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PubMed2006

Single quantum dot-micelles coated with silica shell as potentially non-cytotoxic fluorescent cell tracers.

The present study describes a stabilization of single quantum dot (QD) micelles by hydrophobic silica precursors and an extension of the silica layer to form a silica shell around the micelle. The obtained product consists of up to 92% of single nanocrystals (CdSe, CdSe/ZnS, or CdSe/ZnSe/ZnS quantum dots) in the silica micelles, coated with silica shell. The thickness of silica shell could vary, starting from 3 to 4 nm. Increasing the shell thickness increases the photoluminescent characteristics of QDs in aqueous solution. The silica-shelled single CdSe/ZnS QD micelles possess a high quantum yield in aqueous solution, a controlled small size, sharp photoluminescence spectra (fwhm approximately 30 nm), an absence of aggregation, and a high transparency. The presence of a hydrophobic layer between the QD and silica shell ensures an incorporation of other hydrophobic molecules (with interesting properties) in the close proximity of nanocrystal. Thus, it is possible to combine the characteristics of hybrid material with the priority of small size. The nanoparticles are amino functionalized and ready for conjugation. A comparatively good biocompatibility is demonstrated. The nanoparticles show ability for intracellular delivery and are noncytotoxic during long-term incubation with viable cells in the absence of light exposure, which makes them appropriate for cell tracing and drug delivery.

Biocompatible Materials↗
PubMed2005

Evidence for rigid binding of rhodamine 6G to silica surfaces in aqueous solution based on fluorescence anisotropy decay analysis.

Strong ionic binding of the cationic probe rhodamine 6G (R6G) to the anionic surface of silica particles in water provides a convenient labeling procedure to study both particle growth kinetics and surface modification by time-resolved fluorescence anisotropy (TRFA). The decays for R6G dispersed in diluted Ludox silica sols usually fit to a sum of picosecond and nanosecond decay components, along with a significant residual anisotropy component. The origin of the nanosecond decay component (phi2) is not fully understood, and has been ascribed to wobbling of the probe on the silica surface, the presence of a subpopulation of small nanoparticles in the Ludox sol, or rapid exchange between free and bound R6G. To elucidate the physical meaning of phi2, measurements were performed in various silica-based colloidal systems using different concentrations of silica. We found that the fraction of phi2 was generally higher in Ludox than in aqueous sodium silicate and decreased with increasing silica concentration; phi2 vanished upon gelation of sodium silicate at pH 7 leading to a total loss of R6G depolarization (r(t) = const). These results rule out the presence of local R6G wobbling when bound ionically to colloidal silica and support the rigid sphere model to describe the TRFA decays for R6G-Ludox. This conclusion is entirely supported by steady-state anisotropy data and structural considerations for the R6G molecule and the silica surface.

Journal Article↗
PubMed2006

Phase domain of the cubic Im3m mesoporous silica in the EO106PO70EO106-butanol-H2O system.

n-butanol has been chosen as an organic additive in the SiO(2)-EO(106)PO(70)EO(106)-H(2)O system at low HCl concentrations, for the generation of large-pore mesoporous silicas with easily tailored textural and structural properties. As opposed to previous reports on syntheses of cubic mesoporous silica that are usually performed in a very narrow composition range, we report now the possibility of preparing large-pore cagelike mesoporous silicas in a wide range of synthesis mixture compositions. Particularly, the cubic Imm silica with large interconnected cagelike pores (SBA-16) can easily be synthesized with controlled pore sizes and wall thicknesses, depending upon the synthesis mixture composition. The primary mesopore volume of the SBA-16 cages can be tuned from 0.27 to 0.56 cm(3) g(-)(1), and the mesopore size is shown to range from 4.7 to 7.2 nm, by performing a simple adjustment of the starting mixture composition. With the synthesis parameters varied, we describe the first complete diagram of the product phase domains obtained for silica mesophases in a SiO(2)-EO(106)PO(70)EO(106)-butanol-H(2)O system. Other ordered mesophases also observed in this system are the face-centered cubic Fmm silica mesophase and a 2D hexagonal-like mesostructure. Importantly here, the use of a low acid catalyst concentration regime allowed the preparation of silica mesophases in almost thermodynamically controlled conditions because of slow condensation kinetics of the inorganics. Such conditions enabled the introduction of n-butanol as the phase-controlling agent in the system, providing efficient tuning of the mesophase topology. The description of the phase domains provides a future basis for the design of large-pore mesoporous silicas with tailored textural and structural properties. Mesoporous samples obtained within the composition ranges of the phase domains are characterized by powder X-ray diffraction (PXRD) and nitrogen physisorption measurements.

