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PubMed2004

Crystalline silica induces apoptosis in human endothelial cells in vitro.

We investigated whether incubation of cultured human aortic endothelial cells (HAEC) with crystalline silica at the concentration 1 cm2/ml (chosen on the basis of a pilot experiment) leads to alterations typical of apoptosis. The binding of annexin V as early, and DNA fragmentation as late events of apoptosis were measured besides the number of cells with depolarized mitochondria. The generation of reactive oxygen species (ROS) by HAEC in presence of silica was determined as well as silica ability to in vitro generate hydroxyl radicals was investigated. After 18 h of silica incubation, about 30% of viable cells bound annexin V. After 24 h of silica treatment, the percentage of cells with fragmented DNA (Tunel positive) was 27% and it increased up to 50% after 48 h, whereas in untreated cells this percentage was 7% and 11% after 24 and 48 h, respectively. The presence of fragmented DNA in cells treated with silica was confirmed by agarose gel electrophoresis. In agreement with these results showing an induction of HAEC apoptosis by silica incubation, the number of cells with depolarized mitochondria was significantly higher after silica treatment as compared to the control. Apoptosis was also obtained with silica added to aliquots of anti-C5a-absorbed-medium. In the cells exposed to silica there was a significant increasing of ROS generation in comparison to the untreated cells. Apoptosis might be due to peroxidative stress since silica can generate hydroxyl radicals.

Annexin A5↗
PubMed2003

Silica accelerated systemic autoimmune disease in lupus-prone New Zealand mixed mice.

The genetic backgrounds of lupus-prone murine models are a valuable resource for studying the influence of environmental exposure on autoimmune diseases in sensitive populations. Epidemiological studies have shown associations between silica exposure and several autoimmune diseases, including scleroderma and systemic lupus erythematosus. To determine whether silica exposure can exacerbate systemic autoimmunity in genetically predisposed animals, New Zealand mixed mice were intranasally instilled twice with saline or saline suspensions of 1 mg silica or 500 micro g TiO2, a dose equivalent in surface area, and were evaluated with respect to health and immune status. Survival in silica exposed NZM mice was decreased compared to saline and TiO2 exposed mice. Proteinuria levels were elevated in silica exposed mice. Levels of circulating immune complexes, autoantibodies to nuclear antigen (ANA), histone, and double stranded DNA were measured every two weeks by ELISA. Circulating immune complexes showed a trend towards an increased acceleration in levels in the silica exposed mice compared to saline and TiO2 exposed mice. ANA levels were significantly higher in silica exposed animals compared to saline and TiO2 exposed animals (0.237 +/- 0.03 versus 0.140 +/- 0.029 and 0.125 +/- 0.03, P < 0.05) 16 weeks postexposure. Autoantibodies to histone were also significantly elevated after 16 weeks in silica exposed animals compared to saline and TiO2 exposed animals (0.227 +/- 0.03 versus 0.073 +/- 0.015 and 0.05 +/- 0.03, P < 0.05). In contrast, serum IgG levels were decreased in silica exposed NZM mice compared to the saline controls, however, IgM levels were unaffected. Lungs of the silica-exposed mice had increased inflammatory infiltrates as well as fibrotic lesions characterized by excess collagen deposition. Therefore, although NZM mice are susceptible to SLE, silica exposure significantly exacerbated the course of disease.

Animals↗
PubMed2000

Induction of activator protein-1 through reactive oxygen species by crystalline silica in JB6 cells.

