Journal of Applied Toxicology

Our medical research library holds 17 studies published in Journal of Applied Toxicology (1983–2024). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 17 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it.

About the journal

• Publisher: John Wiley And Sons
• Published: 1981 to the present, England
• Language: English
• ISSN: 0260-437X (print), 1099-1263 (electronic)
• Its record in the NLM Catalog

2020s

• Toxicity and inflammatory potential of mineral fibres: The contribute of released soluble metals versus cell contact direct effects. V. Almonti, S. Vernazza, S. Mirata, et al. 2024;44(8):1166-1183. PubMed · Publisher

  Abstract

  Asbestos fibres have been considered an environmental hazard for decades. However, little is known about the attempts of circulating immune cells to counteract their toxicity. We addressed the early effects of fibre-released soluble factors (i.e. heavy metals) in naïve immune cells, circulating immediately below the alveolar/endothelial cell layer. By comparison, the direct fibre effects on endotheliocytes were also studied since these cells are known to sustain inflammatory processes. The three mineral fibres analysed showed that mainly chrysotile (CHR) and erionite (ERI) were able to release toxic metals in extracellular media respect to crocidolite (CRO), during the first 24 h. Nevertheless, all three fibres were able to induce oxidative stress and genotoxic damage in indirectly challenged naïve THP-1 monocytes (separated by a membrane). Conversely, only CHR-released metal ions induced apoptosis, NF-κB activation, cytokines and CD163 gene overexpression, indicating a differentiation towards the M0 macrophage phenotype. On the other hand, all three mineral fibres in direct contact with HECV endothelial cells showed cytotoxic, genotoxic and apoptotic effects, cytokines and ICAM-I overexpression, indicating the ability of these cells to promote an inflammatory environment in the lung independently from the type of inhaled fibre. Our study highlights the different cellular responses to mineral fibres resulting from both the nature of the cells and their function, but also from the chemical-physical characteristics of the fibres. In conclusion, CHR represented the main pro-inflammatory trigger, able to recruit and activate circulating naïve monocytes, through its released metals, already in the first 24 h after inhalation.

  © 2024 John Wiley & Sons Ltd.

• Characteristics of transcription profile, adhesion and migration of SETD2-loss Met-5A mesothelial cells exposed with crocidolite. D. Yang, C. Chen, H. Xia, et al. 2023;43(10):1511-1521. PubMed · Publisher

  Abstract

  Asbestos is a fibrous silicate mineral exhibiting biopersistence and carcinogenic properties and contributes to mesothelioma. Despite the concept of gene-environmental interaction in pathogenesis of mesothelioma, the possible pathophysiological changes of mesothelial cells simultaneously with SET domain containing 2 (SETD2) loss and asbestos exposure remains obscure. Herein, CRISPR/Cas9-mediated SETD2 knockout Met-5A mesothelial cells (Met-5ASETD2-KO ) were established and exposed with crocidolite, an amphibole asbestos. Cell viability of Met-5ASETD2-KO appeared to dramatically decrease with ≥2.5 μg/cm2 crocidolite exposure as compared with Met-5A, although no cytotoxicity and apoptosis changes of Met-5ASETD2-KO and Met-5A was evident with 1.25 μg/cm2 crocidolite exposure for 48 h. RNA sequencing uncovered top 50 differentially expressed genes (DEGs) between 1.25 μg/cm2 crocidolite exposed Met-5ASETD2-KO (Cro-Met-5ASETD2-KO ) and 1.25 μg/cm2 crocidolite exposed Met-5A (Cro-Met-5A), and ITGA4, THBS2, MYL7, RAC2, CADM1, and CLDN11 appeared to be the primary DEGs involved with adhesion in gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Cro-Met-5ASETD2-KO had strong migration but mild adhesion behavior as compared with Cro-Met-5A. Additionally, crocidolite tended to increase migration of Met-5ASETD2-KO but inhibited migration of Met-5A when compared with their corresponding cells without crocidolite exposure, although no further adhesion property changes was evident for both cells in response to crocidolite. Therefore, crocidolite may affect adhesion-related gene expression and modify adhesion and migration behavior for SETD2-depleted Met-5A, which could provide preliminary insight regarding the potential role of SETD2 in the cell behavior of asbestos-related malignant mesothelial cell.

