Oxidative stress in mouse plasma and lungs induced by cigarette smoke and lipopolysaccharide

Valença, Samuel Santos; Bezerra, Frank Silva; Lopes, Alan Aguiar; Romana‐Souza, Bruna; Cavalcante, Moisés C.M.; Lima, Aline Brando; Koatz, Vera Lúcia Gonçalves; Pôrto, Luís Cristóvão

doi:10.1016/j.envres.2008.07.001

Cited by 78 publications

(66 citation statements)

References 38 publications

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“…ERS plays a critical role in the regulation of apoptosis caused by a variety of toxic insults that damage mammalian cells, including oxidative stress, hypoxia, chemicals, Ca 2ϩ -homeostasis imbalance, and heavy metals (4,26). Previous studies have revealed that the oxidative stress and ERS pathways are activated in the lungs of LPS-treated mice (13,43). Thus, we examined a number of ERSrelated molecules and stress-activated signaling pathways, such as GRP78, CHOP, caspase-12, ASK1/JNK, and p38 cascades.…”

Section: R E T R a C T E Dmentioning

confidence: 99%

Reactive Oxygen Species-Triggered Trophoblast Apoptosis Is Initiated by Endoplasmic Reticulum Stress via Activation of Caspase-12, CHOP, and the JNK Pathway in Toxoplasma gondii Infection in Mice

Liu

Zhang

et al. 2012

Infect Immun

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dToxoplasma gondii infection in pregnant women may result in abortion or in fetal teratogenesis; however, the underlying mechanisms are still unclear. In this paper, based on a murine model, we showed that maternal infection with RH strain T. gondii tachyzoites induced elevated production of reactive oxygen species (ROS), local oxidative stress, and subsequent apoptosis of placental trophoblasts. PCR array analysis of 84 oxidative stress-related genes demonstrated that 27 genes were upregulated at least 2-fold and that 9 genes were downregulated at least 2-fold in the T. gondii infection group compared with levels in the control group. The expression of NADPH oxidase 1 (Nox1) and glutathione peroxidase 6 (Gpx6) increased significantly, about 25-fold. The levels of malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) increased significantly with T. gondii infection, and levels of glutathione (GSH) decreased rapidly. T. gondii infection increased the early expression of endoplasmic reticulum stress (ERS) markers, followed by cleavage of caspase-12, activation of ASK1/JNK, and increased apoptosis of trophoblasts, both in vivo and in vitro. The apoptosis of trophoblasts, the activation of caspase-12 and the ASK1/JNK pathway, and the production of peroxides were dramatically inhibited by pretreatment with N-acetylcysteine (NAC). The upregulation of Nox1 was contact dependent and preceded the increase in levels of ERS markers and the activation of the proapoptosis cascade. Thus, we concluded that apoptosis in placental trophoblasts was initiated predominantly by ROS-mediated ERS via activation of caspase-12, CHOP, and the JNK pathway in acute T. gondii infection. Elevated ROS production is the central event in T. gondiiinduced apoptosis of placental trophoblasts.

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Section: R E T R a C T E Dmentioning

confidence: 99%

Reactive Oxygen Species-Triggered Trophoblast Apoptosis Is Initiated by Endoplasmic Reticulum Stress via Activation of Caspase-12, CHOP, and the JNK Pathway in Toxoplasma gondii Infection in Mice

Liu

Zhang

et al. 2012

Infect Immun

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“…5 This excess ROS disturbs the balance between oxidants and antioxidants, resulting in oxidative stress. 16 Induced sputum, bronchoalveolar lavage fluid, or bronchial biopsy are among the invasive methods used for direct assessment of airway inflammation. EBC obtained by cooling exhaled air during spontaneous breathing is a simple, safe, and noninvasive method.…”

Section: Discussionmentioning

confidence: 99%

“…27 Increased MDA levels has been reported in smokers. 16,28 Corradi et al reported that MDA levels were increased in subjects with COPD in comparison to both non-smoking and smoking control subjects. 29 We did not detect any difference between the levels of MDA between groups.…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress Levels in Exhaled Breath Condensate Associated With COPD and Smoking