We reported previously that freshly fractured silica (FFSi) induces activator protein-1 (AP-1) activation through extracellular signal-regulated protein kinases (ERKs) and p38 kinase pathways. In the present study, the biologic activities of FFSi and aged silica (ASi) were compared by measuring their effects on the AP-1 activation and phosphorylation of ERKs and p38 kinase. The roles of reactive oxygen species (ROS) in this silica-induced AP-1 activation were also investigated. We found that FFSi-induced AP-1 activation was four times higher than that of ASi in JB6 cells. FFSi also caused greater phosphorylation of ERKs and p38 kinase than ASi. FFSi generated more ROS than ASi when incubated with the cells as measured by electron spin resonance (ESR). Studies using ROS-sensitive dyes and oxygen consumption support the conclusion that ROS are generated by silica-treated cells. N-Acetylcysteine (an antioxidant) and polyvinyl pyridine-N-oxide (an agent that binds to Si-OH groups on silica surfaces) decreased AP-1 activation and phosphorylation of ERKs and p38 kinase. Catalase inhibited phosphorylation of ERKs and p38 kinase, as well as AP-1 activation induced by FFSi, suggesting the involvement of H(2)O(2) in the mechanism of silica-induced AP-1 activation. Sodium formate (an ( small middle dot)OH scavenger) had no influence on silica-induced MAPKs or AP-1 activation. Superoxide dismutase enhanced both AP-1 and MAPKs activation, indicating that H(2)O(2), but not O(2), may play a critical role in silica-induced AP-1 activation. These studies indicate that freshly ground silica is more biologically active than aged silica and that ROS, in particular H(2)O(2), play a significant role in silica-induced AP-1 activation.

Animals↗
PubMed1998

Regulation of nitric oxide production by rat alveolar macrophages in response to silica exposure.

In the present study, it was confirmed that in vivo exposure of rats to silica significantly increases nitric oxide (NO) production by bronchoalveolar lavage cells (BALC), a population of cells that includes alveolar macrophages. Possible mechanisms whereby NO production could be upregulated by rat alveolar macrophages following silica exposure were examined to determine if there is a direct effect of silica on alveolar macrophage NO production or if other factors are involved. BALC were obtained from normal male rats and cultured for 2 h. Nonadherent cells were then removed and the enriched alveolar macrophage cell populations were exposed to test agents for 18-20 h. Media nitrate and nitrite (NOx) concentrations were used to assess NO production and, in some cases, inducible NO synthase mRNA levels were indexed. In vitro exposure to silica (0.1-100 micrograms/ml) had no significant effect on basal NO levels. Furthermore, NO generation was not additionally increased above levels induced by interferon gamma (IFN), lipopolysaccharide (LPS), or other cytokines during simultaneous incubations with silica and IFN, a 2-h pretreatment with silica followed by IFN, or preincubation with IFN, LPS, and/or other cytokines before the addition of silica. To evaluate whether cell-cell interactions might be required for the induction of NO production during silica challenge, alveolar macrophages were cultured with splenic lymphocytes or blood-derived polymorphonuclear leukocytes. Coculture of splenic lymphocytes with alveolar macrophages resulted in media NOx levels that were greater than the additive levels from each cell type. However, the presence of silica was without additional effect on NO production by either of these cell types. Furthermore, it was found that conditioned media, derived from adherent BALC following silica treatment in vivo, could induce NO production by naive alveolar macrophages. In summary, the collective results from these experiments suggest that cell-cell communication factors, involving the interaction of pneumocytes following in vivo silica exposure, are necessary for the induction of NO by alveolar macrophages.

Animals↗
PubMed1999

Use of tetrandrine to differentiate between mechanisms involved in silica-versus bleomycin-induced fibrosis.

Animals exposed to silica or bleomycin (BLM) develop pulmonary fibrosis. Tetrandrine (TT) has been shown to inhibit stimulant-induced macrophage respiratory burst and effectively reduce silica-induced lung injury. The present study employed TT as a probe to assess the differences in mechanisms involved in silica- and BLM-induced pulmonary responses. Rats received a single intratracheal instillation of silica (40 mg/rat, sacrificed 4 wk postexposure) or BLM (1 mg/kg or approximately 0.25 mg/rat, sacrificed up to 2 wk postexposure). TT was administered orally at 18 mg/kg, 3 times/wk for desired time periods beginning 5 d before silica or BLM exposure. Both the silica and BLM exposures resulted in a significant increase in lung weight, total protein, lactate dehydrogenase (LDH), and phospholipids (PL) content in the acellular fluid from the first lavage, and hydroxyproline content in the lung tissue. Alveolar macrophages (AM) isolated from rats exposed to silica or BLM exhibited significant increases in secretion of interleukin-1 (IL-1), tumor necrosis factor alpha (TNF-alpha), and transforming growth factor beta (TGF-beta). TT treatment significantly lowered the silica- or BLM-induced increase in lung weight, while marginally reducing the release of IL-1 and TNF-alpha by AM. TT, however, markedly inhibited the silica-induced increase in the acellular protein, LDH and PL, hydroxyproline content, and the production of TGF-beta by AM but had no marked effect on these same parameters in BLM-exposed rats. Histological examination of rats exposed to BLM for 14 d showed pulmonary inflammation and fibrosis. TT treatment had only a small effect on limiting the extent of these lesions and did not significantly affect their severity. In summary, data indicate that many inflammatory and fibrotic effects of in vivo silica exposure are substantially attenuated by TT, whereas the stimulation by BLM is only marginally affected by this drug. Since TT acts to attenuate AM-mediated reactions, these results suggest that AM may play a pivotal role in silica-induced fibrotic development and may be less involved in the pathogenesis of BLM-induced fibrosis.

