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作者应用体外培养和透射电镜技术探讨了人参皂甙抗石棉尘的细胞毒作用。结果表明:加入人参皂甙的石棉组较单纯石棉组在存活率、吞噬功能上有所提高,培养上清中LDH、ACP和MDA产生量减少,超微结构损伤减轻。本实验为石棉肺的预防性给药及石棉的脂质过氧化机理研究提供了参考。 相似文献
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石棉工人肺功能5年前后比较 总被引:2,自引:0,他引:2
为寻找反应石棉工人肺功能损伤的最早、最敏感的指标,作者采用水封式肺量计和弥散功能测定仪对119名男性石棉作业工人1989年和1994年的肺功能进行了测定,并比较其5年前后各项指标的变化情况。其中健康接尘组50例,石棉肺观察对象25例,I期石棉肺患者36例,Ⅱ期石棉肺患者8例。结果显示:5年后4组工人的用力肺活量(FVC),第一秒呼气量(FEV1)和弥散数(DLco)值均有降低,其中FVC和DLco 相似文献
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为探讨青石棉与P53基因突变之间的关系,采用PCR-SSCP分析方法,对8株青石棉衣发的BALB/c 3T3转化细胞进行P53基因的突变检测和分析。结果:从8株转化细胞P53基因上的11个显子中共发现7处突变,其中2个位于外显子4-6,5个位于外显子9-11;大多数检出的异常表现为比野生型多1条带;突变随机地分布于各个青石棉剂量组。 相似文献
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石棉诱发大鼠胸膜间皮瘤的形态发生学观察 总被引:2,自引:0,他引:2
In order to observe the lesions of pleural mesothelia caused by asbestos, we injected asbestos fiber into the pleural cavity of Wistar rats. The result showed that there Was an obvious process for the morphological genesis of mesothelioma. Simple hyperplasia and stratified pleomorphic hyperplasia of mesothelial cells were found on the 30th and 106th day after the injection of asbestos fiber, respectively. The benign and malignant mesotheliomas were noted on the 300th day. Meanwhile, a two-way differentiation may be observed in the process of mesothelial hyperplasia. 相似文献
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家犬于石棉车间自然吸入染尘1~3年后,其呼吸性细支气管、肺泡管及膜性细支气管均显示不同程度的粉尘沉着伴纤维化。病变程度亦随染尘时间延长而逐渐加重,酷似人体石棉肺小气道病变。肺病灶内尘粒能谱分析揭示其病因相当复杂,原则上是一种混合粉尘,以硅酸盐为主,石棉占绝对优势,且闪石类多于温石棉,并存在明显剂量效应关系。 相似文献
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作者对23例大鼠间皮瘤作了超微结构研究,其中7例混合型作了免疫组化研究。结果说明,间皮瘤可能来自间皮下多功能的原始间叶细胞。作者还就本组间皮瘤与人和其他动物的间皮瘤进行了比较,并对电镜及免疫组化在研究间皮瘤中的作用进行了讨论。 相似文献
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Titanium dioxide (TiO2) dust has generally been regarded as a "nuisance dust" in experimental animals and men. In this experiment, 16 dogs were exposed intratracheally to TiO2 dust for 9-15 months. The scanning electron microscopy with energy dispersive analysis of X-ray (SEM-EDAX), performed to identify the elemental composition of dust particles used in the study and in the focal lesions of the lungs, showed that dust particles were nearly pure titanium. Dust in the lung deposited mainly in the respiratory bronchioles and adjacent alveoli, with many alveoli filled by compacted dust particles. The pulmonary responses consisted of slight alveolitis, centrilobular emphysema, focal collapse of alveoli, and fibroblast hyperplasia with a few collagen fibres surrounding some of the TiO2-dust foci. Electron microscopically, many alveolar macrophages with intact nuclei contained a great amount of dust particles in their lysosomes, and in the dust foci, most of type I pneumocytes disappeared and type I pneumocytes showed hyperplasia. The alveolar subepithelial basement membrane were markedly thickened and bundles of collagen fibres were formed in the interstice. These findings suggest that TiO2 dust is one of the sorts which probably induce mild lung fibrosis in case a large amount is deposited in the lung tissue. 相似文献
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新康短纤维温石棉诱发大鼠支气管肺泡炎的病理研究 总被引:2,自引:2,他引:0