  © 2023 John Wiley & Sons Ltd.

• Mortality of workers employed in refractory ceramic fiber manufacturing: An update. G. LeMasters, J.E. Lockey, T.J. Hilbert, et al. 2022;42(7):1287-1293. PubMed · Publisher

  Abstract

  This study evaluates the possible association between refractory ceramic fiber (RCF) exposure and all causes of death. Current and former employees (n = 1,119) hired from 1952 to 1999 at manufacturing facilities in New York (NY) state and Indiana were included. Work histories and quarterly plant-wide sampling from 1987 to 2015 provided cumulative fiber exposure (CFE) estimates. The full cohort was evaluated as well as individuals with lower and higher exposure, <45 and ≥45 fiber-months/cc. The Life-Table-Analysis-System was used for all standardized mortality rates (SMRs). Person-years at risk were accumulated from start of employment until 12/31/2019 or date of death. There was no significant association with all causes, all cancers, or lung cancer in any group. In the higher exposed, there was a significant elevation in both malignancies of the "urinary organs" (SMR = 3.59, 95% confidence interval [CI] 1.44, 7.40) and "bladder or other urinary site" (SMR = 4.04, 95% CI 1.10, 10.36), which persisted in comparison to regional mortality rates from NY state and Niagara County. However, six of the nine workers with urinary cancers were known smokers. In the lower exposed, there was a significant elevation in malignancies of the lymphatic and hematopoietic system (SMR = 2.54, 95% CI 1.27, 4.55) and leukemia (SMR = 4.21, 95% CI 1.69, 8.67). There was one pathologically unconfirmed mesothelioma death. A second employee currently living with a pathologically confirmed mesothelioma was identified, but the SMR was non-significant when both were included in the analyses. The association of these two mesothelioma cases with RCF exposure alone is unclear because of potential past exposure to asbestos.

  © 2022 John Wiley & Sons, Ltd.

• A nontoxic dose of chrysotile can malignantly transform Met-5A cells, in which microRNA-28 has inhibitory effects. F. Zhang, X. Yuan, H. Sun, et al. 2021;41(11):1879-1892. PubMed · Publisher

  Abstract

  Chrysotile, which is classified as a class I carcinogen by the International Agency for Research on Cancer (IARC), has extensive application in the industry and can lead to lung or other cancers. However, whether chrysotile causes malignant mesothelioma and its molecular mechanism remain debatable. Thus, this study aimed to demonstrate the mesothelioma-inducing potential of chrysotile at the mesothelial cellular level and the function of microRNA-28 in malignantly transformed mesothelial MeT-5A cells. MeT-5A cells malignantly transformed by a nontoxic dose of chrysotile were named Asb-T, and miR-28 expression was downregulated in Asb-T cells. Restoration of miR-28 expression inhibited the proliferation, migration and invasion of Asb-T cells. We verified that IMPDH is a putative target of miR-28. The expression of IMPDH was significantly higher in Asb-T MeT-5A cells than in control cells, whereas the opposite trend was observed with miR-28 overexpression. Additionally, inhibition of IMPDH had similar effects as miR-28 overexpression. After miR-28 was elevated or IMPDH was inhibited, Ras activation was reduced, and its downstream pathways (the Erk and Akt signalling pathways) were inhibited. Surprisingly, the content of miR-28 in the blood of mesothelioma patients was higher than that in control subjects. Overall, nontoxic doses of chrysotile can cause malignant transformation of MeT-5A cells. Moreover, miR-28 inhibits the proliferation, migration and invasion of Asb-T MeT-5A cells, negatively regulates the expression of IMPDH through the Ras signalling pathway and may be an important therapeutic target.

