Selective adsorption of serum proteins by chrysotile and crocidolite

Two distinct and contemporaneous adsorption mechanisms occur when serum proteins are incubated with chrysotile and crocidolite. The first one appears to be reversible and nonspecific, independent of the characteristics of the protein and the fiber surface. The second process seems to depend on fiber type and to involve only some protein species that are strongly concentrated on the fiber surface. This latter adsorption mechanism appears to be electrostatic in nature.     

多壁碳纳米管长期染毒对人胸膜间皮细胞的影响

目的:探讨低剂量多壁碳纳米管（MWCNT）长期慢性染毒对人胸膜间皮细胞的毒性效应及可能机制。方法:于2016年,使用10 μg/cm 2 MWCNT对人胸膜间皮细胞MeT-5A反复持续染毒1年作为染毒组,每4周收集1次细胞并观察细胞形态和计数增殖情况。对照组细胞同期培养但不进行染毒处理。染毒后细胞经流式细胞...     

青石棉致胸膜间皮瘤42例临床分析

分析42例资料完整的接触青石棉致胸膜间皮瘤病例的临床症状及诊断方法,并结合该病的发病机理,探讨本地区胸膜间皮瘤高发的原因。     

The effects of chrysotile and crocidolite asbestos on the lower respiratory tract: analysis of bronchoalveolar lavage constituents

This study was designed to evaluate the effects of amphibole and serpentine asbestos inhalation on the constituents of the lower respiratory tract. Bronchoalveolar lavage (BAL) analyses were performed on three groups of rats: one group was exposed to chrysotile (serpentine) asbestos, another group was exposed to crocidolite amphibole asbestos, while a third group was sham-exposed. Intermittent inhalational exposures lasted three months. The total BAL cell yields and the macrophage content of BAL cells were significantly lower after asbestos exposure, especially in the chrysotile-exposed group. These effects persisted for as long as 1 year after the cessation of exposure. Multinucleated macrophages were seen in BAL cells from both asbestos-exposed groups. Striking ultrastructural alterations of macrophage morphology were noted in BAL cells from both groups of asbestos-exposed rats. Chrysotile fibers were not seen in any BAL cells from chrysotile-exposed animals. However, 15 months after terminating the exposure regimen, a sizeable proportion of BAL macrophages from crocidolite-exposed rats contained phagocytosed asbestos fibers. Significantly higher beta-glucuronidase and lactate dehydrogenase activity was found in BAL fluids from both asbestos-exposed groups and was detected 17-18 months after exposure had ceased. These observations have served as useful correlates of asbestos-mediated injury to the lower respiratory tract. They have also provided evidence of continual pathological sequelae occurring long after withdrawal from asbestos exposure.     

Dielectric changes in membrane properties and cell interiors of human mesothelial cells in vitro after crocidolite asbestos exposure

Asbestos induces cytogenetic and genotoxic effects in cultured cell lines in vitro. For further investigations of the fiber-induced cellular changes, electrorotation (ROT) measurements can be used to determine early changes of surface properties and dielectric cellular changes. In the present study, human mesothelial cells (HMC) were exposed to nontoxic concentrations of crocidolite asbestos (1 microg/cm(2)) for 12, 24, 30, 50, and 72 hr, and were investigated for changes in dielectric properties, morphologic and biochemical changes using ROT measurements, electron microscopy, and flow cytometry, respectively. The results of ROT measurements revealed slightly increased internal conductivity and decreased membrane conductance of HMC during the first 12 hr of exposure to crocidolite. This may be due to functional changes of ion channels of the cellular membrane. However, after exposures of >= 30 hr, reduced internal conductivity and increased membrane conductance of HMC occurred. These effects may be caused by permeabilization of the cell membrane and the leakage of ions into the surrounding medium. The membrane capacitance of HMC is always decreased during exposure of cells to crocidolite fibers. This decreased membrane capacitance may result from the observed reduction in the number of microvilli and from the shrinkage of cells as observed by electron microscopy and flow cytometry. Changes in composition of the plasma membrane were also observed after the labeling of phosphatidylserines (PS) on the cell surface. These observed changes can be related to apoptotic events. Whereas during the first 50 hr of exposure only a small number of HMC with increased exposure of PS on the cell surface was detected by flow cytometry, the dielectric properties of HMC showed marked changes during this time. Our results show that surface property changes of the cellular membrane of HMC as well as interior dielectric changes occur after the exposure of cells to crocidolite fibers. The observed changes are discussed in terms of complex combined cellular effects after amphibole asbestos exposure.     

