• 한국수의병리학회:학술대회논문집
• /
• 한국수의병리학회 2005년도 Proceedings of The 2nd Asian Society of Veterinary Pathology Symposium(Vol.2) and 2005 Annual Meeting of The Korean Society of Veterinary Pathology(Vol.9)
• /
• pp.88-88
• /
• 2005

• 한국수의병리학회:학술대회논문집
• /
• 한국수의병리학회 2005년도 Proceedings of The 2nd Asian Society of Veterinary Pathology Symposium(Vol.2) and 2005 Annual Meeting of The Korean Society of Veterinary Pathology(Vol.9)
• /
• pp.87-87
• /
• 2005

• Journal of Preventive Medicine and Public Health
• /
• 제33권2호
• /
• pp.165-173
• /
• 2000

Objectives : To assess the availability of the glycophorin A (GPA) assay to detect the biological effect of ionizing radiation in workers exposed to low-doses of radiation. Methods : Information on confounding factors, such as age and cigarette smoking was obtained on 144 nuclear power plant workers and 32 hospital workers, by a self-administered questionnaire. Information on physical exposure levels was obtained from the registries of radiation exposure monitoring and control at each facility. The GPA mutant assay was performed using the BR6 method with modification by using a FACScan flow cytometer. Results : As confounders, age and cigarette smoking habits showed increasing trends with GPA variants, but these were of no statistical significance. Hospital workers showed a higher frequency of the GPA variant than nuclear power plant workers in terms of the NO variant. Significant dose-response relationships were obtained from in simple and multiple linear regression models. The slope of the regression equation for nuclear power plant workers was much smaller than that of hospital workers. These findings suggest that there may be apparent dose-rate effects. Conclusion : In population exposed to chronic low-dose radiation, the GPA assay has a potential to be used as an effective biologic marker for assessing the bone marrow cumulative exposure dose.

• Environmental Analysis Health and Toxicology
• /
• 제29권
• /
• pp.10.1-10.6
• /
• 2014

Objectives Cigarette smoking had been recorded as the main cause of impaired endothelium-dependent vasodilation in smokers by reducing nitric oxide (NO), a production of endothelial nitric oxide synthase (eNOS). However, the mechanism of NO impairment via eNOS activity is unclear until now. In this study, cell passage is suggested to be a relevant factor to eNOS expression under cigarette smoking stress. Methods Bovine aortic endothelial cells (BAECs) were chosen as the research subject with passages ranking from 6 to 9 (6P to 9P). After exposure of cigarette smoking extract (CSE) solution, MTT assay and Western blot method were performed to check the cell viability as well as eNOS protein concentration. In these experiments, four concentrations of CSE at 0.5, 1, 2, and 4% were selected for treatment. Results Our results showed that cells almost died at 4% of CSE. Besides, eNOS protein mass had a linear decrease under the increase of CSE concentration. In addition, the effect of CSE on eNOS expression was dissimilar between different passages. Conclusions This study indicated that CSE had effect on both cell viability and eNOS expression. Besides, a reduction in protein mass was matched with the decrease of cell viability due to CSE tress. Last but not least, the response of eNOS protein to different concentration of CSE at different passages was disparate, making the hypothesis about cell passage related inhibition of eNOS caused by CSE solution.

• Tuberculosis and Respiratory Diseases
• /
• 제76권4호
• /
• pp.188-191
• /
• 2014

Acute eosinophilic pneumonia (AEP) is a disease characterized by an acute febrile onset, eosinophilia in bronchoalveolar lavage fluid, and a dramatic response to corticosteroids. Although many studies have reported a close relationship between direct cigarette smoking and AEP, few studies have identified an association between passive smoking and AEP. Here, we report a case of AEP in a 19-year-old female with cough, fever, and dyspnea after 4 weeks of intense exposure to secondhand smoke for 6 to 8 hours a day in an enclosed area.

• Tuberculosis and Respiratory Diseases
• /
• 제81권2호
• /
• pp.138-147
• /
• 2018

Background: Recent studies show that mitophagy, the autophagy-dependent turnover of mitochondria, mediates pulmonary epithelial cell death in response to cigarette smoke extract (CSE) exposure and contributes to the development of emphysema in vivo during chronic cigarette smoke (CS) exposure, although the underlying mechanisms remain unclear. Methods: In this study, we investigated the role of mitophagy in the regulation of CSE-exposed lung bronchial epithelial cell (Beas-2B) death. We also investigated the role of a phosphodiesterase 4 inhibitor, roflumilast, in CSE-induced mitophagy-dependent cell death. Results: Our results demonstrated that CSE induces mitophagy in Beas-2B cells through mitochondrial dysfunction and increased the expression levels of the mitophagy regulator protein, PTEN-induced putative kinase-1 (PINK1), and the mitochondrial fission protein, dynamin-1-like protein (DRP1). CSE-induced epithelial cell death was significantly increased in Beas-2B cells exposed to CSE but was decreased by small interfering RNA-dependent knockdown of DRP1. Treatment with roflumilast in Beas-2B cells inhibited CSE-induced mitochondrial dysfunction and mitophagy by inhibiting the expression of phospho-DRP1 and -PINK1. Roflumilast protected against cell death and increased cell viability, as determined by the lactate dehydrogenase release test and the MTT assay, respectively, in Beas-2B cells exposed to CSE. Conclusion: These findings suggest that roflumilast plays a protective role in CS-induced mitophagy-dependent cell death.

