

...

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Tobacco Smoke ◽

Biofilm Formation ◽

Smoke Exposure ◽

Bacterial Biofilm ◽

Tobacco Smoke Exposure ◽

University Of Pennsylvania ◽

Biofilm Growth

Objective To evaluate changes in the expression of biofilm-related genes when exposed to tobacco smoke and oxidative stress. Study Design Experimental, in vitro. Setting Laboratories of Rhinology and Microbiology, University of Pennsylvania. Subjects and Methods Bacterial biofilm mass was measured using crystal violet staining and measurement of the optical density. Biofilm-related genes of the Pseudomonas aeruginosa PAO1 strain ( pilF, flgK, lasI, lasB, rhlA, and algC) were studied following repetitive exposure to exogenous tobacco smoke and hydrogen peroxide. This was done using a reporter plasmid. Results After 1 exposure to smoke, there was no change in biofilm formation. However, after 2 and 3 exposures, the biofilm formed had an increased mass ( P < .05). With respect to oxidative stress in the form of H2O2, bacterial cultures demonstrated a dose- and time-dependent induction of biofilm formation compared with control conditions. Gene expression following repetitive smoke exposure demonstrated an increase in expression of pilF, flgK, algC, and lasI genes ( P < .05); a decrease in rhlA ( P < .05); and no significant change in the lasB gene ( P = 0.1). Gene expression following H2O2 exposure demonstrated an increase in pilF ( P < .05), whereas the other genes failed to demonstrate a statistical change. Conclusions Repetitive tobacco smoke exposure leads to molecular changes in biofilm-related genes, and exposure to oxidative stress in the form of H2O2 induces biofilm growth in PAO1. This could represent adaptative changes due to oxidative stress or chemically mediated through any of the several chemicals encountered in tobacco smoke and may explain increased biofilm formation in microbes isolated from smokers.

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