Alkaloids↗
PubMed2006

Silica-induced apoptosis in alveolar macrophages: evidence of in vivo thiol depletion and the activation of mitochondrial pathway.

Studies have shown that silica induces apoptosis through mechanisms that also regulate the inflammatory responses of lung cells to silica exposure. Although implicated in cell culture studies, the major in vivo pathway through which silica induces apoptosis has not been characterized. The present study is to study the role of mitochondria in silica-induced oxidative stress and apoptosis in vivo. Rats were intratracheally instilled with saline or silica (20 mg/kg) and sacrificed at 3 days post-exposure unless otherwise specified. Alveolar macrophages (AM) were harvested by bronchoalveolar lavage and measured for apoptosis and secretion of inflammatory mediators in the presence or absence of appropriate inhibitors. Concurrent studies were carried out to determine the presence of intracellular reactive oxygen species (ROS) via confocal microscopy, mitochondrial trans-membrane potential by flow cytometry, mitochondrial release of cytochrome c, and the activation of caspase activities in AM by Western blot analysis. Silica was shown to induce elevated levels of intracellular ROS, resulting in a marked decrease in intracellular glutathione (GSH) and cysteine and a sustained presence of apoptotic AM in silica-exposed rats up to two weeks post-exposure. The apoptotic AM were characterized by decreased mitochondrial trans-membrane potential, increased mitochondrial release of cytochrome c, activated caspase 9 (but not caspase 8) and caspase 3 activities, and PARP degradation, comparing to cells from the saline control. Silica induced AM production of IL-1 and TNF-alpha, which may be inhibited by ex vivo treatment of cells with N-acetylcysteine (NAC) or microtubule modifiers such as tetrandrine and taxol. NAC was shown to prevent intracellular GSH depletion and silica-induced production of IL-1beta and TNF-alpha but not apoptosis in AM from silica-exposed rats. These results show that silica-induced apoptosis is mediated through the mitochondrial pathway but not through cellular production of inflammatory cytokines, ROS generation, however, induces both apoptosis and cellular secretion of inflammatory mediators.

Acetylcysteine↗
PubMed2004

Progression of lung inflammation and damage in rats after cessation of silica inhalation.

Human epidemiologic studies have found that silicosis may develop or progress even after occupational exposure has ended, suggesting that there is a threshold lung burden above which silica-induced pulmonary disease progresses without further exposure. We previously described the time course of rat pulmonary responses to silica inhalation as biphasic, the initial phase characterized by increased but controlled pulmonary inflammation and damage. However, after a threshold lung burden was exceeded, rapid progression of silica-induced pulmonary disease occurred. To test the hypothesis that there is a threshold lung burden above which silica-induced pulmonary disease progresses without further exposure we initiated a study to investigate the relationship between silica exposure, the initiation and progression of silica-induced pulmonary disease, and recovery. Rats were exposed to silica (15 mg/m(3), 6 h/day) for either 20, 40, or 60 days. A portion of the rats from each exposure were maintained without further exposure for 36 days to examine recovery. The major findings of this study are: (1) silica-exposed rats were not in pulmonary overload, and lung silica burden decreased with recovery; (2) pulmonary inflammation, damage and lipidosis increased with recovery for rats exposed to silica for 40 and 60 days, but not 20 days; (3) histopathology revealed changes in silica-induced alveolitis, epithelial hypertrophy and hyperplasia, and alveolar lipoproteinosis consistent with bronchoalveolar lavage (BAL) endpoints; and (4) pulmonary fibrosis developed even when exposure was stopped prior to its initial development.

