Effect of Cigarette Smoking on Selected Antioxidant Enzymes and Oxidative Stress Biomarkers

Joshi, B.P.; Singh, Sangeeta; Sharma, Preeti; Mohapatra, Tapan Kumar; Kumar, Pradeep

doi:10.7860/jcdr/2020/45948.14138

Cited by 7 publications

(8 citation statements)

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“…Tobacco use has been reported to be responsible for 8 million deaths each year, with more than 7 million of these deaths accruing from direct tobacco use and 1.2 million from secondhand smoke ( 2 ). Adverse effects of cigarette smoking have been linked to the diverse effects of the complex mixture of chemical constituents of cigarette smoke (CS) on biological systems which can be influenced by age, sex, race, genetic variations, individual genetic susceptibility as well as variations in smoking pattern ( 3 , 4 ).…”

Section: Introductionmentioning

confidence: 99%

Risk of Pulmonary-Reproductive Dysfunctions, Inflammation and Oxidative DNA Damage in Exposure to Polycyclic Aromatic Hydrocarbon in Cigarette Smokers

Nsonwu-Anyanwu

Egom

Eworo

et al. 2022

Med. J. Islam. Republ. Iran

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Background: Exposure to cigarette smoke has been associated with pulmonary and reproductive dysfunctions; inflammatory response, oxidative stress and oxidative DNA damage induced by polycyclic aromatic hydrocarbons (PAHs) present in cigarette smoke have been implicated in the pathogenesis of these disorders. The peak expiratory flow rate (PEFR), a biomarker of inflammation and oxidative DNA damage (8-hydroxy-2-deoxyguanosine (8-OHdG), tumor necrosis factor alpha (TNF-α)), reproductive hormones (testosterone (TST), luteinizing hormone (LH), follicle stimulating hormone (FSH)) cotinine and urinary PAH metabolite (1-hydroxypyrene (1-HOP)) were estimated in male active smokers. Methods: One hundred men aged 20-47 years, comprising 50 active male smokers and 50 non-smokers, were randomly recruited into this comparative cross-sectional study. The PEFR was measured using a peak flow meter, serum levels of cotinine, FSH, LH, TST, TNF-α, and urine 8-OHdG by enzyme-linked immunosorbent assay and 1-HOP by high-performance liquid chromatography. Data analysis was done using a t-test and correlation analysis at p ≤0.05. Results: Smokers had significantly higher cotinine (49.73±31.76 versus 0.51±0.69 ng/ml, p ≤0.001), 8-OHdG (16.34±12.10 versus 5.79±2.14 ng/ml, p ≤0.001) and lower PEFR (309.20±56.05 versus 452.80±45.76 L/min, p ≤0.001) and LH (5.75±2.06 versus 6.97±2.79 mIU/ml, p =0.015) compared to non-smokers. Duration of exposure to cigarette smoke correlated positively with cotinine (r=0.937, p ≤0.001) and 1-HOP (r=0.813, p ≤0.001) while cotinine correlated positively with 1-HOP (r=0.863, p ≤0.001) only in smokers. Conclusion: Reduced lung function and luteinizing hormone and concurrent increase in oxidative DNA damage associated with exposure to cigarette smoke may suggest the involvement of PAH-induced DNA damage in the development of pulmonary and reproductive impairment in smokers.

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Section: Introductionmentioning

confidence: 99%

Risk of Pulmonary-Reproductive Dysfunctions, Inflammation and Oxidative DNA Damage in Exposure to Polycyclic Aromatic Hydrocarbon in Cigarette Smokers

Nsonwu-Anyanwu

Egom

Eworo

et al. 2022

Med. J. Islam. Republ. Iran

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“…However, other studies did not take into consideration nutritional status, it is important because nutritional status can modify metDNA patterns [92]. One plausible explanation of the oxidative stressinduced signi cant decrease in metDNA level in the smokers could be that the saturation levels of the antioxidant enzymatic systems such as the superoxide dismutase (SOD) enzyme activities, which is one of the most important antioxidant systems [93], were decreased in smokers as compared with non-smokers [94,95]. Although, the SOD levels of smokers were normal [96], the levels of their cofactors were high [94].…”

Section: Discussionmentioning

confidence: 99%

Effects of Cigarette Smoke Exposure on Placental Global DNA Methylation and 8-hydroxy-2’-deoxyguanosine Levels in Mother-new-born Binomials

