黄酮类成分黄芩素、槲皮素、丹参素钠对吸烟致细胞毒性和DNA损伤的保护作用

目的评价吸烟致细胞毒性和DNA损伤以及黄酮类成分黄芩素、槲皮素、丹参素钠的保护作用。方法以自动吸烟机按照FTC协议吸烟产生的主流烟雾在线染毒B-16细胞和人颊黏膜细胞两种真核细胞,通过MTT比色法和单细胞凝胶电泳法检测吸烟所致的细胞毒性和DNA损伤,并考察黄芩素、槲皮素、丹参素钠的保护作用。结果吸烟可致体外培养的B-16细胞活力明显下降,两种细胞的DNA明显损伤。随着烟气作用时间的延长,表征细胞内DNA损伤程度的彗星尾矩、Olive尾矩都有增加;1 mmol/L槲皮素、黄芩素和丹参素均可明显缓解吸烟引起的细胞毒性和DNA损伤,对B-16细胞的活力提升50%左右,对人颊黏膜细胞的DNA保护效果超过60%。结论吸烟可致细胞毒性和细胞DNA损伤,但是黄酮类成分黄芩素、槲皮素、丹参素钠均对细胞和DNA具有保护作用。     

Anti-HIV Activity of Cucurbitacin-D against Cigarette Smoke Condensate-Induced HIV Replication in the U1 Macrophages

Chemodietary agents are emerging as promising adjuvant therapies in treating various disease conditions. However, there are no adjuvant therapies available to minimize the neurotoxicity of currently existing antiretroviral drugs (ARVs). In this study, we investigated the anti-HIV effect of a chemodietary agent, Cucurbitacin-D (Cur-D), in HIV-infected macrophages using an in-vitro blood–brain barrier (BBB) model. Since tobacco smoking is prevalent in the HIV population, and it exacerbates HIV replication, we also tested the effect of Cur-D against cigarette smoke condensate (CSC)-induced HIV replication. Our results showed that Cur-D treatment reduces the viral load in a dose-dependent (0–1 μM) manner without causing significant toxicity at <1 μM concentration. Further, a daily dose of Cur-D (0.1 μM) not only reduced p24 in control conditions, but also reduced CSC (10 μg/mL)-induced p24 in U1 cells. Similarly, Cur-D (single dose of 0.4 μM) significantly reduced the CSC (single dose of 40 μg/mL)-induced HIV replication across the BBB model. In addition, treatment with Cur-D reduced the level of pro-inflammatory cytokine IL-1β. Therefore, Cur-D, as an adjuvant therapy, may be used not only to suppress HIV in the brain, but also to reduce the CNS toxicity of currently existing ARVs.     

WHERE THERE'S SMOKING,THERE'S FIRE: THE EFFECTS OF SMOKING POLICIES ON THE INCIDENCE OF FIRES IN THE USA

Fires and burns are among the leading causes of unintentional death in the USA. Most of these deaths occur in residences, and cigarettes are a primary cause. In this paper, I explore the relationship between smoking, cigarette policies, and fires. As smoking rates decline, there are fewer opportunities for fires; however, the magnitude of any reduction is in question. Using a state‐level panel, I find that increases in cigarette prices are associated with fewer residential fires and deaths. However, laws regulating indoor smoking are associated with more fires; in particular, restaurant and bar smoking bans are associated with an increase in fires at eating and drinking establishments. This increase is important given the growing popularity of smoking bans in the USA and around the world. As workplaces, schools, and businesses ban smoking and remove ashtrays, smokers who continue to smoke are left without safe options for disposal of cigarettes, leading to more opportunities for fires to start. Copyright © 2013 John Wiley & Sons, Ltd.     

Acute effects of second-hand smoke on complete blood count

We assessed the acute effects of a 1-h exposure to second-hand smoke (SHS) on complete blood count (CBC) markers in a controlled simulated bar/restaurant environment. Nineteen adult never-smokers completed a 1-h .exposure to SHS at bar/restaurant levels, and a 1-h exposure to normal room air. Blood samples were collected at the baseline at 30?min during each exposure, and at 0, 0.5, 1, 2, 3, and 4?h after each exposure. The values of white blood cells (WBC) at 1?h (p?=?0.010), 3?h (p?=?0.040), and 4?h (p?=?0.008) following SHS were significantly increased compared with the baseline values. Also, there was a positive association between the WBC and cotinine levels (r?=?0.28, p?=?0.007). A 1-h exposure to SHS at bar/restaurant levels significantly increased the WBC for at least 4?h following the exposure time. This effect of SHS on WBC has dose–response characteristics and should be considered to prescribing CBC.     