  © 2021 John Wiley & Sons, Ltd.

• Using benchmark dose modeling for the quantitative risk assessment: Carbon nanotubes, asbestos, glyphosate. A. Korchevskiy. 2021;41(1):148-160. Case report · Review PubMed · Publisher

  Abstract

  Benchmark dose method is one of the most famous quantitative approaches available for toxicological risks prediction. However, it is not fully clear how occupational health professionals can use it for specific workplace scenarios requiring carcinogen risk assessment. The paper explores the hypothesis that benchmark dose method allows to effectively approximate dose-response data on carcinogenic response, providing reasonable estimations of risks in the situations when a choice between more complex models is not warranted for practical purposes. Three case studies were analyzed for the agents with different levels of scientific confidence in human carcinogenicity: carbon nanotubes, amosite asbestos, and glyphosate. For each agent, a critical study was determined, and a dose-response slope factor was quantified, based on the weighted average lower bound benchmark dose. The linear slope factors of 0.111 lifetime excess cases of lung carcinoma per mg/m3 of MWCNT-7 (in rats exposure equivalent), 0.009 cases of mesothelioma per f/cc-years of cumulative exposure to amosite asbestos, and 0.000094 cases of malignant lymphoma per mg/kg/day of glyphosate (in mice equivalent) were determined. The correlations between the proposed linear predictive models and observed data points were R = 0.96 (R2 = 0.92) for carbon nanotubes, R = 0.97 (R2 = 0.95) for amosite asbestos, and R = 0.89 (R2 = 0.79) for glyphosate. In all three cases, the linear extrapolation yielded comparable level of risk estimations with the "best fit" nonlinear model; for nanoparticles and amosite asbestos, linear estimations were more conservative. By performing a simulation study, it was demonstrated that a weighted average benchmark dose expressed the highest correlation with multistage and quantal-linear models.

  © 2020 John Wiley & Sons, Ltd.

• Modeling mesothelioma risk factors from amphibole fiber dimensionality: mineralogical and epidemiological perspective. A.G. Wylie, A. Korchevskiy, A.M. Segrave, et al. 2020;40(4):515-524. PubMed · Publisher

  Abstract

  Amphiboles are common rock-forming minerals but when they form asbestos, they are known carcinogens. Mesothelioma mortality among miners and millers per the unit of asbestiform amphibole exposure varies significantly across cohorts when asbestos exposure measurements are based on the membrane filter method. Because the cohorts were exposed to different occurrences of asbestiform amphibole, variance in mesothelioma potency (RM ) among cohorts is likely due to differences in exposure characteristics not reflected by the membrane filter method. In this paper using both linear and nonlinear models we correlate RM from four mining and milling cohorts with two-dimensional parameters of the exposure. The parameters are based on the proportion of elongated minerals that are >5 μm in length from each occurrence that also have either (a) width ≤ 0.15 μm, or (b) width ≤ 0.25 μm. Based on the models we derived, it was possible to quantify RM for the occurrences of asbestiform amphibole associated with mesothelioma excess but for which epidemiologically based RM has not been published. It was demonstrated that modeled RM for amphibole occurrences in nonasbestiform habits are lower (fibrous glaucophane) or not significant (cleavage fragments). The results of the study can be used in a risk assessment of elongated mineral particles and have implications for public policy and regulations.

  © 2020 John Wiley & Sons, Ltd.

