scholarly journals Oxidative damage induced by cigarette smoke exposure in mice: impact on lung tissue and diaphragm muscle,

2014 ◽  
Vol 40 (4) ◽  
pp. 411-420 ◽  
Author(s):  
Samanta Portão de Carlos ◽  
Alexandre Simões Dias ◽  
Luiz Alberto Forgiarini Júnior ◽  
Patrícia Damiani Patricio ◽  
Thaise Graciano ◽  
...  

OBJECTIVE: To evaluate oxidative damage (lipid oxidation, protein oxidation, thiobarbituric acid-reactive substances [TBARS], and carbonylation) and inflammation (expression of phosphorylated AMP-activated protein kinase and mammalian target of rapamycin [p-AMPK and p-mTOR, respectively]) in the lung parenchyma and diaphragm muscles of male C57BL-6 mice exposed to cigarette smoke (CS) for 7, 15, 30, 45, or 60 days. METHODS: Thirty-six male C57BL-6 mice were divided into six groups (n = 6/group): a control group; and five groups exposed to CS for 7, 15, 30, 45, and 60 days, respectively. RESULTS: Compared with control mice, CS-exposed mice presented lower body weights at 30 days. In CS-exposed mice (compared with control mice), the greatest differences (increases) in TBARS levels were observed on day 7 in diaphragm-muscle, compared with day 45 in lung tissue; the greatest differences (increases) in carbonyl levels were observed on day 7 in both tissue types; and sulfhydryl levels were lower, in both tissue types, at all time points. In lung tissue and diaphragm muscle, p-AMPK expression exhibited behavior similar to that of TBARS. Expression of p-mTOR was higher than the control value on days 7 and 15 in lung tissue, as it was on day 45 in diaphragm muscle. CONCLUSION: Our data demonstrate that CS exposure produces oxidative damage, not only in lung tissue but also (primarily) in muscle tissue, having an additional effect on respiratory muscle, as is frequently observed in smokers with COPD.

2021 ◽  
Vol 12 (2) ◽  
pp. 85-92
Author(s):  
Rivan Virlando Suryadinata ◽  
Dita Sukmaya Prawitasari ◽  
Indira Pradita Rochim

Background. Free radicals in cigarette smoke will hurt health when they enter to the respiratory tract. An excessive increase of free radicals in the body will cause oxidative stress. Free radicals are generated physiologically by the body's metabolism and can neutralize antioxidants in the body. An imbalance number of free radicals will result in cell damage and death. It has characterized by an increase in malondialdehyde levels in the blood and alveolar macrophages in the lung tissue. Giving red mulberry (Morus rubra) as an intake of antioxidants from outside the body can prevent adverse effects of cigarette smoke. Objective. This study analyses flavonoids' impact on red mulberry in reducing free radicals due to exposure to cigarette smoke by lowering levels of malondialdehyde and alveolar macrophages. Method. This research is experimental with a post-test control group design using male Wistar rats (Rattus novergicus) as experimental animals. Treatment of experimental animals through red mulberry per oral and exposure to cigarette smoke had conducted for 30 days. The parameters used were levels of malondialdehyde and alveolar macrophages in the lung tissue. Results. The research showed an increase in free radicals in the group exposed to cigarette smoke. Increasing intake of red mulberry can further reduce malondialdehyde levels and the number of alveolar macrophages (p<0.05). Conclusions. The antioxidants in red mulberry can reduce malondialdehyde levels in the blood and the number of alveolar macrophages in lung tissue due to exposure to cigarette smoke.


2021 ◽  
pp. 1-7
Author(s):  
Oktay Aslaner

<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.


2020 ◽  
Vol 107 (1) ◽  
pp. 55-66
Author(s):  
B. Mammel ◽  
T. Kvárik ◽  
Zs. Szabó ◽  
J. Gyarmati ◽  
T. Ertl ◽  
...  

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).


2020 ◽  
Vol 8 (1) ◽  
pp. 45
Author(s):  
Alfreda Sabrina Widyanti ◽  
Martha Ardiaria ◽  
Nurmasari Widyastuti

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.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Giulia Pintarelli ◽  
Sara Noci ◽  
Davide Maspero ◽  
Angela Pettinicchio ◽  
Matteo Dugo ◽  
...  