Journal Article↗
PubMed2006

Fabrication of arrays of sub-20-nm silica walls via photolithography and solution-based molecular coating.

We report herein fabrication of arrays of sub-20-nm silica walls via photolithography and the surface sol-gel process. A photolithographically fabricated line template on a silicon wafer was coated with a silica nanolayer using the surface sol-gel process, and then the topmost portion of the silica layer and the template were successively removed using CHF(3) and oxygen plasma, respectively, leaving the sidewalls of the silica layers remaining on the substrate. These walls were fully self-supporting, and the thicknesses of silica wall were 6, 8, and 12 nm at 20, 30, and 60 cycles, respectively. The height/width ratio of the wall was 38 at the 30-cycle coating. This ratio is surprisingly high when compared to that of the conventional photolithography processes. Successive formation of the silica, polymer, and silica layers yielded a trilayer sidewall, and the spacer polymer layer could be selectively removed to form a doubled sidewall. Size reduction and proliferation of sub-20-nm silica wall was thus achieved. The reported method is simple and cost-efficient and opens a gateway to further miniaturization of nanostructures.

Journal Article↗
PubMed2005

Biological control of terrestrial silica cycling and export fluxes to watersheds.

Silicon has a crucial role in many biogeochemical processes--for example, as a nutrient for marine and terrestrial biota, in buffering soil acidification and in the regulation of atmospheric carbon dioxide. Traditionally, silica fluxes to soil solutions and stream waters are thought to be controlled by the weathering and subsequent dissolution of silicate minerals. Rates of mineral dissolution can be enhanced by biological processes. But plants also take up considerable quantities of silica from soil solution, which is recycled into the soil from falling litter in a separate soil-plant silica cycle that can be significant in comparison with weathering input and hydrologic output. Here we analyse soil water in basaltic soils across the Hawaiian islands to assess the relative contributions of weathering and biogenic silica cycling by using the distinct signatures of the two processes in germanium/silicon ratios. Our data imply that most of the silica released to Hawaiian stream water has passed through the biogenic silica pool, whereas direct mineral-water reactions account for a smaller fraction of the stream silica flux. We expect that other systems exhibiting strong Si depletion of the mineral soils and/or high Si uptake rates by biomass will also have strong biological control on silica cycling and export.

Biomass↗
PubMed2006

MARCO mediates silica uptake and toxicity in alveolar macrophages from C57BL/6 mice.

Scavenger receptors (SR), on the surface of the macrophage, appear to be responsible for silica uptake and cell death signaling in the macrophage. The purpose of this study was to isolate which SRs (macrophage receptor with collagenous structure (MARCO), CD204, or CD36) were involved using a variety of SR single and double null mice. The findings indicated that MARCO was the critical SR involved in silica uptake and cytotoxicity in the primary alveolar macrophages (AM) from C57BL/6 mice, as there was no particle uptake or cell death in the absence of this SR. The level of MARCO expression on AM changed significantly with the absence of other SR, and silica uptake was proportional to cell surface MARCO expression. In addition, silica uptake and cytotoxicity were completely blocked by an anti-mouse MARCO antibody. Transfection of Chinese hamster ovary cells with human MARCO supported these conclusions, as silica particles bound to and initiated apoptosis in the MARCO-transfected cells. Strain differences with regard to SR distribution were also examined. There was a differential expression of these SR on AM from each strain, with MARCO dominant for C57BL/6, CD36 dominant on BALB/c, and all three SR expressed on 129/SvJ mice. Similar to the results with C57BL/6 AM, MARCO was involved with silica-induced cell death in the 129/SvJ strain. In contrast, BALB/c AM used an unidentified mechanism for silica uptake because the SR antibodies failed to block particle internalization. Taken together, these results indicate MARCO is the primary AM receptor interacting with silica, depending on mouse strain and level of constitutive expression.

