Antioxidant responses following active and passive smoking of tobacco and electronic cigarettes

Context: 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.

Objective: To examine the acute effects of active and passive e-cigarette and tobacco cigarette smoking on selected redox status markers.

Methods: 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?m³ environmental chamber) and a passive e-cigarette smoking session (exposure of 1?h to air enriched with pre- determined number of puffs in a 60?m³ environmental chamber). Total antioxidant capacity (TAC), catalase activity (CAT) and reduced glutathione (GSH) were assessed in participants’ blood prior to, immediately after, and 1-h post-exposure.

Results: TAC, CAT and GSH remained similar to baseline levels immediately after and 1-h-post exposure (p?>?0.05) in all trials.

Conclusions: Tobacco and e-cigarette smoking exposure do not acutely alter the response of the antioxidant system, neither under active nor passive smoking conditions. Overall, there is not distinction between tobacco and e-cigarette active and passive smoking effects on specific redox status indices.     

醛糖还原酶和晚期糖基化终末产物受体对糖尿病视网膜病变神经元凋亡的影响

目的　探究醛糖还原酶和晚期糖基化终末产物受体对糖尿病视网膜病变神经元凋亡的影响。方法　Wistar大鼠36只，随机分为对照组、模型组、转染组，后两组建立糖尿病大鼠模型。模型建立成功后，构建含有晚期糖基化终末产物受体siRNA的质粒并利用慢病毒转染入转染组大鼠体内。造模后4周、8周、12周，记录各组大鼠体质量及空腹血糖。造模后9周，禁食6 h，测定口服葡萄糖耐量。造模后12周，处死全部大鼠后，TUNEL法检测各组大鼠视网膜神经元凋亡情况，荧光分光光度计测定醛糖还原酶活性，Western blotting法测定晚期糖基化终末产物受体的表达，RT-PCR检测视网膜中Bcl-2和Bax mRNA相对表达量。结果　造模后4周、8周、12周，转染组和模型组的大鼠体质量均低于对照组（均为P<0.05）；造模后12周，转染组大鼠体质量高于模型组（P<0.05）。造模后4周、8周、12周，各组内大鼠空腹血糖水平均无明显变化（均为P>0.05），转染组和模型组大鼠的空腹血糖水平均高于对照组（均为P<0.05）。模型组和转染组大鼠在口服葡萄糖后30 min时，血糖水平均高于对照组（均为P<0.05）；在120 min时分别下降至最低，但仍高于对照组（均为P<0.05）。模型组和转染组的视网膜神经元凋亡指数、醛糖还原酶活性、晚期糖基化终末产物受体和Bax mRNA相对表达量均高于对照组（均为P<0.05），且转染组均高于模型组（均为P<0.05）。模型组和转染组的Bcl-2 mRNA相对表达量均低于对照组（均为P<0.05），转染组低于模型组（P<0.05）。结论　晚期糖基化终末产物结合受体后产生大量的氧自由基损伤，可能是导致糖尿病视网膜神经元凋亡，进而导致糖尿病视网膜病变发生的机制之一。     

Redox Polymer–Based Nano‐Objects via Polymerization‐Induced Self‐Assembly

Poly(2,2,6,6‐tetramethylpiperidinyloxy‐4‐yl‐methacrylate) (PTMA) redox polymer–based nano‐objects are synthesized by polymerization‐induced self‐assembly with poly[oligo(ethylene glycol) methyl ether methacrylate] and poly[(4‐methacryloyloxy)‐2,2,6,6‐tetramethylpiperidinium chloride] as hydrophilic macro‐chain transfer agents. These hydrophilic blocks are used in order to stabilize hydrophobic PTMA blocks in aqueous medium. The accordingly obtained spherical nano‐objects are observed via transmission electron microscopy analysis. Cyclic voltammetry measurements indicate that the nature and the length of coronal blocks influence the redox process of the PTMA core blocks. Moreover, these electroactive nano‐objects display low viscosities with a shear‐thinning behavior, making them suitable as cathode‐active materials for aqueous flow‐assisted electrochemical systems.     