Abstract Alterations in the gene expression of organs in contact with the environment may signal exposure to toxins. To identify genes in lung tissue whose expression levels are altered by cigarette smoking, we compared the transcriptomes of lung tissue between 118 ever smokers and 58 never smokers. In all cases, the tissue studied was non-involved lung tissue obtained at lobectomy from patients with lung adenocarcinoma. Of the 17,097 genes analyzed, 357 were differentially expressed between ever smokers and never smokers (FDR < 0.05), including 290 genes that were up-regulated and 67 down-regulated in ever smokers. For 85 genes, the absolute value of the fold change was ≥2. The gene with the smallest FDR was MYO1A (FDR = 6.9 × 10−4) while the gene with the largest difference between groups was FGG (fold change = 31.60). Overall, 100 of the genes identified in this study (38.6%) had previously been found to associate with smoking in at least one of four previously reported datasets of non-involved lung tissue. Seven genes (KMO, CD1A, SPINK5, TREM2, CYBB, DNASE2B, FGG) were differentially expressed between ever and never smokers in all five datasets, with concordant higher expression in ever smokers. Smoking-induced up-regulation of six of these genes was also observed in a transcription dataset from lung tissue of non-cancer patients. Among the three most significant gene networks, two are involved in immunity and inflammation and one in cell death. Overall, this study shows that the lung parenchyma transcriptome of smokers has altered gene expression and that these alterations are reproducible in different series of smokers across countries. Moreover, this study identified a seven-gene panel that reflects lung tissue exposure to cigarette smoke.


1994 ◽  
Vol 266 (4) ◽  
pp. L382-L388 ◽  
Author(s):  
A. J. Ghio ◽  
J. Stonehuerner ◽  
D. R. Quigley

Deposition of pigmented matter in the lower respiratory tract correlates with the extent of emphysema in smokers as well as with free radical generation and iron accumulation. Pulmonary emphysema is postulated to be mediated by free radical generation which is either directly or indirectly associated with cigarette smoke exposure. The hypothesis was tested that 1) incomplete combustion of tobacco yields humic-like substances (HLS) which 2) deposit in the lung as pigmented particulates, 3) complex iron cations in vitro and in vivo, and 4) have a capacity to catalyze oxidant formation. HLS, isolated by alkali extraction of cigarette smoke condensate (CSC) (Tobacco Health Research Institute, University of Kentucky), demonstrated a high carbon and low carboxylate content on elemental and functional group analyses, respectively, compared with values for HLS sequestered from soils. The HLS isolated from CSC had a capacity to complex iron in vitro and accumulated the metal in vivo after intratracheal instillation in an animal model. Both HLS and its iron complex generated free radicals, and some portion of this oxidant generation was metal dependent. Lung tissue collected at autopsy from smokers contained HLS with an infrared spectrum almost identical to that of the material isolated from CSC. Associations between particulate deposition, metal accumulation, and free radical generation suggest a possible role of HLS in the induction of lung disease following cigarette exposure.


2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Garrett Pehote ◽  
Manish Bodas ◽  
Kathryn Brucia ◽  
Neeraj Vij

Introduction. Cigarette smoke (CS) exposure is the leading risk factor for COPD-emphysema pathogenesis. A common characteristic of COPD is impaired phagocytosis that causes frequent exacerbations in patients leading to increased morbidity. However, the underlying mechanism is unclear. Hence, we investigated if CS exposure causes autophagy impairment as a mechanism for diminished bacterial clearance via phagocytosis by utilizing murine macrophages (RAW264.7 cells) and Pseudomonas aeruginosa (PA01-GFP) as an experimental model. Methods. Briefly, RAW cells were treated with cigarette smoke extract (CSE), chloroquine (autophagy inhibitor), TFEB-shRNA, CFTR(inh)-172, and/or fisetin prior to bacterial infection for functional analysis. Results. Bacterial clearance of PA01-GFP was significantly impaired while its survival was promoted by CSE (p<0.01), autophagy inhibition (p<0.05; p<0.01), TFEB knockdown (p<0.01; p<0.001), and inhibition of CFTR function (p<0.001; p<0.01) in comparison to the control group(s) that was significantly recovered by autophagy-inducing antioxidant drug, fisetin, treatment (p<0.05; p<0.01; and p<0.001). Moreover, investigations into other pharmacological properties of fisetin show that it has significant mucolytic and bactericidal activities (p<0.01; p<0.001), which warrants further investigation. Conclusions. Our data suggests that CS-mediated autophagy impairment as a critical mechanism involved in the resulting phagocytic defect, as well as the therapeutic potential of autophagy-inducing drugs in restoring is CS-impaired phagocytosis.


