Passive smoke exposure induces oxidative damage in brains of rat pups: Protective role of diphenyl diselenide

Stangherlin, Eluza Curte; Luchese, Cristiane; Ardais, Ana Paula; Nogueira, Cristina W.

doi:10.1080/08958370802526881

Cited by 18 publications

(9 citation statements)

References 40 publications

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“…In this study total-SH, protein-SH, and NP-SH levels were significantly lowered in the brain of rats exposed to cigarette smoke. These results are consistent with previous studies (Stangherlin et al 2009;Jaques et al 2013). Besides, these reports are in agreement with the finding above that the brain NO concentration is elevated in cigarette smoke-exposed rats, which enhances peroxynitrite and peroxynitrate formation and can subsequently deplete cellular thiols and promote apoptotic cell death (Pryor and Stone 1993).…”

Section: Discussionsupporting

confidence: 94%

Brain oxidative damage restored by Sesbania grandiflora in cigarette smoke-exposed rats

et al. 2015

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Cigarette smoking has been associated with high risk of neurological diseases such as stroke, Alzheimer's disease, multiple sclerosis, etc., The present study was designed to evaluate the restorative effects of Sesbania grandiflora (S. grandiflora) on oxidative damage induced by cigarette smoke exposure in the brain of rats. Adult male Wistar-Kyoto rats were exposed to cigarette smoke for a period of 90 days and consecutively treated with S. grandiflora aqueous suspension (SGAS, 1000 mg/kg body weight per day by oral gavage) for a period of 3 weeks. The levels of protein carbonyl, nitric oxide, and activities of cytochrome P450, NADPH oxidase and xanthine oxidase were significantly increased, whereas the levels of total thiol, protein thiol, non-protein thiol, nucleic acids, tissue protein and the activities of Na(+)/K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase were significantly diminished in the brain of rats exposed to cigarette smoke as compared with control rats. Also cigarette smoke exposure resulted in a significant alteration in brain total lipid, total cholesterol, triglycerides and phospholipids content. Treatment of SGAS is regressed these alterations induced by cigarette smoke. The results of our study suggest that S. grandiflora restores the brain from cigarette smoke induced oxidative damage. S. grandiflora could have rendered protection to the brain by stabilizing their cell membranes and prevented the protein oxidation, probably through its free radical scavenging and anti-peroxidative effect.

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Section: Discussionsupporting

confidence: 94%

Brain oxidative damage restored by Sesbania grandiflora in cigarette smoke-exposed rats

et al. 2015

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“…25 These effects may be mediated through injury inflicted by proinflammatory agents, such as cytokines 26 or smoking-induced oxidative stress. 27 …”

Section: Discussionmentioning

confidence: 99%

Secondhand Smoke and Periodontal Disease: Atherosclerosis Risk in Communities Study

Sanders

Slade²,

Beck³

et al. 2011

Am J Public Health

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Objectives We investigated the relationship between secondhand smoke and periodontal disease in nonsmokers. Methods We undertook a cross-sectional analysis of the Atherosclerosis Risk in Communities study with 2739 lifetime nonsmokers aged 53–74 years, unexposed to other sources of tobacco, who received a complete periodontal examination at visit 4. Exposure was reported as average hours per week in close contact with a smoker in the preceding year. We defined severe periodontitis as 5 or more periodontal sites with probing pocket depth of 5 millimeters or more and clinical attachment levels of 3 millimeters or more in those sites. Other outcomes were extent of periodontal probing depths of 4 millimeters or more and extent of clinical attachment levels of 3 millimeters or more. Results In a binary logistic regression model, adjusted odds of severe periodontitis for those exposed to secondhand smoke 1 to 25 hours per week increased 29% (95% confidence interval=1.0, 1.7); for those exposed to secondhand smoke 26 hours per week, the odds were twice as high (95% confidence interval=1.2, 3.4) as for those who were unexposed. Conclusions Exposure to secondhand smoke and severe periodontitis among nonsmokers had a dose-dependent relationship.

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“…), and reduction of antioxidant enzymes (Stangherlin et al. ) including SOD (Luchese et al. ), catalase (Luchese et al.…”

Section: Laboratory/biological Studiesmentioning

confidence: 99%

How cigarette smoking may increase the risk of anxiety symptoms and anxiety disorders: a critical review of biological pathways

et al. 2013

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Multiple studies have demonstrated an association between cigarette smoking and increased anxiety symptoms or disorders, with early life exposures potentially predisposing to enhanced anxiety responses in later life. Explanatory models support a potential role for neurotransmitter systems, inflammation, oxidative and nitrosative stress, mitochondrial dysfunction, neurotrophins and neurogenesis, and epigenetic effects, in anxiety pathogenesis. All of these pathways are affected by exposure to cigarette smoke components, including nicotine and free radicals. This review critically examines and summarizes the literature exploring the role of these systems in increased anxiety and how exposure to cigarette smoke may contribute to this pathology at a biological level. Further, this review explores the effects of cigarette smoke on normal neurodevelopment and anxiety control, suggesting how exposure in early life (prenatal, infancy, and adolescence) may predispose to higher anxiety in later life. A large heterogenous literature was reviewed that detailed the association between cigarette smoking and anxiety symptoms and disorders with structural brain changes, inflammation, and cell-mediated immune markers, markers of oxidative and nitrosative stress, mitochondrial function, neurotransmitter systems, neurotrophins and neurogenesis. Some preliminary data were found for potential epigenetic effects. The literature provides some support for a potential interaction between cigarette smoking, anxiety symptoms and disorders, and the above pathways; however, limitations exist particularly in delineating causative effects. The literature also provides insight into potential effects of cigarette smoke, in particular nicotine, on neurodevelopment. The potential treatment implications of these findings are discussed in regards to future therapeutic targets for anxiety. The aforementioned pathways may help mediate increased anxiety seen in people who smoke. Further research into the specific actions of nicotine and other cigarette components on these pathways, and how these pathways interact, may provide insights that lead to new treatment for anxiety and a greater understanding of anxiety pathogenesis.

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Passive smoke exposure induces oxidative damage in brains of rat pups: Protective role of diphenyl diselenide

Cited by 18 publications

References 40 publications

Brain oxidative damage restored by Sesbania grandiflora in cigarette smoke-exposed rats

Brain oxidative damage restored by Sesbania grandiflora in cigarette smoke-exposed rats

Secondhand Smoke and Periodontal Disease: Atherosclerosis Risk in Communities Study

How cigarette smoking may increase the risk of anxiety symptoms and anxiety disorders: a critical review of biological pathways

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