Changes in lipid ordering of model phospholipid membranes treated with chrysotile and crocidolite asbestos

A variety of inorganic particles bind to cell membranes and cause alterations in phagocytosis, migration, and metabolism leading to eventual cell death. The mechanism which mediate these events at the complex membrane level are not known. In attempting to define the mechanisms of asbestos-induced membrane changes, we have prepared small unilamellar vesicles (SUV) of dipalmitoyl phosphatidylcholine as a simplified model of the cell membrane. Negatively stained preparations for electron microscopy demonstrated that the SUVs bind to both chrysotile and crocidolite asbestos fibers. Electron spin resonance showed that both asbestos types caused increased membrane rigidity at the level of the 12th carbon, whereas chrysotile induced increased rigidity at the 5th carbon level as well. Studies using DPPC membranes compared to SUVs made of phosphatidylcholine from egg yolk support the view that lipid peroxidation may play no significant role in alterations of membrane rigidity induced by the asbestos particle binding. Similar alterations of membrane rigidity and lipid peroxidation at the depth of the 12th carbon have been reported in complex naturally occurring erythrocyte membranes. This suggests that our observations may be relevant to biological membranes and that the model system of SUVs is appropriate for additional studies on the mechanisms of particle-induced membrane injury.     

Natural history of pleural thickening after exposure to crocidolite

Serial plain chest radiographs of 384 men who worked at the Wittenoom crocidolite mine and mill between 1943 and 1966 and who applied for pneumoconiosis compensation between 1948 and 1982 have been examined independently by two trained observers for pleural disease using the 1980 ILO-UICC classification of radiographs to record width and extent of pleural disease. Radiographs covering follow up periods of from two to 38 years were examined (median number of films per subject was nine). The degree of crocidolite exposure was estimated from employment records and a survey of airborne fibre concentrations performed in 1966. Agreement between the observers on the presence and degree of pleural disease in the final film for each subject was moderately close (Kendall's tau B = 0.62) and was least for subjects with thickening less than 5 mm in width. Diffuse pleural thickening extending for greater than 50% of the lateral chest wall was the most common type recorded by both observers. Minor pleural thickening frequently progressed in extent along the lateral chest wall but progression beyond 5 mm in thickness was less common. Pleural plaques were not seen to progress beyond their initial thickness or extent. The rate of onset of thickening in this population increased continually from the time of first exposure and also increased slightly with age. There was evidence that the level of total cumulative exposure to crocidolite increased the rate of onset of pleural thickening in the period between five and 15 years after first exposure. Rate of progression of established thickening was greatest in subjects who first developed thickening early after first exposure. The relative rate of progression decreased slowly with time from first signs of thickening and there was no evidence of any progression more than 15 years after onset.     

Adsorption of proteins by chrysotile and crocidolite: role of molecular weight and charge density

Transferrin, gamma-globulin, fibrinogen, aldolase, albumin, and cytochrome c at concentration of 0.45 muMole/liter were treated with chrysotile and crocidolite fibers. Specific adsorption for each protein and correlations between protein molecular weight and charge density in experimental conditions were evaluated. Chrysotile showed the highest absorption capability, particularly toward albumin and cytochrome c. Affinity for fibers was poorly linked to protein molecular weight; on the contrary, a good correlation with protein charge density was found. The sign of charge on fibers and proteins seemed to play a minor role in adsorption.     

The effects of chrysotile and crocidolite asbestos on the lower respiratory tract: Analysis of bronchoalveolar lavage constituents

This study was designed to evaluate the effects of amphibole and serpentine asbestos inhalation on the constituents of the lower respiratory tract. Bronchoalveolar lavage (BAL) analyses were performed on three groups of rats: one group was exposed to chrysotile (serpentine) asbestos, another group was exposed to crocidolite amphibole asbestos, while a third group was sham-exposed. Intermittent inhalational exposures lasted three months. The total BAL cell yields and the macrophage content of BAL cells were significantly lower after asbestos exposure, especially in the chrysotile-exposed group. These effects persisted for as long as 1 year after the cessation of exposure. Multinucleated macrophages were seen in BAL cells from both asbestos-exposed groups. Striking ultrastructural alterations of macrophage morphology were noted in BAL cells from both groups of asbestos-exposed rats. Chrysotile fibers were not seen in any BAL cells from chrysotile-exposed animals. However, 15 months after terminating the exposure regimen, a sizeable proportion of BAL macrophages from crocidolite-exposed rats contained phagocytosed asbestos fibers. Significantly higher β-glucuronidase and lactate dehydrogenase activity was found in BAL fluids from both asbestos-exposed groups and was detected 17–18 months after exposure had ceased. These observations have served as useful correlates of asbestos-mediated injury to the lower respiratory tract. They have also provided evidence of continual pathological sequelae occurring long after withdrawal from asbestos exposure.     