2021 ◽  
Vol 10 (2) ◽  
Author(s):  
Rivan Virlando Suryadinata ◽  
Bambang Wirjatmadi ◽  
Amelia Lorensia

Background: Most people believe that electric cigarettes have no negative effect on health,  which causes them to use it more. However, exposure to the smoke from these cigarettes is bad for the health and causes cell damage. Antioxidants play an important role in preventing cell damage, and they can be obtained through the oral administration of selenomethionine.Design and methods: This study used an experimental method and a post-test control group design. Male Wistar rats, which were exposed to cigarette smoke were given selenomethionine orally and then tested for the presence of free radicals. The measurement of lung tissue damage was conducted by assessing the level of malondialdehyde in the blood and immunohistochemistry (IHC) of the lung tissue.Result: The study showed that differences in the time of administration of selenomethionine affect the levels of malondialdehyde in the blood and expression of malondialdehyde in the lung tissue (p<0.05). Consequently, the two groups showed a strong (r=0.861) and significant (p=0.000) relationship with each other.Conclusion: The early application of selenomethionine can prevent increased levels of malondialdehyde in the blood and lung tissue due to exposure to e-cigarette smoke.


2018 ◽  
Vol 54 (1) ◽  
pp. 34
Author(s):  
Nyna Puspa Ningrum ◽  
Hermanto Tri Joewono ◽  
Widjiati Widjiati

Folic acid contains 5-methyltetrahydrofolate (5-MTHF), one of antioxidants that can be used to inhibit reaction caused by cigarette smoke exposure. Folic acid is able to inhibit the levels of Reactive Oxygen Species (ROS) so as to reduce the occurrence of neuronal apoptosis. The objectives of this study was to determine the effect of folic acid intake during pregnancy whose mother was exposed to cigarette smoke on brain neurons apoptosis index and quantity of mice (Mus musculus) offspring. This study was an experimental laboratory study with posttest-only control group design. The subjects were 24 female mice divided into 4 groups consisting of one control group and three treatment groups. Sampling used simple random sampling, each group consisting of 6 animals. Control group 1 was not given treatment during pregnancy, group 2 was given with folic acid orally on days 0-17 of gestational age as much as 0.06 mg/day/mice. Group 3 was given with cigarette smoke exposure on days 7-17 of gestational age, amounting to 2 cigarettes/day. Group 4 was given with cigarette smoke exposure on days 7-17 of gestational age, amounting to 2 cigarettes/day and folic acid orally on days 0-17 of gestational age as much as 0.06 mg/day/mice. The result showed significant differences in all variables. In neurons apoptosis index, there were significant differences between groups 1 and 3, groups 2 and 3, groups 3 and 4, significant differences in the quantity of neurons between groups 1 and 3, groups 2 and 3, groups 2 and 4. The study concluded that there were significant difference in neural apoptosis index between all groups, and there were also significant differences in the quantity of neurons between all groups.


2019 ◽  
Vol 3 (2) ◽  
pp. 122-128
Author(s):  
Andita Ayu Mandasari ◽  
Siti Nur Asiyah ◽  
Kurnia Lintang

Smoking is one of the habits that can affect human health. One type of cigarette that is currently the choice is electric cigarettes. The e-cigarette content includes nicotine, propylene glycol, flavorings and glycerin. The purpose of this study was to determine the effect of exposure to e-cigarette smoke on mice strain balb / c with the parameters of the number of spermatozoa. This study used 15 male mice which were 8-10 weeks old and weighed 25-30 grams of male mice which were divided into 3 treatment groups namely control group, treatment group one and treatment group two. In the control group no exposure to cigarette smoke was carried out while in the treatment group one was exposed to cigarette smoke in mice with a dose of 0 mg nicotine and the second treatment group was exposed to e-cigarette smoke at a dose of 18 mg nicotine. Electric cigarette smoke exposure is carried out for 30 days using a suction device from a syringe. The exposure of cigarette smoke is carried out every day with successive doses of 20 times as much as 3 times with a time lag of 10 minutes (5 minutes the chamber is closed and 5 minutes of the chamber is opened). The results showed that the average number of spermatozoa in the control group was 16.816 million / ml. The average number of spermatozoa in treatment one was 10.432 million / ml and the average number of spermatozoa in treatment two was 5.234 million / ml. This shows that exposure to cigarette smoke can reduce the number of spermatozoa from the control group to the first treatment by 42.56% and the second treatment shows a decrease from the first group by 34.65%.


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