Eighty-four rats were exposed intratracheally to 25 mg of locally produced Xinkang short-fiber chrysotile asbestos (98% of the fibers are less than 5 microns in length). In 1 to 3 d after instillation, the pathological changes in rat lungs demonstrated that the affection was mainly acute bronchio-alveolitis characterized by acute inflammatory exudation and injuries of the small airways and alveolar structural units. The four main manifestations of alveolitis induced by the chrysotile asbestos were of the neutrophilic, serous, alveolar macrophages and granulomatous varieties. Three types of pulmonary fibrosis developed gradually from 7 to 90 d following the exposure to the asbestos, i.e. the intraluminal, murally incorporated, and interstitial fibrosis. Findings showed the complete process from the acute inflammatory exudation and the damage to lung tissue, with the following repair and proliferation of injuried lung tissue and organization of exudate, to the final fibrosis and destruction of the lung. The results suggested that the persistent and irreversible damage to the epithelial cells of respiratory bronchioles and pneumocytes, and denudation and destruction of the basement membrane played an important role in the development of pulmonary fibrosis by forming a channel for the inflammatory exudates and fibroblasts migrating into the bronchioalveolar spaces. Therefore, the experimental results have proved that Xinkang chrysotile asbestos fibers less than 5 microns in length certainly have a fibrogenic effect. 相似文献
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We studied the Syrian hamster embryo (SHE) cell transformation by focus assay for detecting the carcinogenicity of chrysotile asbestos fibers collected from Sichuan Xinkang Asbestos Mine and particulate coal dusts from Jiayang Coal Mine. Both these mines belong to Sichuan Province. Results showed that transformed foci were found in the methylcholanthrene group and in the two asbestos dosing groups (8 micrograms/ml and 4 micrograms/ml), whereas no transformed foci were noted in the coal dust groups and no spontaneous transformation in the negative control groups. Morphologically, the transformed foci were documented by light and electronmicroscopy. Significant differences between the positive transformed groups and the negative control groups were demonstrated by statistic analysis. The results indicate that Sichuan Xinkang chrysotile asbestos fibers are of carcinogenic potentiality, and Jiayang coal dusts do not induce transformation in SHE cells. 相似文献
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本文报告用MNNG溶液(250ug/ml),拌喂普通食物复制家狗胃癌模型的实验结果。在10只狗中,三只诱发了微小胃癌。共发现16个癌灶。分布在胃体和胃底、大小弯,为多发性;组织类型为高分化管状腺癌(9/16),及印戒细胞癌(7/16),位于粘膜内或粘膜下浸润;肉眼类型属Ⅱ_(b-c)型。系统地观察了各种癌前期病变的病理组织学变化及其与胃癌发生的关系。研究表明:重度慢性萎缩性胃炎伴重度非典型腺体增生是重要的癌前期病变,并提出了狗微小胃癌组织发生模式的初步设想。 相似文献
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Omics Approaches for Exploring Pneumoconiosis: A Review 总被引:1,自引:0,他引:1
LUO Ya QI Xian Mei PANG Jun Ling WANG Jing WANG Chen 《Biomedical and environmental sciences : BES》2021,34(1):71-82
Pneumoconiosis,a fatal lung disease caused by dust inhalation and deposition,is one of the leading occupational diseases worldwide[1].The dust is primarily inorganic particles,such as silica particles,coal dust,and asbestos fibers.If the diameter of dust is less than 5μm,it is defined as‘respirable dust’that can easily reach the distal airways and alveoli[2]. 相似文献
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对10例临床诊断为Ⅰ期生肺的稻谷加工工人肺活检标本进行了病理组织学观察。主要病变为弥漫性肺纤维化,有纤维细胞结节形成。小气道管壁纤维化和小血管玻璃样变均较明显。肺组织内有大量粉尘沉着。 相似文献