Animals↗
PubMed2006

Silica in grasses as a defence against insect herbivores: contrasting effects on folivores and a phloem feeder.

1. Silica, deposited as opaline phytoliths in the leaves of grasses, constitutes 2-5% of dry leaf mass, yet its function remains unclear. It has been proposed that silica may act as an antiherbivore defence by increasing the abrasiveness and reducing the digestibility of grass leaves, although there is little direct experimental evidence to support this. 2. We investigated the effects of manipulated silica levels on the abrasiveness of the leaves of five grass species. We also examined the effects of silica levels on the feeding preferences, growth performance and digestion efficiency of two folivorous insects and one phloem-feeding insect. 3. Silica addition resulted in increases to leaf abrasiveness in four of the five grass species studied. Silica addition also deterred feeding by both folivores and reduced their growth rates and digestion efficiency. 4. These effects resulted in lower pupal mass of the lepidopteron larvae Spodoptera exempta and compensatory feeding by the orthopteran, Schistocerca gregaria. In contrast, silica had no effects on the feeding preference or the population growth of the phloem feeder, Sitobion avenae. 5. Our results demonstrate that silica is an effective defence against folivorous insects, both as a feeding deterrent, possibly mediated by increased abrasiveness, and as a digestibility reducer. The effects of silica on pupal mass and development time may impact on herbivore fitness and exposure to natural enemies. 6. These results are the first demonstration of a direct effect of silica on the abrasiveness of grasses and the adverse impact of silica on herbivore preference and performance.

Animals↗
PubMed2004

Essential role of p53 in silica-induced apoptosis.

Occupational exposure to mineral dusts, such as silica, has been associated with progressive pulmonary inflammation, lung cancer, and fibrosis. However, the mechanisms involved in this process are poorly understood. Because p53 is a key transcription factor regulating many important apoptosis-related genes, we hypothesized that p53 may play a key role in silica-induced apoptosis and that abnormal regulation of p53 by silica may contribute to development of lung cancer as well as silicosis. We used both in vitro and in vivo studies to test this hypothesis. Treatment of JB6 cells carrying a p53-luciferase reporter plasmid with silica caused dose-dependent p53 transactivation. Western blot indicates that silica not only stimulated p53 protein expression but also caused p53 phosphorylation at Ser392. TUNEL and DNA fragmentation analysis show that silica caused apoptosis in both JB6 cells and wild-type p53 (p53+/+) fibroblasts but not in p53-deficient (p53-/-) fibroblasts. Similar results were obtained by in vivo studies. Intratracheal instillation of mice with silica induced apoptosis in the lung of p53+/+ mice, whereas this induction was significantly inhibited in p53-/- mice. Confocal image analysis indicates that most apoptotic cells induced by silica were alveolar macrophages. These results demonstrate for the first time that silica induces p53 transactivation via induction of p53 protein expression and phosphorylation of p53 protein and that p53 plays a crucial role in the signal transduction pathways of silica-induced apoptosis. This finding may provide an important link in understanding the molecular mechanisms of silica-induced carcinogenesis and pathogenesis in the lung.

Animals↗
PubMed1992

Diminished arachidonic acid metabolite release by bovine alveolar macrophages exposed to surface-modified silica.

Modification of the silica surface has been shown to reduce its cytotoxicity in vitro and its fibrogenic activity in vivo. We have shown silica to be a potent stimulator of arachidonic acid (AA) metabolism in bovine alveolar macrophages (BAM). To determine the effect of surface-modified silica on AA metabolism in BAM, we exposed BAM in vitro to silica treated with aluminum lactate or polyvinylpyridine-N-oxide (PVPNO). BAM were prelabeled with [3H]AA and incubated with 3 and 5 mg of silica. Unmodified silica at these doses elicited maximal AA metabolite release from BAM. AA metabolites were analyzed by high performance liquid chromatography. Lactate dehydrogenase release was quantitated to determine the cytotoxicity of treated and untreated silica on BAM. Treating silica with aluminum lactate or PVPNO significantly (P less than or equal to 0.05) reduced 5-lipoxygenase metabolite release and significantly (P less than or equal to 0.05) increased cyclooxygenase metabolite release. These changes in AA metabolite release were accompanied by a significant (P less than or equal to 0.05) reduction in the cytotoxicities of the treated silicas compared with untreated silica. Our results suggest that the reduced inflammatory and fibrogenic activity of surface-modified silica may in part be due to reduced AA metabolite release from exposed macrophages.