2010s

• Size-dependent superparamagnetic iron oxide nanoparticles dictate interleukin-1β release from mouse bone marrow-derived macrophages. S. Chen, S. Chen, Y. Zeng, et al. 2018;38(7):978-986. PubMed · Publisher

  Abstract

  Superparamagnetic iron oxide nanoparticles (SPIONs) have been widely investigated for their biomedical applications in magnetic resonance imaging, targeting therapy, cell labeling, etc. It has been well documented that macrophages produce interleukin (IL)-1β via several signaling pathways, such as inflammasome activation in response to particles including silica, asbestos and urea crystals with lipopolysaccharide priming. However, the size and dose effects of SPIONs on macrophages and the mechanisms remain unclear. In this study, we explored the cytotoxicity and mechanisms of the synthesized SPIONs with different size distributions of 30, 80 and 120 nm, and compared their potential capability in inducing IL-1β release in mouse bone marrow-derived macrophages (BMMs). We found that SPIONs induced IL-1β release in a size- and dose-dependent manner, in which the smallest SPIONs triggered the highest IL-1β in BMMs. When cellular uptake of SPIONs was inhibited by the actin polymerization inhibitor, cytochalasin D, SPION-induced IL-1β release was suppressed in BMMs. Preventing lysosome damage with bafilomycin A1 or CA-074-Me also counteracted SPION-induced IL-1β release. Moreover, SPION-activated IL-1β release was also attenuated by reactive oxygen species scavengers, diphenylene iodonium or N-acetylcysteine. Our results elucidated the effects of size and dose on the cytotoxicity and mechanisms of IL-1β release of SPIONs on macrophages, which facilitate the theoretical and experimental application of SPIONs in biotechnology and biomedicine in the future.

  Copyright © 2018 John Wiley & Sons, Ltd.

• Anthophyllite asbestos: state of the science review. S.H. Gaffney, M. Grespin, L. Garnick, et al. 2017;37(1):38-49. Review PubMed · Publisher

  Abstract

  Anthophyllite is an amphibole form of asbestos historically used in only a limited number of products. No published resource currently exists that offers a complete overview of anthophyllite toxicity or of its effects on exposed human populations. We performed a review focusing on how anthophyllite toxicity was understood over time by conducting a comprehensive search of publicly available documents that discussed the use, mining, properties, toxicity, exposure and potential health effects of anthophyllite. Over 200 documents were identified; 114 contained relevant and useful information which we present chronologically in this assessment. Our analysis confirms that anthophyllite toxicity has not been well studied compared to other asbestos types. We found that toxicology studies in animals from the 1970s onward have indicated that, at sufficient doses, anthophyllite can cause asbestosis, lung cancer and mesothelioma. Studies of Finnish anthophyllite miners, conducted in the 1970s, found an increased incidence of asbestosis and lung cancer, but not mesothelioma. Not until the mid-1990s was an epidemiological link with mesothelioma in humans observed. Its presence in talc has been of recent significance in relation to potential asbestos exposure through the use of talc-containing products. Characterizing the health risks of anthophyllite is difficult, and distinguishing between its asbestiform and non-asbestiform mineral form is essential from both a toxicological and regulatory perspective. Anthophyllite toxicity has generally been assumed to be similar to other amphiboles from a regulatory standpoint, but some notable exceptions exist. In order to reach a more clear understanding of anthophyllite toxicity, significant additional study is needed. Copyright © 2016 John Wiley & Sons, Ltd.

  Copyright © 2016 John Wiley & Sons, Ltd.

2000s

• Pulmonary toxicity of wollastonite in vivo and in vitro. E. Tátrai, Z. Kováciková, M. Brózik, et al. 2004;24(2):147-54. PubMed · Publisher