Díaz-García

Vilchis-Gil

Castro-Cerritos

et al. 2021

Preprint

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Background: Smoking is practiced worldwide for both men and women, and it is associated with different diseases and deleterious effects on gestational products, chiefly during pregnancy. Epigenetic alterations induced by cigarette smoke must be related to perinatal abnormalities. Methods: 219 pregnant women, aged 16 to 34 years, with or without a history of cigarette consumption (1–5/day) during the first trimester of pregnancy and their offspring were studied in this work. A validated dietary questionnaire was used to estimate daily consumptions of macronutrients and micronutrients, including total energy, during pregnancy. As a marker of DNA damage, 8-hydroxy-2’-deoxyguanosine (8-OHdG) levels were determined in plasma of women, before delivery, in umbilical cord blood after delivery, in the new-borns. The proportion of methylated DNA in the placentas (metDNA) was determined by ultra-high-performance liquid chromatography coupled with high-resolution mass spectrometry (UPLC-HRMS). Results: Non-significant differences were observed between smoking and non-smoking women groups, or between the new-borns groups (p > 0.05). Smoking women showed up higher intakes of vitamins, lipids, proteins, and carbohydrates in comparison with non-smoking women (p < 0.01). 8-OHdG levels correlated among the mothers and new-borns (p = 5.386e-15) and were lower in the smoking binomials in comparison with non-smoking binomials (β = −1.20 to −64). Negative correlations were found between micronutrients and macronutrients but Vitamin C, and 8-OHdG levels of the women (p < 0.01). However, the new-borns 8-OHdG correlated with proteins, vitamin A, and vitamin B12 (p < 0.05). Cigarettes consumed per day correlated to the 8-8HdG levels (Rho = −0.247, p = 0.012), alcohol consumption (Rho = 0.219, p = 0.001), to macronutrients (Rho = 212 to 332, p < 0.01), micronutrients (Rho = 186 to 289, p < 0.01), and to energy (Rho = 0.286, p = 0.001). Finally, metDNA deceased in the smoking women than in the non-smoking women (β = −0.12, p < 0.05), and correlated with the number of cigarettes consumed per day (Rho = −0.229, p = 0.009). Conclusion: Cigarette smoking alters metDNA levels of the placenta, however, their clinical effects come out over years or transgenerationally.

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“…Asap rokok mengandung sejumlah besar oksidan yang memiliki efek buruk pada jaringan melalui kerusakan oksidatif (de Carlos et al, 2014). Berdasarkan penelitian Joshi et al (2020), menjelaskan bahwa durasi merokok secara signifikan mempengaruhi oksidanoksidan pada subjek merokok dimana asap rokok kaya akan ROS dan RNS yang dapat menyebabkan produksi radikal bebas dan meningkatkan stres oksidatif melalui pembentukan ROS yang pada akhirnya dapat menyebabkan peroksidasi lipid dan disfungsi sel endotel. Asap rokok juga kaya akan molekul karsinogenik, mutagenik, radikal bebas, dan logam berat, yang menghasilkan ROS dan spesies nitrogen reaktif (RNS) yang mudah bereaksi dengan biomolekul, menyebabkan cedera DNA dan peroksidasi lipid dalam jaringan serta merokok dapat mengkonversi asam lemak tak jenuh ganda menjadi hidroperoksida, endoperoksida, aldehida (misalnya, MDA) dan alkana (misalnya, etana dan pentana) (Boehm et al, 2020).…”

Section: Pembahasanunclassified

Pengaruh Pemberian Dehydroepiandrosterone (DHEA) terhadap Aktivitas Peroksidasi Lipid dan Kadar Nitrit Oksida pada Aorta Tikus Wistar Jantan yang Terpapar Asap Rokok

2022

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The research aimed to investigate the effect of dehydroepiandrosterone (DHEA) on lipid peroxidation activity and nitric oxide concentration in the aorta of male Wistar rats due to exposure to cigarette smoke. This study was a laboratory experiment using 21 rats that were divided into 3 groups: KN-14 (negative control that is given smoke exposure within 14 days), DHEA-1 (15 mg/kgBW + smoke exposure for 14 days), and DHEA-2 (30 mg/kgBW + smoke exposure for 14 days). The exposure was carried out in 25-45 minutes with 4 cigarettes/day. Surgery was performed in the 15th days to remove the aorta to examine malondialdehyde (MDA) as a biomarker of lipid peroxidation and nitric oxide (NO) concentration using Enzyme-linked Immunosorbent Assay (ELISA). The results showed that a significant increase in MDA concentrations was found in the group administered with DHEA, particularly at a dose of 30 mg/kgBW (p<0.05). Meanwhile, the administration of DHEA at doses of 15 and 30 mg/kgBW did not have a significant effect (p>0,05) on aortic NO concentrations compared to the group KN-14. Therefore, it can be concluded that the administration of DHEA could increase lipid peroxidation activity, as indicated by a significant increase in aortic MDA concentrations, without affecting aortic NO concentrations in rats exposed to cigarette smoke for 14 days.Keyword: Dehydroepiandrosterone (DHEA), MDA, NO, lipid peroxidation, exposure of cigarettes smoke

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Effect of Cigarette Smoking on Selected Antioxidant Enzymes and Oxidative Stress Biomarkers

Cited by 7 publications

References 0 publications

Risk of Pulmonary-Reproductive Dysfunctions, Inflammation and Oxidative DNA Damage in Exposure to Polycyclic Aromatic Hydrocarbon in Cigarette Smokers

Risk of Pulmonary-Reproductive Dysfunctions, Inflammation and Oxidative DNA Damage in Exposure to Polycyclic Aromatic Hydrocarbon in Cigarette Smokers

Effects of Cigarette Smoke Exposure on Placental Global DNA Methylation and 8-hydroxy-2’-deoxyguanosine Levels in Mother-new-born Binomials

Pengaruh Pemberian Dehydroepiandrosterone (DHEA) terhadap Aktivitas Peroksidasi Lipid dan Kadar Nitrit Oksida pada Aorta Tikus Wistar Jantan yang Terpapar Asap Rokok

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