Animals↗
PubMed2006

Synthesis and properties of water-soluble core-shell-shell silica-CdSe/CdS-silica nanoparticles.

This paper describes the synthesis of highly water-soluble and fluorescent core-shell-shell silica-CdSe/CdS-silica nanoparticles (CSS silica-QDs-silica NPs). We used cadmium nitrate and 1,1-dimethyl-2-selenourea precursors to synthesize CdSe quantum dots (QDs) in aqueous solution under simultaneous illumination with a diode-pumped solid state green laser and a Xe-Hg lamp. After passivation of the CdSe QDs with CdS, the CdSe/CdS QDs were then conjugated covalently to (3-mercaptopropyl)trimethoxysilane (MPS); we call these nanoparticles "MPS-QDs". We mixed the MPS-QDs with tetraethoxysilane (TEOS), ethanol, and NH3. By controlling the concentrations of the reagents, the stirring speed, and the reaction time, we synthesized CSS silica-QDs-silica NPs having sizes ranging from 75 to 190 nm. The incubation time for preparing the MPS-QDs and their concentrations are important parameters in determining the morphologies of the CSS silica-QDs-silica NPs. When we mixed 50 nM MPS-QDs, 1.1 mM TEOS, and 78 mM NH3 and reacted them at a stirring speed of 750 rpm, we obtained 85-nm-diameter CSS silica-QDs-silica NPs having a QD shell thickness of about 20 nm. The CSS silica-QDs-silica NPs provide a strong photoluminescence intensity (quantum yield 88%) and exhibit enhanced stability both photochemically and in high-conductivity media (e.g., 1.0 M NaCl).

Cadmium Compounds↗
PubMed1999

Surface composition of silica particles embedded in an Australian bituminous coal.

The composition and structure of the surface layers of a series of silica particles (10-20 microns across), embedded in a bituminous coal from the Whybrow seam, Sydney Basin, Australia, have been characterized in situ using time-of-flight secondary ion mass spectrometry (TOFSIMS), ion imaging, and depth profiling. The silica particles investigated are typically encased in a multilayered shell, the composition of which differs from average composition of both the silica and the bulk coal. The analysis directly demonstrates the presence of a silanol-rich (Si-OH) interfacial layer 3 nm in thickness. This silanol-rich region separates the bulk silica and a complex non-silica layer encasing the particles. The interfacial region also shows significant lithium enrichment (approximately fivefold over bulk) which implies diffusion and precipitation of lithium-containing species during the authigenetic formation of the surface layers of the silica grains. The outer layer encasing the silica particles is 10 nm in thickness and is composed of clays and carbonates, and, in some cases, includes organic material. The elemental constituents of this layer include aluminium, sodium, potassium, magnesium, iron, and lesser amounts of titanium and copper. The variation in the aluminium concentration from the outermost surface to the deeper layers is less than that of other non-silica species. A relatively high amount of calcium is found associated with the silica bulk. Although only non-respirable-sized silica particles are examined in this work, the methods of analysis developed have potential in providing an insight into the surface composition of respirable particles and in further studies of the surface bioavailability of silica species.

Air Pollutants, Occupational↗
PubMed2004

Spectroscopic evidence of silica-lignin complexes: implications for treatment of non-wood pulp wastewater.

This research examined the hypothesis that lignin compounds form aqueous complexes with silica increasing its solubility, thereby inhibiting its precipitation. An experimental program using four lignin model compounds was conducted to test the hypothesis. Laser Raman spectroscopy (LRS) was used to characterize, qualitatively, the interaction between lignin and aqueous silica, and to identify the possibility of silica-lignin complexation. Solubility studies were then performed by analyzing the solubility of silica in presence and absence of lignin within the relevant pH range to confirm the results of LRS, and to obtain a quantitative assessment of the relative solubility. The findings have established the formation of silica-ferulic, silica-vanillic, and silica-4-methoxycinnamic acid complexes, but no evidence was detected for the formation of silica-veratryl alcohol complex. In fact, the black liquor undoubtedly contains much more complex lignin materials than the simple model compounds used in this work. The more complex lignin compounds are likely to have an even greater tendency to form silica complexes, thus contributing to the initial hypothesis. This finding provides a fundamental understanding as to why previous efforts to precipitate silica by lowering the pH from 10-11 (for black liquor) to less than 9 did not achieve satisfactory silica separation, and why alternative strategies need to be investigated.