保元抗癌口服溶液清除超氧自由基与DPPH作用

目的考察保元抗癌口服溶液对超氧自由基（O－2）和1,1 二苯基 2 苦肼自由基（DPPH）的清除作用。方法采用电子自旋共振（ESR）技术,以DPPH和 O－2为检测项目,测定保元抗癌口服溶液对自由基的清除效果。结果保元抗癌口服溶液稀释50倍时清除O－2和DPPH自由基分别为81.32%和98.47%。结论保元抗癌口服溶液对O－2和DPPH自由基均有较好清除作用,并呈一定的量效关系。     

Oxidative stress indices in COPD--Broncho-alveolar lavage and salivary analysis

OBJECTIVE: It has been suggested that oxidative stress plays a role in the pathogenesis of chronic obstructive pulmonary disease (COPD), though this role has yet to be fully elucidated. The purpose of this study was to further evaluate this role as concomitantly expressed in the saliva and broncho-alveolar lavage (BAL/'lavage'). DESIGN: Forty consenting patients (mean age 62+/-13-year-old), with/without COPD and/or smoking habit, participated in the study. The following antioxidant profile was examined both in saliva and lavage of the patients: total antioxidant status (TAS), uric acid (UA), peroxidase and super oxide dismutase (SOD). Total protein (TP) and albumin (Alb) were also evaluated in both saliva and lavage while amylase was measured only in saliva. RESULTS: Increase of TAS (by 100%) and of SOD activity levels (by 60%) in the lavage of COPD patients indicated oxidative stress. The salivary UA in COPD patients was 125% higher (p = 0.05) while the peroxidase was 20% higher. Another novel finding was that levels of salivary antioxidants in smoking versus non-smoking COPD patients were lower by 25-48% (for all four: TAS, UA, peroxidase and SOD) while the albumin was significantly reduced by 60% (p = 0.018). CONCLUSION: Oxidative-stress-related changes demonstrated both in the lavage and saliva of the COPD and/or smoking patient indicate cumulative effects of both, also emphasizing the pathogenetic role of free radicals in COPD. Salivary analysis, which is less invasive and much easier to perform as compared with lavage analysis, is suggested as a new and effective diagnostic tool in COPD patients.     

Levels of lipid peroxides and antioxidants in smokers and nonsmokers

BACKGROUND AND OBJECTIVE: The aim of the study was to evaluate the relationship between cigarette smoking and periodontal damage in terms of the levels of free radicals and antioxidants. MATERIAL AND METHODS: Thirty-five healthy subjects in the age group 25-56 yr and with chronic moderate inflammatory periodontal disease (attachment loss of 3-4 mm) were selected. All subjects were matched with respect to the clinical parameters plaque index, gingival index and attachment loss. Of the 35 subjects, 25 were smokers (smoking a minimum of 15 cigarettes/day) and 10 were nonsmokers. Smokers were subdivided into three subgroups: group I (10 subjects smoking 15-20 cigarettes/day); group II (10 subjects smoking 21-30 cigarettes/day) and group III (five subjects smoking > 50 cigarettes/day). Gingival tissue (obtained during Modified Widman surgery) and blood samples were collected from each of the subjects and analyzed for the following parameters: lipid peroxide, superoxide dismutase, catalase, glutathione and total thiol. RESULTS: The level of lipid peroxide was lowest in nonsmokers (2.242 +/- 0.775 in tissue and 1.352 +/- 0.414 in blood) and highest in smokers smoking > 50 cigarettes/day (6.81 +/- 1.971 in tissue and 4.96 +/- 0.890 in blood), both in tissue and in blood. The increase was statistically significant in all groups, except in tissue of group I smokers. Catalase showed a similar trend, where the levels increased from 0.245 +/- 0.043 in controls to 0.610 +/- 0.076 in group III smokers for tissue, and from 0.231 +/- 0.040 in controls to 0.568 +/- 0.104 in group III smokers for blood. The increase was statistically significant for all groups. Total thiol levels were also higher in smokers than in controls (0.222 +/- 0.050 in controls vs. 0.480 +/- 0.072 in group III smokers in tissue; 0.297 +/- 0.078 in controls vs. 0.617 +/- 0.042 in group III smokers in blood). Except for group I in both tissue and blood, the increase was statistically significant. The superoxide dismutase (SOD) level was higher in nonsmokers (2.406 +/- 0.477 in tissue and 2.611 +/- 0.508 in blood) than in group III smokers (1.072 +/- 0.367 in tissue and 0.938 +/- 0.367 in blood), both in tissue and in blood, but this was significant only in the case of blood and for group III smokers in tissue. The glutathione level in tissue was consistently lower in smokers than in controls, showing a decrease from 121.208 +/- 37.367 in controls to 46.426 +/- 14.750 in group III smokers, but the decrease was not significant in group I smokers. In the case of blood, the glutathione level dropped from 262.074 +/- 68.751 in controls to 154.242 +/- 51.721 in group III smokers, but was statistically significant only for group III smokers. CONCLUSION: The study results show that smoking increases the level of free radicals in periodontal tissues, which in turn may be responsible for the destruction seen in periodontal diseases.     