Cytologic features of vaping‐induced lung injury: A case report

Vaping‐induced lung injury is a recently recognized phenomenon owing to the rising popularity of e‐cigarette use. A cluster of cases of varying severity, including six deaths, was recently reported in the United States by the Centers for Disease Control. The objective of this report is to highlight the cytologic features suggestive of vaping‐induced lung injury. A 20‐year‐old previously healthy man presented with a 7‐day history of progressively worsening respiratory symptoms including dyspnea on exertion, cough, and fever, with no improvement after initiating a course of antibiotics. No relevant travel or occupational history was reported, but patient endorsed daily use of e‐cigarette with a fluid containing both tetrahydrocannabinol and nicotine. Radiographic studies demonstrated scattered areas of interlobular septal thickening and diffuse ground‐glass opacities in both lungs. Laboratory tests for HIV and influenza were negative. Bronchoscopy and bronchoalveolar lavage were performed, with cytologic study showing clusters of benign bronchial cells and an increase in lipid‐laden macrophages by Oil Red O stain. Patient was placed on steroid and steadily improved for the next 2 days. He was discharged on a steroid taper and follow‐up with respiratory clinic. Case reports and series have shown a variety of lung injury patterns in previously healthy patients who are frequent users of e‐cigarettes and among them features suggestive of lipoid pneumonia with increased lipid‐laden macrophages. The clinical utility of this finding is still unclear.     

Effect of smoking on immunity in human chronic periodontitis

Aim

Evaluate the effects of smoking on dendritic cells (DCs), cytokines, clinical periodontal parameters, and number of teeth in samples of human chronic periodontitis (CP).

Material and methods

Gingival samples were obtained from 24 smokers and 21 non-smokers with CP. Periodontal examination was carried out. Immunohistochemical staining was performed to identify Factor XIIIa+ immature, CD1a+ immature, and CD83+ mature DCs. The inflammatory infiltrate was counted, and IL-2, IL-10, IL-4, IL-6, IFN-γ, TNF-α, and IL-17A were measured using the cytometric bead array (CBA). Inflammatory infiltrate, DCs, cytokines, classification of CP, clinical periodontal parameters, number of teeth, smoking habit in years (SH/years), and number of cigarettes smoked per day (C/day) were correlated and compared.

Results

CD83+ mature DCs decreased in the smokers group. Negative correlations could be observed between the number of C/day with levels of IL-17A and number of teeth. Correlations between smoking, periodontal disease status, and other cytokines were not observed.

Conclusions

Smoking decreases mature DCs in chronic periodontitis. Moreover, a dose-dependent relation can be observed between C/day and number of teeth and levels of IL17A observed. Smokers show a different modulation of the CP immune response.     

LDH enzyme activity in human saliva: The effect of exposure to cigarette smoke and its different components

ObjectiveAldehydes and reactive nitrogen species (RNS) are important chemically active agents in cigarette smoke (CS). Salivary lactate dehydrogenase (LDH) originates predominantly from oral epithelium and was identified as an oral state marker. Its activity in saliva decreases after CS exposure. The aims of the current study were to identify the specific damaging agents in CS responsible for this activity reduction and to understand the mechanisms participating in CS oxidative damage to the salivary enzymes.MethodsPurified and salivary LDH samples were exposed to different levels of CS, pure acrolein, acetaldehyde, peroxynitrite and RNS donors. Each response of the isolated agent to the exposure was examined by a spectrophotometric enzyme activity assay and a Western blot.ResultsCS exposure caused a 34% reduction in LDH activity. Isolated treatment with unsaturated-aldehydes (acrolein, 10 μmol) caused a 61% reduction, while saturated-aldehydes (acetaldehyde, 200 μmol), peroxynitrite (200 μM) and RNS donor (SIN-1, 2 mM) caused no substantial effect. All five LDH isoenzymes reacted similarly. The carbonyl immunoblotting assay revealed a fourfold increase in carbonyl content when treated with CS and a sevenfold increase when treated with acrolein.Conclusionα,β-Unsaturated-aldehydes were identified as the main CS ingredient responsible for salivary LDH activity diminution. The effect of saturated-aldehydes and RNS donors was negligible. Unsaturated-aldehydes are capable of introducing carbonyl group into proteins, causing their dysfunction. This provides a molecular explanation for a decrease in LDH enzymatic activity in saliva.