Effect of alpha-lipoic acid on oxidative stress status in rat kidney subjected to ischemia/reperfusion injury (original) (raw)
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Food and Chemical Toxicology, 2017
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Heliyon, 2021
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Evaluation of Antioxidant Status in Passive Smokers
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Free Radical Biology and Medicine, 2011
Cigarette smoking predisposes to the development of multiple diseases involving oxidative damage. We measured a range of oxidative damage biomarkers to understand which differ between smokers and nonsmokers and if the levels of these biomarkers change further during the act of smoking itself. Despite overnight abstinence from smoking, smokers had higher levels of plasma total and esterified F 2 -isoprostanes, hydroxyeicosatetraenoic acid products (HETEs), F 4 -neuroprostanes, 7-ketocholesterol, and 24-and 27hydroxycholesterol. Levels of urinary F 2 -isoprostanes, HETEs, and 8-hydroxy-2′-deoxyguanosine were also increased compared with age-matched nonsmokers. Several biomarkers (plasma free F 2 -isoprostanes, allantoin, and 7β-hydroxycholesterol and urinary F 2 -isoprostane metabolites) were not elevated. The smokers were then asked to smoke a cigarette; this acute smoking elevated plasma and urinary F 2isoprostanes, plasma allantoin, and certain cholesterol oxidation products compared to presmoking levels, but not plasma HETEs or urinary 8-hydroxy-2′-deoxyguanosine. Smokers showed differences in plasma fatty acid composition. Our findings confirm that certain oxidative damage biomarkers are elevated in smokers even after a period of abstinence from smoking, whereas these plus some others are elevated after acute smoking. Thus, different biomarkers do not measure identical aspects of oxidative stress.
Antioxidant responses following active and passive smoking of tobacco and electronic cigarettes
Toxicology mechanisms and methods, 2016
It has been indicated that acute active and passive tobacco cigarette smoking may cause changes on redox status balance that may result in significant pathologies. However, no study has evaluated the effects of active and passive e-cigarette smoking on redox status of consumers. To examine the acute effects of active and passive e-cigarette and tobacco cigarette smoking on selected redox status markers. Using a randomized single-blind crossover design, 30 participants (15 smokers and 15 nonsmokers) were exposed to three different experimental conditions. Smokers underwent a control session, an active tobacco cigarette smoking session (smoked 2 cigarettes within 30-min) and an active e-cigarette smoking session (smoked a pre-determined number of puffs within 30-min using a liquid with 11 ng/ml nicotine). Similarly, nonsmokers underwent a control session, a passive tobacco cigarette smoking session (exposure of 1 h to 23 ± 1 ppm of CO in a 60 m(3) environmental chamber) and a passive ...
International Journal of Medical Biochemistry
Effects of electronic cigarettes on oxidative stress markers in the rat kidney tissues T he number of tobacco smokers worldwide increased to 1.1 billion in 2019. Tobacco smoke contains various compounds that are harmful to smokers and nonsmokers alike [1]. In 2013, the World Health Organization attributed 6 million deaths worldwide to smoking. Therefore, reducing smoking is a significant public health objective [2]. Most smokers want to quit smoking, but only about one out of every ten adult smokers succeeds [3]. Although traditional techniques to minimize smoking have been employed, such as organizing activities to highlight the dangers of smoking or boosting cigarette taxes, the number of smokers continues to increase. Therefore, there is a clear requirement for novel approaches in this respect [4, 5]. Electronic nicotine delivery devices, known as electronic cigarettes (e-cigarettes), have long been recognized as a safer alternative to traditional cigarettes. These battery-operated devices deliver nicotine to users via an aerosol carrier system, and their use is mainly prevalent among young people [6]. According to the American Center for Disease Control and Prevention, e-cigarette use among college students surged from 1.5% in 2011 to 20.8% in 2018 [7]. However, although it was initially thought that e-smoking reduced smoking and the associated health risks [8], it has more recently been associated with increased oxidative stress and inflammation-related vascular and cardiac dysfunction [7]. Furthermore, cytotoxicity, oxidative stress, airway hyperreactivity, mucin formation, Objectives: Electronic cigarettes (e-cigarettes) are an alternative to traditional cigarettes. Although numerous studies have been conducted regarding the effects of traditional cigarettes on oxidative stress biomarkers in the kidney, there are only a few studies on the effects of e-cigarettes. Methods: A total of 24 male Wistar albino rats were separated into three groups: Group 1 was treated with traditional cigarettes, Group 2 with e-cigarettes, and Group 3 formed the control group. Kidney homogenates and plasma samples were obtained, and the glutathione peroxidase, protein carbonyl, superoxide dismutase (SOD), catalase (CAT), lipid hydroperoxide (LPO), and symmetric dimethylarginine (SDMA) levels were examined. Results: Higher plasma SDMA levels were determined in Group 1 and Group 2 compared with Group 3 (<0.0001). Higher SOD activity was found in Group 1 compared with Group 2 (p=0.0094). Lower CAT activity was found in Group 1 compared with both Group 2 (p=0.0035) and Group 3 (p<0.0001). Higher LPO levels were determined in the traditional cigarette smoking group compared with the control group (p=0.028), and no statistically significant difference was found between the e-cigarette and the control groups. Conclusion: E-cigarettes and traditional cigarettes are associated with the dysregulation of particular oxidative stress markers in the kidney. However, e-cigarettes have less effect on some oxidative stress markers than traditional cigarettes. Long-term use of traditional cigarettes and e-cigarettes causes oxidative stress, which may lead to renal tissue damage and diminished kidney function.
Chemical Research in Toxicology, 2021
To provide insights into the cause of e-cigarette (ecig) associated lung injury, we examined the effects of propylene glycol (PG) and glycerol (G), two common solvent carriers used to deliver nicotine/flavor, on markers of oxidative stress and inflammation in female B6C3F1 mice which had been used successfully in tobacco smoke (TS)-induced lung carcinogenesis. Mice exposed to air and TS were used as negative and positive controls, respectively. Using LC-MS/MS, we showed that PG/G alone, in the absence of nicotine, significantly increased the levels of 8-hydroxy-2′-deoxyguanosine (8-OHdG or its tautomer 8-oxodG), a biomarker of DNA oxidative damage, in lung and plasma of mice; moreover, addition of nicotine (12 and 24 mg/ mL) in e-cig liquid appears to suppress the levels of 8-oxodG. Exposure to e-cig aerosols or TS induced nonsignificant increases of plasma C-reactive protein (CRP), a biomarker of inflammation; nonetheless, the levels of fibronectin (FN), a biomarker of tissue injury, were significantly increased by e-cig aerosols or TS. Although preliminary, our data showed that exposure to e-cig aerosols induced a higher score of lung injury than did control air or TS exposure. Our results indicate that the B6C3F1 mouse model may be suitable for an in-depth examination of the impact of e-cig on lung injury associated with oxidative stress and inflammation and this study adds to the growing evidence that the use of e-cig can lead to lung damage.