间皮细胞检测在胸腔积液诊断中的临床应用

目的 探讨间皮细胞检测在胸腔积液诊断中的临床应用.方法 对36例恶性胸腔积液患者(恶性组)和24例良性胸腔积液患者(良性组)胸腔积液进行间皮细胞检测,判定其在良、恶性胸腔积液中的诊断价值.结果 恶性组未出现间皮细胞消失病例,间皮细胞所占百分比＜1％者1例(2.78％),1％～5％者1例(2.78％),＞5％者34例(94.44％).良性组11例(45.83％)未发现间皮细胞,间皮细胞所占百分比＜1％者8例(33.33％),1％～5％者2例(8.33％),＞5％者3例(12.50％).两组间皮细胞所占百分比比较差异有统计学意义(x2=43.4069,P＜0.01).良、恶性组间皮细胞所占百分比95％可信区间分别为0.28％～5.10％、5.13％ ～ 10.91％,两组可信区间没有相互重叠,因此以胸腔积液间皮细胞所占百分比＞5％作为鉴别良、恶性胸腔积液的标准,其敏感度为94.44％(34/36)、特异度为87.50％(21/24)、准确度为91.67％(55/60).结论 间皮细胞所占百分比是一种简单、易行、经济、快捷诊断良、恶性胸腔积液的方法,具有较高的敏感度、特异度和准确度,在临床诊断中有一定的参考价值.     

Effect of chrysotile asbestos fibers on germ cells of mice

An Indian form of chrysotile asbestos procured from a local asbestos factory (Hyderabad) was tested for its toxic effects on spermatocytes and sperm of mice. Swiss albino male mice were fed orally with chrysotile asbestos suspended in water. The concentration tested was 20 mg/kg/day. Chronic oral administration of chrysotile failed to induce chromosomal aberrations and abnormal sperms in mice.     

Natural history of pleural thickening after exposure to crocidolite.

Serial plain chest radiographs of 384 men who worked at the Wittenoom crocidolite mine and mill between 1943 and 1966 and who applied for pneumoconiosis compensation between 1948 and 1982 have been examined independently by two trained observers for pleural disease using the 1980 ILO-UICC classification of radiographs to record width and extent of pleural disease. Radiographs covering follow up periods of from two to 38 years were examined (median number of films per subject was nine). The degree of crocidolite exposure was estimated from employment records and a survey of airborne fibre concentrations performed in 1966. Agreement between the observers on the presence and degree of pleural disease in the final film for each subject was moderately close (Kendall's tau B = 0.62) and was least for subjects with thickening less than 5 mm in width. Diffuse pleural thickening extending for greater than 50% of the lateral chest wall was the most common type recorded by both observers. Minor pleural thickening frequently progressed in extent along the lateral chest wall but progression beyond 5 mm in thickness was less common. Pleural plaques were not seen to progress beyond their initial thickness or extent. The rate of onset of thickening in this population increased continually from the time of first exposure and also increased slightly with age. There was evidence that the level of total cumulative exposure to crocidolite increased the rate of onset of pleural thickening in the period between five and 15 years after first exposure. Rate of progression of established thickening was greatest in subjects who first developed thickening early after first exposure. The relative rate of progression decreased slowly with time from first signs of thickening and there was no evidence of any progression more than 15 years after onset.     

Production of interleukin 1 by rat pleural leucocytes in culture after intratracheal instillation of crocidolite asbestos.

This study was undertaken to investigate the production of interleukin 1 (IL-1) by pleural leucocytes in culture and to evaluate the influence of intratracheal instillation of crocidolite asbestos on this production. Normal pleural leucocytes spontaneously released IL-1 in culture and stimulation with lipopolysaccharide (LPS) dramatically increased production. Intratracheal instillation with crocidolite asbestos induced recruitment of pleural leucocytes in the longer term and changed IL-1 production by the leucocytes. Reduced production of IL-1 was found by one day after instillation of asbestos and this was correlated with the dose of asbestos. With increasing time after instillation, however, release of IL-1 by pleural leucocytes gradually recovered to normal until, one month after asbestos injection, the leucocytes produced augmented IL-1 in culture compared with control pleural leucocytes. Our data show that pleural leucocytes possess the potential to produce IL-1 in vitro and this capability is altered by intratracheal instillation of crocidolite asbestos. This may be relevant to development of pleural diseases associated with inhalation of asbestos.     

Effect of crocidolite fibers on the cathepsin B-like enzyme activity in HL-60 cells]

In a previous study, we found that crocidolite (an asbestos fiber) had an inhibitory effect on the differentiation process of HL-60 cells induced by dimethyl sulfoxide (DMSO). Here we describe the cathepsin B-like enzyme HL-60 cells and the changes of its activity during cell differentiation with or without crocidolite treatment. The cathepsin B-like enzyme in HL-60 cell extracts had almost the same characteristics and the already known cathepsin B as for the pH optima and the effects of proteinase inhibitors. The cathepsin B-like enzyme activity increased according to the cell differentiation induced by DMSO, however, its activity was depressed by crocidolite treatment.