Chemical Precipitation↗
PubMed2006

[Effect of Ligustrazine on type I, III collagen synthesis in lung tissue of silica-treated rat].

OBJECTIVE: To study the effect of Ligustrazine on type I, III collagen synthesis in lung tissue of silica-treated rat. METHODS: The 128 experimental rats were randomly divided into control, silica and Ligustrazine group. 1ml silica (50g/L) was injected intratracheally in silica group and Ligustrazine group, while Ligustrazine group were injected intraperitoneally 50mg/(kg x d) Ligustrazine. Samples were collected on the 1st, 3rd, 7th, 14th, 21st, 28th day after injected silica. Type I , III collagen on paraffin-embedded lung sections were stained with sirius red, detected by polarized light microscopy and quantified by Image-Pro Plus. RESULTS: On the 3rd day after silica instillation, type III collagen began to appear, while type I collagen formed on the 7th day. Thereafter Type I, III collagen increased progressively. Compared with control group, type I, III collagen expression of silica group increased. At different time points type I, III collagen expression of Ligustrazine group decreased than silica group. There was significant difference of type I collagen area percentage on the 7th, 14th, 28th day, type III collagen area percentage on the 28th day between Ligustrazine group and silica group. CONCLUSION: Silica dioxide could induce the increase of type I, III collagen production in lung tissue, and their stages are different. Ligustrazine could suppress type I, III collagen production in lung tissue of silica-treated rat, and it's mechanism would be studied.

Animals↗
PubMed1981

Canine Silica Urolithiasis.

Silica "jack-stone" uroliths developed in the urinary bladder and urethra of 83 dogs living in the United States. Naturally occurring silica jack stones have not been encountered prior to 1976. German Shepherd Dogs comprised more than 1/3 of affected animals; the remainder encompassed 26 other breeds. In this series, 81 were males and 2 were females. The mean age of the dogs was 5.8 years, with a range of 1.5 to 12 years. Several observations prompt the hypothesis that development of silica uroliths may be related to diet. Although most silica uroliths had a characteristic jack-stone appearance, not all silica uroliths had a jack-stone configuration and not all jack stones were composed of silica. Some calculi were comprised of a combination of silica and struvite. Silica uroliths were radiodense, compared with adjacent tissue, but were not associated with identifiable crystals in urine. The urine pH of affected dogs varied from acid to alkaline. Silica urolithiasis recurred in 5 dogs following surgery. Urinary tract infections, when they occurred, appeared to be a sequela of silica urolithiasis. Pending further studies, management of silica uroliths should include their removal from the urinary tract and eradication of associated urinary tract infections. Prophylactic measures should include attempts to augment urine volume and change of diet.

Animals↗
PubMed1999

Cancer mortality in women with probable exposure to silica: a death certificate study in 24 states of the U.S.

BACKGROUND: Silica exposure is known to cause an increased risk of pneumoconiosis and some types of cancers. Exposure to silica is becoming an increasingly common occupational hazard for women. Studies contradict each other on whether or not women suffer more occupational pneumoconiosis than men, but no studies have evaluated cancer risks among women exposed to silica. METHODS: Death certificate data on occupation and industry from 24 states in the U.S. between 1984 and 1993 were used to calculate proportional mortality ratios (PMRs) for workers exposed to silica. RESULTS: Over 20,000 deaths (4% of all deaths in persons with possible work-related silica-exposure) occurred among women. The PMR for pneumoconiosis among women working in occupations or industries with possible silica exposure was 13.6 (95% CI: 7.2-23.2), for men 3.8 (CI: 3.7-4.0). Both men and women had higher than expected PMRs for respiratory diseases, lung and esophageal cancers, and external causes of death. In the group with probable silica exposure (both occupation and industry associated with silica), women had elevated PMRs for thyroid cancer (PMR = 5.5), multiple myeloma (PMR = 1.3), digestive organ cancers (PMR = 1.2), whereas men had no increased PMRs for these cancers. Both genders had significantly decreased PMRs for breast cancer, cerebrovascular diseases, nervous system diseases, and brain and other central nervous system cancers. CONCLUSIONS: An in depth look at the types of silica exposures (specific work duties) and adjustment for confounders is warranted to determine the importance of these gender-specific excess mortalities associated with possible silica exposure.