  Abstract

  Pulmonary toxicity of wollastonite has been studied in both in vivo long-term sequential and in vitro methods in Sprague-Dawley rats. Wollastonite was administered by intratracheal instillation and the lungs were examined after 1, 3 and 6 months by morphological methods. UICC crocidolite was applied as the positive control. In addition, the effects of both fibres were examined in primary cultures of pulmonary alveolar macrophages and type II pneumocytes to determine the effects of the fibres on the membranes of these cells, the activity of Cu,Zn/superoxide dismutase and the redox system and the release of proinflammatory peptides: macrophage chemoattractant protein-1 (MCP-1) and macrophage inhibitory protein-1alpha (MIP-1alpha). By the end of six months wollastonite had induced mild pulmonary interstitial fibrosis, whereas crocidolite induced progressive interstitial fibrosis as a function of time. The membranes of macrophages and pneumocytes were disrupted at the lowest concentration of crocidolite. The activity of enzymes of the redox system and cytoplasmic superoxide dismutase significantly decreased with crocidolite. Wollastonite decreased only the activity of gamma-glutamyl transpeptidase and glutathione peroxidase. Crocidolite induced expression of the proinflammatory peptides at the lowest concentration (1 micro g ml(-1)) but wollastonite increased production of these peptides only at medium and high concentrations (5 and 10 micro g ml(-1)). These results underline the importance of further human epidemiological studies and the need for the determination of a hygienic standard.

  Copyright 2004 John Wiley & Sons, Ltd.

• Pulmonary and intraperitoneal inflammation induced by cellulose fibres. R.T. Cullen, A. Searl, B.G. Miller, et al. 2000;20(1):49-60. PubMed · Publisher

  Abstract

  The inflammatory effects of respirable cellulose fibres were studied in two short-term animal models: intraperitoneal injection in mice, and inhalation in rats. The mouse peritoneal cavity is particularly sensitive to fibrous compared to non-fibrous particles. Both cellulose fibres and the positive control fibre, crocidolite asbestos, were administered in doses ranging from 10(4) to 10(8) fibres and caused marked, dose-dependent recruitment of inflammatory cells to the mouse peritoneal cavity, which was highest 1 day following injection. Crocidolite was much more active than cellulose, despite the mass dose of cellulose being 66 times greater for an equivalent number of fibres. Crocidolite at the higher doses caused inflammation to persist through 7 days. For the inhalation study, rats were exposed daily, 5 days per week, to aerosols of cellulose dust for ca. 3 weeks at a concentration of 1000 fibres ml(-1). Inhalation exposure induced an early inflammatory response in rat lungs, as determined by bronchoalveolar lavage, which peaked at 1 day following the start of inhalation and thereafter declined, despite a further 13 days of exposure over a period of 18 calendar days. In vitro production of the pro-inflammatory cytokine tumour necrosis factor alpha (TNF-alpha) by lavaged alveolar macrophages was markedly depressed by the end of the exposure period in cellulose-exposed animals, compared to sham-exposed controls, and this effect was still present in rats that had been allowed to recover for 28 days beyond the end of exposure. We conclude that the cellulose material studied is less inflammogenic than crocidolite and that the extent of the inflammatory response within the lung appears to reduce with continued exposure over a 14-day period.

  Copyright 2000 John Wiley & Sons, Ltd.

1990s

• In vivo pulmonary toxicity of cellulose in rats. E. Tátrai, M. Brozik, Z. Adamis, et al. 1996;16(2):129-35. PubMed · Publisher

  Abstract

  Cellulose after a single intratracheal dose (15 mg per animal) brought about fibrosing granulomatous alveobronchiolitis and an increase of IgA production in the bronchoalveolar lavage. Fibrosing alveolitis showed moderate progression as a function of time. With different morphological methods, injury of type I pneumocytes and the incomplete repair of type II pneumocytes were detected. The damage of the alveolar epithelium initiated and activated a series of processes that led to definite pulmonary alterations: pulmonary fibrosis leading to the disintegration of the alveolo-capillary morphological functional unit.

• Nitric oxide (NO) synthase activity in the lung and NO synthesis in alveolar macrophages of rats increased on exposure to asbestos. H. Iguchi, S. Kojo, M. Ikeda. 1996;16(4):309-15. PubMed · Publisher