Animals↗
PubMed2000

Silica-induced nuclear factor-kappaB activation: involvement of reactive oxygen species and protein tyrosine kinase activation.

Nuclear factor-kappaB (NF-kappaB) is a multiprotein complex that may regulate a variety of inflammatory cytokines involved in the initiation and progression of silicosis. The present study documents the ability of in vitro silica exposure to induce DNA-binding activity of NF-kappaB in a mouse peritoneal macrophage cell line (RAW264.7 cells) and investigates the role of reactive oxygen species (ROS) and/or protein tyrosine kinase in this activation. In vitro exposure of mouse macrophages to silica (100 microg/ml) resulted in a twofold increase in ROS production, measured as the generation of chemiluminescence (CL), and caused activation of NF-kappaB. Silica-induced CL was inhibited 100% by superoxide dismutase (SOD) and 75% by catalase, while NF-kappaB activation was inhibited by a variety of antioxidants (catalase, superoxide dismutase, alpha-tocopherol, pyrrolidine dithiocarbamate, or N-acetylcysteine). Further evidence for the involvement of ROS in NF-kappaB activation is that 1 mM H2O2 enhanced NF-kappaB/DNA binding and that this activation was inhibited by catalase. Specific inhibitors of protein tyrosine kinase, such as herbimycin A, genistein, and AG-494, prevented NF-kappaB activation in silica-treated cells. Genistein and AG-494 also reduced NF-kappaB activation in H2O2-treated cells. Results confirm that tyrosine phosphorylation of several cellular proteins (approximate molecular mass of 39, 58-70, and 103 kD) was increased in silica-exposed macrophages and that genistein inhibited this silica-induced phosphorylation. In contrast, inhibitors of protein kinase A or C, such as H89, staurosporin, calphostin C, and H7, had no marked inhibitory effect on silica-induced NF-kappaB activation. The results suggest that ROS may play a role in silica-induced NF-kappaB activation in macrophages and that phosphorylation events mediated by tyrosine kinase may be involved in this activation.

Animals↗
PubMed1996

Exposure to crystalline silica or treatment with chlorphentermine increases vitamin E levels in rat alveolar lavage materials.

Previous studies have shown that vitamin E may be an integral part of lung surfactant and may function to protect this material from oxidant damage. Therefore, we measured the vitamin E levels in alveolar lavage materials from rats exposed to crystalline silica or treated with chlorphentermine (CP), two treatments that are known to increase surfactant phospholipids (PL) by different mechanisms. Silica exposure leads to increased PL synthesis, and CP treatment causes a reduction in PL degradation. Two different silica preparations, HCL-washed and unwashed silica, were used because exposure to each of them leads to different degrees of phospholipidosis. Exposure to HCL-washed silica results in a more than 17-fold increase in lavage PL and protein levels and a 12.2-fold increase in the amount of vitamin E. Exposure to unwashed silica leads to an approximately 7-fold increase in PL and proteins and a 5.8-fold increase in lavage vitamin E. Following treatment of rats with CP, there is a 15- to 19-fold increase in lavage PL and proteins and a 13.6-fold increase in vitamin E. When the results are expressed as micrograms vitamin E per milligram of lavage PL or protein, there is not much difference between controls and each treatment group. Because surfactant synthesis occurs in the endoplasmic reticulum, we also measured vitamin E in lung microsomes. Both silica exposure and CP treatment also lead to 1.8- to 2.5-fold increases, respectively, in the lung microsomal levels of vitamin E. These results demonstrate that alveolar lavage vitamin E levels are elevated along with lavage PL and proteins, and lung microsomal vitamin E levels are increased following exposure of rats to silica or treatment of the animals with CP.

Animals↗
PubMed2003

Modeling of gel barrier formation by using colloidal silica in saturated media.