Hyper-reactive mononuclear cells and neutrophils in chronic periodontitis

OBJECTIVES: Stimulated mono- and polymorphonuclear cells from patients with periodontitis have shown increased release of interleukin-1beta (IL-1beta) and oxygen radicals, respectively. The aim was to study whether this hyper-reactivity could be found both in mono- and polymorphonuclear cells from the same patient, and whether there was a relation to the gene coding for IL-1beta (IL-1beta(+3953)). MATERIAL AND METHODS: Peripheral mononuclear cells from 14 non-smoking and well-treated patients and pair-matched controls were incubated with opsonized Staphylococcus aureus and lipopolysaccharide (LPS). Released IL-1beta and tumour necrosis factor (TNF)-alpha were determined with ELISA. Generation of oxygen radicals from the Fcgamma-receptor-stimulated neutrophils was measured with chemiluminescence and the polymorphism at IL-1beta(+3953) was measured with polymerase chainreaction. RESULTS: The mononuclear cells from the patients released more IL-1beta after incubation with LPS (p<0.001) and with bacteria (p<0.05). The release of TNF-alpha tended to be higher in the patient group. The peripheral neutrophils from the patients generated more oxygen radicals (p<0.06). We found no differences between the study groups regarding the IL-1beta(+3953) polymorphism. CONCLUSION: The similarity in systemic inflammation between patients and controls suggests that the increased release/generation of IL-1beta and oxygen radicals from peripheral leukocytes in periodontitis patients is of a constitutional nature and of pathogenic relevance.     

Nano-purification of raw semen minimises oxidative stress with improvement in post-thaw quality of buffalo spermatozoa

The study consisted of application of anti-ubiquitin antibodies (Abs)-coated iron oxide-nanoparticles (IONPs) for minimisation of oxidative stress to contemporary live spermatozoa from the raw semen. Round-shaped IONPs (12.09 ± 0.91 nm) after two-stage functionalisation (silanisation and pegylation) were conjugated with Abs. Four aliquots from each of the 24 ejaculates (4 buffalo bulls) formed Control (Group I) and treatment (II, III and IV) groups; each containing 150 ± 25 million dead/damaged spermatozoa. IONPs-Abs complex were added at ratio of 1:1 (0.5 µg/ml), 1:2 (1.0 µg/ml) and 1:4 (2.0 µg/ml), respectively, in Groups II, III and IV. The semen quality parameters showed improvement at lag-stage (post-nano-purification before processing for cryopreservation). The mean post-thaw motility (%) in Group IV was found to be greater (p < .05) than Group I. Moreover, the overall DNA integrity (%) at post-thaw stage was improved in the nano-purified semen samples. The value of malondialdehyde was greater (p < .001) in Group I than Groups II, III and IV. The mean total antioxidant capacity and superoxide dismutase (U/mg protein) activity values in Group IV was greater (p < .05) than Group I. The study results show that IONPs conjugated with anti-ubiquitin Abs at 2.0 µg/ml can be an effective dose for depletion of dead/damaged spermatozoa from buffalo ejaculates to minimise oxidative stress.     

儿茶素对拟衰老大鼠耳蜗氧自由基生成的影响

【目的】观察儿茶素对衰老大鼠动物模型耳蜗氧自由基生成的影响,初步探讨儿茶素对听觉老化的保护效应及其机制。【方法】通过腹腔注射D-半乳糖（D-gal）建立大鼠衰老动物模型,以腹腔注射生理盐水为阴性对照组,检测其听觉脑干诱发电位（ABR）明确衰老动物听力减退情况,检测大鼠耳蜗组织丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性;并观察胃内灌注儿茶素后衰老动物模型上述指标的变化。【结果】衰老模型组大鼠与对照组大鼠相比较,ABR阈值增高,耳蜗组织中MDA含量明显增高,SOD活性明显降低（P〈0.05）;儿茶素保护组大鼠耳蜗组织中MDA含量和SOD活性水平较对照组无变化（P〉0.05）,而与衰老模型组相比却逆转上述指标变化,并能提高听力（P〈0.05）。【结论】氧自由基及其引发的脂质过氧化反应参与了听觉老化过程,儿茶素可能通过提高SOD活性、减少MDA生成发挥清除自由基抗氧化作用,从而改善听觉功能。