  Abstract

  We examined whether the lung of rats induced nitric oxide synthase (NOS) on instillation of Union Internationale Contre le Cancer (UICC) asbestos into the trachea, and whether alveolar macrophages (M phi s) of rats increased synthesis of nitric oxide (NO) on exposure to the asbestos. Instillation of chrysotile asbestos (CH) into rat tracheas increased NOS activity in the lung up to fourfold compared with that of normal control rats. On instillation of amosite asbestos (AM), the activity did not significantly increase. In the culture of alveolar M phi s with CH, NO2-, a stable oxidation product of NO, in the conditioned medium markedly increased while in the culture with AM or crocidolite (CR) asbestos it was comparable to that in the control culture without asbestos. Thus, it was assumed that the lung as well as alveolar M phi s induced NOS on exposure to CH. Viability of M phi s was lower in the culture with CH than in the culture with AM or CR. When alveolar M phi s were cultured in the presence of lipopolysaccharide (LPS), a potent inducer of NOS, NO2- in the medium dramatically increased, indicating a possible induction of NOS, while NO2- was decreased significantly in the presence of both LPS and CH, AM or CR. On the other hand, when M phi s which had previously been stimulated with LPS were cultured in LPS-free medium, NO2- synthesis retained a significantly increased level, irrespective of the presence or absence of asbestos. Thus, the three kinds of asbestos used seemed to interfere with LPS in inducing NOS and to decrease subsequently the synthesis of NO2-, but not to affect the synthesis of NO2- by LPS-induced NOS. Taken altogether, lung or alveolar M phi s of rats induced NOS to increase NO synthesis on exposure to CH.

• Red blood cell damage by wollastonite: in vitro study. M. Aslam, M.J. Arif, O. Rahman. 1995;15(1):27-31. PubMed · Publisher

  Abstract

  Asbestos is known to cause lung diseases in occupationally exposed workers. These properties have restricted its use. Industries have been exploring the possibility of other mineral fibres to replace the asbestos. In this direction, wollastonite has gained great attention owing to its high thermal resistance. In the present paper, the toxicity of three samples of Indian wollastonite was compared to that of chrysotile. Dust suspensions were added to the red blood cell suspensions to obtain a final dust concentration of 1.0-5.0 mg ml-1 in the system. The wollastonite varieties were found to have smaller haemolytic potential in human red blood cells than that of chrysotile in vitro. Chrysotile also was more effective in inducting peroxidative damage of polyunsaturated fatty acid (PUFA) than wollastonites in the present system. The peroxidative damage of PUFA and the haemolysis were both time and dose dependent. A higher value of malonaldehyde (a lipid peroxidation product) formation in low-speed supernatant of haemolysate was observed than in the intact cells. As the free-radical scavengers vitamin E and reduced glutathione prevent haemolysis and lipid peroxidation, these data are consistent with the involvement of lipid peroxidation in the haemolytic process.

• Lipid peroxidation and disintegration of the cell membrane structure in cultures of rat lung fibroblasts treated with asbestos. H. Iguchi, S. Kojo, M. Ikeda. 1993;13(4):269-75. PubMed · Publisher

  Abstract

  Rat lung fibroblasts were cultured for 24 and 48 h with UICC standard reference asbestos samples of amosite, crocidolite or Canadian chrysotile at various concentrations, and thiobarbituric acid-reactive substances (TBARS) in the media and the cells were measured. Tests by the trypan blue dye-exclusion method showed that cell viability was 80 +/- 5% (mean +/- SD) and 71 +/- 6% when cultured for 48 h in the presence of 500 micrograms ml-1 of amosite and crocidolite, respectively, but was not affected by chrysotile. In cultures for 24 and 48 h, both chrysotile and crocidolite at > 250 micrograms ml-1 significantly increased TBARS in the medium, whereas amosite did so at > 500 micrograms ml-1. TBARS in the cells was not increased significantly by chrysotile at any concentration in the cultures for 24 and 48 h, but crocidolite at > 250 micrograms ml-1 significantly increased TBARS in the cells when cultured for 24 or 48 h. Although amosite at all concentrations tested did not increase significantly TBARS in the cells of the 24-h culture, it did increase TBARS significantly in the cells when cultured for 48 h at a concentration of 500 micrograms ml-1 amosite. The increases of TBARS in media of the cultures with asbestos were accompanied by increases of lactate dehydrogenase (LDH) activity in the media, indicating the leakage of the enzyme from the cell into the media. The activity of LDH and the amount of TBARS showed a good correlation with each other, with a significant correlation coefficient value of 0.655.(ABSTRACT TRUNCATED AT 250 WORDS)