The applicability of constructing a subsurface barrier by injecting a Colloidal Silica solution directly into the saturated medium was examined through numerical experiments. Investigations ascertain that the construction of this Colloidal Silica-based subsurface barrier in the saturated medium might be a promising containment technology. According to the results of numerical studies, gel formation takes place in the region were more than 90% of introductory concentration of the Colloidal Silica solution is maintained at a time equal to the gel-point. By using a point injection method, the radius of the solidified Colloidal Silica mass increases proportional to the respective ratios of the gel-points and the injection pressure heads. With higher injection pressures and longer gel-points, a larger volume of injected Colloidal Silica solution is diluted. The effect of subsurface water flow is significant when the solution has a slower gelation rate and the spherical shape of the solidified mass is less distorted with increasing injection rate. The degree of distoration of the solidified Colloidal Silica mass is much less than that of the rest of the Colloidal Silica solution surrounding the solidified Colloidal Silica mass

Colloids↗
PubMed2004

Role of inducible nitric oxide synthase-derived nitric oxide in silica-induced pulmonary inflammation and fibrosis.

Inhalation of crystalline silica can produce lung inflammation and fibrosis. Inducible nitric oxide synthase (iNOS)-derived nitric oxide (NO) is believed to be involved in silica-induced lung disease. To investigate the role of iNOS-derived NO in this disease, the responses of iNOS knockout (KO) versus C57Bl/6J wild-type (WT) mice to silica were compared. Male mice (8-10 wk old, mean body weight 24.0 g) were anesthetized and exposed, by aspiration, to silica (40 mg/kg) or saline. At 24 h and 42 d postexposure, lungs were lavaged with saline. The first bronchoalveolar lavage (BAL) fluid supernatant was analyzed for lactate dehydrogenase (LDH) activity, levels of albumin, tumor necrosis factor-alpha (TNF-alpha), and macrophage inflammatory protein-2 (MIP-2), as well as total antioxidant capacity (TAC). The cellular fraction of the total BAL was used to determine alveolar macrophage (AM) and polymorphonuclear leukocyte (PMN) counts, and zymosanstimulated AM chemiluminescence (AM-CL). In separate mice, lung histopathological changes were evaluated 42 d postexposure. Acute (24-h) silica exposure decreased AMs, increased PMNs, increased LDH activity and levels of albumin, TNF-alpha, and MIP-2 in BAL fluid, and enhanced AM-CL in both iNOS KO and WT mice. However, iNOS KO mice exhibited less AM activation (defined as increased AM-CL and decreased AM yield) than WT. Furthermore, TAC following acute silica decreased in WT but was maintained in iNOS KO mice. Pulmonary reactions to subchronic (42 d) silica exposure were similar to acute. However, histopathological and BAL fluid indices of lung damage and inflammation, AM activation, and lung hydroxyproline levels were significantly less in iNOS KO compared to WT mice. These results suggest that iNOS-derived NO contributes to the pathogenesis of silica-induced lung disease in this mouse model.

Animals↗
PubMed1997

Amorphous silica: a review of health effects from inhalation exposure with particular reference to cancer.

Silicas and silicates are some of the most abundant compounds found naturally in the earth's crust. Excessive exposure to crystalline silicas can cause serious lung disease such as silicosis and has been associated with lung cancer in some studies, but the potential health effects of amorphous silicas (silicon dioxide without crystalline structure) have not been well studied. Results from animal studies of amorphous silicas, unlike those seen with crystalline silicas, have suggested limited and largely reversible cytotoxic and possibly fibrogenic effects associated with some forms, but data on cancer outcomes are scanty and for the most part negative. Epidemiologic investigations to date for any potential cancer risk are not informative because the effects of crystalline and amorphous silicas have not been separated. Any future epidemiologic study should attempt to clarify the health effects of amorphous silicas from those of crystalline silicas, particularly with regard to any potential for carcinogenicity.

Administration, Inhalation↗
PubMedDate not supplied

Exposure to respirable crystalline silica in eastern North Carolina farm workers.