Inonu¹,

Doruk²,

Sahin³

et al. 2012

Respir Care

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BACKGROUND: COPD is characterized by chronic air-flow limitation. Smoking is the most important factor in the pathogenesis of COPD. Smoking is associated with increased oxidative stress in the lungs. In this study our aim was to evaluate the differences in the burden of oxidative stress in patients with COPD, smokers, and non-smokers by measuring hydrogen peroxide (H 2 O 2 ), malondialdehyde (MDA), and 8-isoprostane levels in the exhaled breath condensate (EBC) samples. METHODS: Eighty subjects were included in the study. Group I (no. ‫؍‬ 25) had COPD, Group II (no. ‫؍‬ 26) was smokers, and Group III (no. ‫؍‬ 29) was nonsmokers. The severity of the COPD and dyspnea was assessed according to the results of pulmonary function tests (PFTs) and Medical Research Council (MRC) scale. RESULTS: The mean age of the subjects was 58 ؎ 8.9 years. While 8-isoprostane and H 2 O 2 levels were significantly higher in subjects with COPD (44.8 ؎ 40.2 pg/mL and 1.9 ؎ 0.8 mol/L) and smokers (41.3 ؎ 26 pg/mL and 1.7 ؎ 0.7 mol/L) than non-smokers (15.8 ؎ 6.9 pg/mL and 0.8 ؎ 0.4 mol/L), levels were similar between smokers and COPD subjects. MDA levels were similar between the 3 groups (P ‫؍‬ .31). There was no correlation between 8-isoprostane and H 2 O 2 levels and PFT parameters. There was a significant positive correlation between dyspnea grade on the MRC scale and 8-isoprostane levels (r ‫؍‬ 0.805, P < .001). CON-CLUSIONS: Even if respiratory function tests are within normal limits, oxidant burden in lungs of smokers is equivalent to that in COPD patients. 8-isoprostane could be useful in assessing symptom severity and health status of COPD patients.

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“…Taken together, these results show that THS exposure reduces the antioxidant potential of the liver and leads to increased oxidative stress. Furthermore, the increased levels of H 2 O 2 can react with Fe 2+ ions in the tissue and undergo the Fenton reaction leading to production of hydroxyl radicals [18][19][20][21]. These, in turn, can lead to protein modification, formation of DNA adducts, and lipid peroxidation.…”

Section: Time Required For Ths Exposure To Cause Oxidative Stressmentioning

confidence: 99%

Biomarkers of disease can be detected in mice as early as 4 weeks after initiation of exposure to third-hand smoke levels equivalent to those found in homes of smokers

2017

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Third-hand smoke (THS) is a newly discovered environmental health hazard that results from accumulation and aging of second-hand smoke (SHS) toxins on surfaces where smoking has occurred. Our objective was to determine whether there is a time-dependent effect of THS exposure on health. Using an in vivo exposure mouse system that mimics exposure of humans to THS, we investigated its effects on biomarkers found in serum, and in liver and brain tissues. Mice were exposed to THS for 1, 2, 4, or 6 months and brain, liver, and serum were collected. We found that THS exposure, as early as 1 month, resulted in increased circulating inflammatory cytokines, tumor necrosis factor by an order of magnitude of 2 and granulocyte macrophage colony-stimulating factor by an order of magnitude of 1.5 and in increases in the stress hormone epinephrine and the liver damage biomarker aspartate aminotransferase (AST), increased in magnitude 1.5 and 2.5 times compared with controls, respectively. THS exposure for 2 months resulted in further damage and at 4 and 6 months, many factors related to oxidative stress were altered and caused molecular damage. We also found that the mice became hyperglycemic and hyperinsulinimic suggesting that insulin resistance (IR) may be a significant consequence of long-term exposure to THS. In conclusion, time-dependent THS exposure has a significant effect on health as early as 1 month after initiation of exposure and these alterations progressively worsen with time. Our studies are important because virtually nothing is known about the effects of increased THS exposure time, they can serve to educate the public on the dangers of THS, and the biomarkers we identified can be used in the clinic, once verified in exposed humans.

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Oxidative stress in mouse plasma and lungs induced by cigarette smoke and lipopolysaccharide

Cited by 78 publications

References 38 publications

Reactive Oxygen Species-Triggered Trophoblast Apoptosis Is Initiated by Endoplasmic Reticulum Stress via Activation of Caspase-12, CHOP, and the JNK Pathway in Toxoplasma gondii Infection in Mice

Reactive Oxygen Species-Triggered Trophoblast Apoptosis Is Initiated by Endoplasmic Reticulum Stress via Activation of Caspase-12, CHOP, and the JNK Pathway in Toxoplasma gondii Infection in Mice

Oxidative Stress Levels in Exhaled Breath Condensate Associated With COPD and Smoking

Biomarkers of disease can be detected in mice as early as 4 weeks after initiation of exposure to third-hand smoke levels equivalent to those found in homes of smokers

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