1980s

• A protocol to evaluate the fibrogenic potential of inhaled materials. I.P. Bennett, G.H. Pigott, K. Isaacs. 1988;8(6):423-9. PubMed · Publisher

  Abstract

  A protocol to provide a more rapid assessment of the fibrogenic potential of an inhaled particulate has been developed. Young rats are exposed nose-only for 6 h/day, 7 days a week for 28 days to a respirable aerosol of the test compound. After exposure the rats are kept for up to 1 year, followed by histopathological assessment of the lung. Interim sacrifices could allow an estimate of the rate and severity of the development of any fibrogenic lesion. The protocol has been evaluated for chrysotile asbestos, alpha-quartz and titanium dioxide using rats of both sexes and two different ages at first exposure. The results indicate that there are no significant differences in either the rate, type or extent of lesion provoked by a 28-day exposure period when compared with the more conventional 1-year exposure period studies. It can be concluded that neither sex nor age at first exposure cause any biologically significant differences in response, although young rats would be used in practice. Only one sex need be investigated. The protocol offers considerable benefits over conventional inhalation studies for fibrogenicity (where a 1-year exposure period followed by a further 1-year holding period is usual) by virtue of time, specificity (in the absence of continued exposure the development of any lesion can be studied free from initial inflammatory response) and cost, and could be incorporated into a standard subacute inhalation study design. The results obtained are also of more physiological relevance than studies based on intratracheal instillation.

• Interrelationship between hemolysis and lipid peroxidation of human erythrocytes induced by silicic acid and silicate dusts. S.V. Singh, Q. Rahman. 1987;7(2):91-6. PubMed · Publisher

  Abstract

  Silicic acid and silicate dusts (slate dust and chrysotile asbestos) cause hemolysis of erythrocytes in vitro. The peroxidation of polyunsaturated fatty acids (PUFA) of erythrocyte membrane lipids is also enhanced by incubating the erythrocytes with silicic acid and silicate dusts in in vitro. Hemolysis of erythrocytes elicited by silicic acid and silicate dusts is inhibited significantly by polyvinyl-pyrrolidone and dipalmitoyl lecithin (DPL). These agents, however, have no effect on silicic acid and silicate dust induced peroxidation of erythrocyte membrane lipids. On the other hand, peroxidation of erythrocyte membrane lipids, induced by silicic acid and silicate dusts, is inhibited almost completely by adding superoxide dismutase and catalase to the incubation system, whilst the hemolysis of erythrocytes induced by silicic acid and silicate dusts is unaffected by these agents. Similarly the lysis of erythrocytes, induced by silicic acid and silicate dusts, proceeds at a much faster rate than silicic acid and silicate dust induced lipid peroxidation. These results indicate that silicic acid and silicate dust induced hemolysis and lipid peroxidation represent two independent processes.

• Binding of silicic acid by proteins and its relation to toxicity of silicate dusts. V. Misra, Q. Rahman, P.N. Viswanathan. 1983;3(3):135-8. PubMed · Publisher

  Abstract

  A possible mechanism of biological effects of silicate dusts is the interaction between silicic acid and tissue constituents, and this has been studied in vitro. On incubating silicic acid with lung homogenate, appreciable amounts of silicon were recovered in the trichloroacetic acid precipitate in both organic solvent extract and residual protein. Polyvinyl pyrrolidone inhibited this interaction as well as reducing the dissolution of silicic acid from asbestos dust. The capacity of serum albumin to bind silicic acid was also observed. Chemical interaction between macromolecules and silicic acid could be one of the factors responsible for the biological effects of silicon-containing dusts.

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