Occupational exposure to crystalline silica has been linked to silicosis, some forms of cancer, and certain autoimmune diseases. Little information exists on exposure levels of respirable silica in the agricultural industry. This study assessed respirable silica exposure of farm workers in eastern North Carolina. Sandy soils in this region have been shown to contain high levels of respirable silica. Personal breathing zone samples (n = 37) were collected from 27 workers at seven farms during various agricultural activities. The highest respirable silica concentrations were measured during sweet potato transplanting (3.91 +/- 2.07 mg/m3). Respirable silica exposure was observed to be associated with agricultural activity, soil moisture, relative humidity, and wind speed. Most of the variation in exposure (79%) was explained by agricultural activity and soil moisture. The observed percentage of silica levels (mean 34.7%) were almost twice as high as was reported in studies of California agriculture. This may be due to the loamy sand and sandy loam soil types in the regions in this study. In agriculture, respirable silica exposure is highly variable, but the potential for exposures above the threshold limit value of 0.05 mg/m3 exists during particular agricultural activities.

Agricultural Workers' Diseases↗
PubMed2003

Excessive exposure to silica in the US construction industry.

Exposures to respirable dust and silica were investigated among 36 construction sites in the USA. Personal measurements (n = 151) were analyzed from 80 workers in four trades, namely bricklayers, painters (while abrasive blasting), operating engineers and laborers. Painters had the highest exposures (median values for respirable dust and silica: 13.5 and 1.28 mg/m(3), respectively), followed by laborers (2.46 and 0.350 mg/m(3)), bricklayers (2.13 and 3.20 mg/m(3)) and operating engineers (0.720 and 0.075 mg/m(3)). Mixed models were fitted to the log-transformed air levels to estimate the means and within- and between-worker variance components of the distributions in each trade. We refer to the likelihood that a typical worker from a given trade would be exposed, on average, above the occupational exposure limit (OEL) as the probability of overexposure. Given US OELs of 0.05 mg/m(3) for respirable silica and 3 mg/m(3) for respirable dust, we estimated probabilities of overexposure as between 64.5 and 100% for silica and between 8.2 and 89.2% for dust; in no instance could it be inferred with certainty that this probability was <10%. This indicates that silica exposures are grossly unacceptable in the US construction industry. While engineering and administrative interventions are needed to reduce overall air levels, the heterogeneous exposures among members of each trade suggest that controls should focus, in part, upon the individual sites, activities and equipment involved. The effects of current controls and workplace characteristics upon silica exposures were investigated among operating engineers and laborers. Silica exposures were significantly reduced by wet dust suppression (approximately 3-fold for laborers) and use of ventilated cabs (approximately 6-fold for operating engineers) and were significantly increased indoors (about 4-fold for laborers). It is concluded that urgent action is required to reduce silica exposures in the US construction industry.

Algorithms↗
PubMed1979

Effect of silica on the innate resistance of inbred mice to Salmonella typhimurium infection.

The role of macrophages in the innate immunity of (CBA/N female X DBA/2N male)F1 female mice to Salmonella typhimurium was assessed with silica, an agent which has been reported to selectively inactivate macrophages. Silica, administered intravenously to mice, markedly decreased the phagocytic capacity of splenic macrophages but had no effect on splenic responsiveness to the B-cell mitogen lipopolysaccharidide or the T-cell mitogen phytohemagglutinin, nor did it affect the frequency of surface immunoglobulin-positive cells (B cells). Silica given to mice 1 day before intraperitoneal challenge decreased the 50% lethal dose of S. typhimurium 100-fold. The incidence of survival of mice given silica up to 14 days before infection with a sublethal dose of organisms was also decreased. This susceptibility could also be demonstrated when silica was given 10 days, but not 20 days, after S. typhimurium infection. Poly-2-vinylpyridine-N-oxide, a lysosomal stabilizing agent, abrogated the silica effect. Deaths among silica-treated mice followed uncontrolled multiplication of the organism in the spleen. These results provide direct evidence that macrophages play an essential role in natural immunity to murine typhoid and demonstrate the efficacy of silica as a tool to analyze macrophage function.

Animals↗
PubMed1983

Protective effect of poly-2-vinylpyridine-N-oxide on susceptibility of silica-treated mice to experimental histoplasmosis.