Cause of Death↗
PubMed1992

Effect of circulating neutrophil depletion on lung injury induced by inhaled silica particles.

Polymorphonuclear leukocytes (PMNs) recruited into the alveolar region during inflammation may injure the lung parenchyma by releasing cytotoxic oxygen radicals and proteases. Because brief exposures to crystalline silica elicit recruitment of PMNs into the alveolar region, which is strongly correlated with parameters of cytotoxicity, increased alveolar epithelial permeability, and lysosomal enzyme release, we sought to evaluate the potential role of PMNs in silica-induced lung injury. Rats were depleted of PMNs by administration of an anti-rat PMN antiserum prior to exposure to silica. Pulmonary inflammatory responses to silica in this group were compared to responses in normal silica-exposed rats as well as sham-exposed normal or PMN-depleted rats. Bronchoalveolar lavage fluids from normal, silica-exposed rats contained 9.7 x 10(6) PMNs immediately after exposure for 3 days, compared to 0.01 x 10(6) PMNs for both normal or PMN-depleted, sham-exposed rats. Bronchoalveolar lavage fluids from successfully PMN-depleted, exposed rats contained significantly fewer (0.7 x 10(6)) PMNs compared to normal silica-exposed rats. In both groups of silica-exposed rats, a variety of biochemical indicators of lung injury were increased significantly compared to measurements from both sham-exposed groups, but there were no differences between PMN-depleted and normal silica-exposed groups. The results suggest that recruitment of PMNs into the alveolar region is not a necessary prerequisite for the observed increases in biochemical indicators of silica-induced acute lung injury.

Acetylglucosaminidase↗
PubMed1997

Physical Adsorption of Bilayer Membranes on Silica

Isotherms for adsorption of bilayer-forming synthetic amphiphiles or phospholipids from vesicles onto hydrophilic silica particles (Aerosil OX-50) are obtained over a range of experimental conditions. Phosphatidylcholine (PC), dipalmitoylphosphatidylcholine (DPPC), dihexadecylphosphate (DHP), and dioctadecyldimethylammonium bromide (DODAB) dispersed in 10 mM Tris, pH 7.4, as small unilamellar vesicles present affinities for silica following the sequence DODAB > DPPC > PC > DHP. Among these, only DHP adsorption is below that expected for one bilayer deposition. Interaction at 65degreesC for 1 h between DPPC (or, at 25degreesC, for PC) vesicles and silica efficiently leads to bilayer deposition at maximal adsorption, if Tris is the buffer used. Preliminary centrifugation of the PC or DPPC vesicle dispersion is necessary to prevent overestimated adsorption. PC affinity for silica and its deposition as a bilayer depend on the nature of buffer used being much higher for Tris than for Hepes at pH 7.4. Formation of ion pairs between protonated amino groups in Tris and silanol groups on silica may lead to Tris adsorption and an increase in density of -OH groups on the solid surface. Therefore, formation of cooperative hydrogen bridges between -P=O in the phosphatidyl of the phospholipid bilayer and the -OH groups of Tris adsorbed on silica increases PC affinity for silica in the presence of Tris. For Hepes as buffer, PC affinity for silica is much lower and no plateau indicative of bilayer deposition is observed in the adsorption isotherm. Stabilization of supported phospholipid bilayers on solid surfaces requires several cooperative hydrogen bridges between the phospholipid and the solid surface. DODAB adsorption was unaffected by vesicle age and physical state of the bilayer vesicle. Adsorption isotherms for DODAB are of the high-affinity type with a maximum indicative of competition between intervesicle interactions and DODAB deposition on silica. Stabilization of DODAB bilayer deposition requires surface charge densities on silica higher than -1 μC/cm2. Copyright 1997Academic Press

Journal Article↗