RESUMEN
Hyperhomocysteinemia was reported to enhance endoplasmic reticulum (ER) stress and subsequent apoptosis in several cells. However, the precise mechanisms of smoking susceptibility associated with hyperhomocysteinemia has not been fully elucidated. This study included 7- to 9-week-old C57BL6 male mice induced with hyperhomocysteinemia and were exposed to cigarette smoke (CS). A549 cells (human alveolar epithelial cell line) were cultured with homocysteine and were exposed to cigarette smoke extract (CSE) to observe cell viability and expression of proteins related to the ER stress. After 6 months of CS exposure, pulmonary emphysema was more severely induced in the group under the condition of hyperhomocysteinemia compared to that in the control group. The apoptotic A549 cells increased as homocysteine concentration increased and that was enhanced by CSE. Protein expression levels of ER stress markers were significantly increased after simultaneous stimulation. Notably, vitamin B12 and folate supplementation improved ER stress after simultaneous stimulation of A549 cells. In this study, we showed that hyperhomocysteinemia exacerbates CS exposure-induced emphysema in mice, suggesting that hyperhomocysteinemia and CS stimulation enhance ER stress and subsequent induced apoptosis in alveolar epithelial cells. It was suggested that there is a synergistic effect between homocysteine and CS.
Asunto(s)
Enfisema , Hiperhomocisteinemia , Enfermedad Pulmonar Obstructiva Crónica , Enfisema Pulmonar , Animales , Apoptosis , Modelos Animales de Enfermedad , Enfisema/etiología , Homocisteína , Humanos , Hiperhomocisteinemia/complicaciones , Masculino , Ratones , Ratones Endogámicos C57BL , Enfermedad Pulmonar Obstructiva Crónica/metabolismo , Enfisema Pulmonar/etiología , Enfisema Pulmonar/metabolismo , Nicotiana/efectos adversosRESUMEN
The effects of the support on the catalytic performance of supported Ni catalysts for the hydrogenation of soybean oil were examined. The turnover frequency (TOF) for Ni/TiO2 was greater than those for other Ni catalysts. Among the examined Ni catalysts, the Ni/TiO2 catalysts were effective for the reduction of trans fatty acid (TFA) levels (minimum 10.5%) in hydrogenated oils at an iodine value (IV) of 70, independent of the difference in the crystalline structure of TiO2. In addition, the oils hydrogenated by Ni/TiO2 had suitable properties for feedstock of margarine and vegetable shortening. The highly dispersed Ni nanoparticles formed by reduction of the NiO monolayer on the surface of TiO2 contribute to increasing the catalytic activity and to reducing the TFA levels.
Asunto(s)
Níquel/química , Aceite de Soja/química , Titanio/química , Ácidos Grasos trans/química , Catálisis , Hidrogenación , Margarina , Nanopartículas del MetalRESUMEN
Smoking is a major risk factor for chronic obstructive pulmonary disease (COPD). Smoking susceptibility is important for the onset and development of COPD. We previously reported an association between serum iron concentrations and pulmonary function in male smokers. However, the mechanism governing smoking susceptibility in relation to iron deficiency is unclear; this study aimed to elucidate this mechanism. C57BL/6 male mice were fed an iron-deficient or normal diet and then exposed to cigarette smoke. BAL, histological analysis, and pulmonary function tests were performed after cigarette smoke exposure. Human alveolar type II epithelial A549 cells were treated with an iron chelator. Subsequently, A549 cells were exposed to cigarette smoke extract. In mice exposed to cigarette smoke for 2 weeks, the concentration of alveolar macrophages in the BAL fluid recovered from iron-deficient mice was significantly higher than that in normal diet mice. IL-6 and MCP-1 (monocyte chemotactic protein 1) concentrations in the BAL fluid increased significantly from baseline in iron-deficient mice, but not in normal diet mice. In mice exposed to cigarette smoke for 8 weeks, the pathological mean linear intercepts, physiological total lung capacity, and functional residual capacity in the lungs of iron-deficient mice were significantly greater than in normal diet mice. Phosphorylation of NF-κB was enhanced in the lungs of iron-deficient mice exposed to cigarette smoke and in the iron-chelating A549 cells exposed to cigarette smoke extract. Iron deficiency exaggerated cigarette smoke-induced pulmonary inflammation, suggesting that it may accelerate COPD development.