• Laboraroty Animal Research
• /
• 제33권1호
• /
• pp.40-47
• /
• 2017

HemoHIM, herbal preparation has designed for immune system recovery. We investigated the anti-inflammatory effect of HemoHIM on cigarette smoke (CS) and lipopolysaccharide (LPS) induced chronic obstructive pulmonary disease (COPD) mouse model. To induce COPD, C57BL/6 mice were exposed to CS for 1 h per day (eight cigarettes per day) for 4 weeks and intranasally received LPS on day 26. HemoHIM was administrated to mice at a dose of 50 or 100 mg/kg 1h before CS exposure. HemoHIM reduced the inflammatory cell count and levels of tumor necrosis factor receptor (TNF)-${\alpha}$, interleukin (IL)-6 and IL-$1{\beta}$ in the broncho-alveolar lavage fluid (BALF) induced by CS+LPS exposure. HemoHIM decreased the inflammatory cell infiltration in the airway and inhibited the expression of iNOS and MMP-9 and phosphorylation of Erk in lung tissue exposed to CS+LPS. In summary, our results indicate that HemoHIM inhibited a reduction in the lung inflammatory response on CS and LPS induced lung inflammation via the Erk pathway. Therefore, we suggest that HemoHIM has the potential to treat pulmonary inflammatory disease such as COPD.

• Preventive Nutrition and Food Science
• /
• 제9권1호
• /
• pp.65-70
• /
• 2004

Side-stream cigarette smoke (SSCS) is a major component of environmental tobacco smoke. The purpose of this study was to investigate the development of lung injury and lipid peroxidation in the lung and liver of immunodeficient (Nude) mice exposed to acute SSCS (a total 5 hours of exposure). The effects of French maritime bark extract (Pycnogeno $l^{ⓡ}$) supplementation of the mice were also determined. SSCS increased pulmonary resistance and lipid peroxidation in these mice. Pycnogeno $l^{ⓡ}$ supplementation increased vitamin E levels in lung and liver. In addition, Pycnogeno $l^{ⓡ}$ attenuated SSCS-mediated lung injury and lipid peroxidation. It appears that the enhanced resistance against SSCS-induced lung injury and lipid peroxidation may be primarily due to the antioxidant property of Pycnogeno $l^{ⓡ}$ in supplemented mice.

• Asian Pacific Journal of Cancer Prevention
• /
• 제16권8호
• /
• pp.3587-3590
• /
• 2015

In spite of limited data regarding the safety or effectiveness of electronic cigarette introduced into the market as a healthier alternative to tobacco smoking, its popularity has increased enormously. E-cigarettes have penetrated the market rapidly owing to the elaborate marketing network and attractive marketing strategies. Stated advantages include the claim that they help quit smoking and produce less exposure than conventional smoking. The list of disadvantages is even more elaborate. While the majority of the studies supporting health claims and efficacy for quitting smoking are not scientifically sound, they are also challenged by studies providing contradictory results. Owing to the limited evidence on the potential advantages and disadvantages of e-cigarettes, the debate on their safety continues.

• 대한화장품학회지
• /
• 제44권2호
• /
• pp.111-116
• /
• 2018

최근 화장품 시장에서 안티폴루션 효능이 있는 화장품은 새로운 피부 건강을 위한 해결책으로 나타나고 있다. 외부(대기) 오염물질에 의해 피부의 산화 기전을 매개하는 주요 원인 인자들로 오존, UV, 미세먼지 및 담배연기 등을 꼽을 수 있다. 담배 연기의 노출은 직 간접적으로 피부 표피 내 지질의 산화를 야기한다. 피부의 지질 산화에 의해 squalene과 squalene monohydroperoxide의 비율 변화가 발생하고, malondialdehyde (MDA)가 지질산화 산물로 생성된다. 따라서, 본 연구에서는 담배연기 노출 시 발생하는 피부 산화에 대하여 레드비트를 함유하는 화장품이 방지할 수 있는 효능이 있는지에 대하여 MDA의 생성량으로 관찰하였다. 시험대상자 전박부를 세 영역(음성대조, 양성대조, 시험제품)으로 나누어 각 지름 3.3 cm의 원으로 구획하고, 15분간 담배연기에 노출 후 피부 표면으로부터 지질막을 걷어낸 후 TBARS assay를 통하여 MDA를 정량 하였다. 음성대조(무도포, 미노출)에 비해 양성대조(무도포, 담배연기 노출)의 MDA 생성량이 3.7배 증가된 결과로, 오염물질인 담배연기에 의한 피부의 산화적 손상을 확인하였다. 반면에 레드비트를 함유하는 화장품을 미리 도포한 영역은 양성대조에 비해 MDA 생성량이 25% 감소하는 결과를 나타내었다. 결론적으로, 담배연기 노출은 피부표피 내 지질 산화를 야기하며, 레드비트를 함유하는 화장품이 이러한 대기환경오염으로부터 방어적 효과(안티폴루션 효과)를 보이는 것을 확인하였다.