We have studied the ability of poly-2-vinylpyridine-N-oxide (PVNO), a lysosomal stabilizing agent, to abrogate the cytotoxic effects of silica on macrophages. Male C3H/HeN mice were pretreated with PVNO and inoculated intravenously with silica particles. At 24 h after silica injection, silica-treated and -untreated mice were challenged intravenously with varying doses of live yeast cells of Histoplasma capsulatum. All mice receiving silica died when challenged with 5 X 10(5) yeast cells of Histoplasma sp. compared with no deaths in PVNO-pretreated animals and 10% mortality in controls not receiving PVNO or silica. When animals were given 2.5 X 10(5) yeast cells (a sublethal dose), the protective effect of PVNO was seen by a reduction in splenomegaly and viable Histoplasma sp. present in the spleen. Furthermore, PVNO alone showed a significant protective effect (P less than 0.05) against a lethal challenge with Histoplasma sp. Prior treatment with PVNO also protected mouse peritoneal macrophages from the cytotoxic effects of silica particles in vitro. These results indicate that PVNO abrogates the cytotoxicity of silica particles on macrophages and also increases the resistance of mice to histoplasmosis.

Animals↗
PubMed2003

Occupational silica exposure and risk of various diseases: an analysis using death certificates from 27 states of the United States.

BACKGROUND: Although crystalline silica exposure is associated with silicosis, lung cancer, pulmonary tuberculosis, and chronic obstructive pulmonary disease (COPD), there is less support for an association with autoimmune disease, and renal disease. METHODS: Using data from the US National Occupational Mortality Surveillance (NOMS) system, a matched case-control design was employed to examine each of several diseases (including silicosis, lung cancer, stomach cancer, oesophageal cancer, COPD, pulmonary tuberculosis, sarcoidosis, systemic lupus erythematosus, systemic sclerosis, rheumatoid arthritis, and various types of renal disease). Cases were subjects whose death certificate mentioned the disease of interest. A separate control group for each of the diseases of interest was selected from among subjects whose death certificate did not mention the disease of interest or any of several diseases reported to be associated with crystalline silica exposure. Subjects were assigned into a qualitative crystalline silica exposure category based on the industry/occupation pairing found on their death certificate. We also investigated whether silicotics had a higher risk of disease compared to those without silicosis. RESULTS: Those postulated to have had detectable crystalline silica exposure had a significantly increased risk for silicosis, COPD, pulmonary tuberculosis, and rheumatoid arthritis. In addition, a significant trend of increasing risk with increasing silica exposure was observed for these same conditions and for lung cancer. Those postulated to have had the greatest crystalline silica exposure had a significantly increased risk for silicosis, lung cancer, COPD, and pulmonary tuberculosis only. Finally, those with silicosis had a significantly increased risk for COPD, pulmonary tuberculosis, and rheumatoid arthritis. CONCLUSIONS: This study corroborates the association between crystalline silica exposure and silicosis, lung cancer, COPD, and pulmonary tuberculosis. In addition, support is provided for an association between crystalline silica exposure and rheumatoid arthritis.

Adult↗
PubMed2006

Essential role of ROS-mediated NFAT activation in TNF-alpha induction by crystalline silica exposure.

Occupational exposure to crystalline silica has been associated with progressive pulmonary silicosis and lung cancer, but the underlying molecular mechanisms are not well understood. Previous studies have shown that crystalline silica exposure can generate reactive oxygen species (ROS) and induce the expression of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in cells. TNF-alpha is believed to be critical in the development of silica-related diseases. Thus it will be of significance to understand the mechanisms of TNF-alpha induction by silica exposure. Given the fact that the transcription factor nuclear factor of activated T cells (NFAT) plays an important role in the regulation of TNF-alpha and can also be activated by ROS, in this study we investigated the potential role of ROS in silica-induced NFAT activity as well as TNF-alpha expression in Cl41 cells. The results showed that exposure of cells to silica led to NFAT transactivation and TNF-alpha induction, where superoxide anion radical (O(2)(-).), but not H(2)O(2), was involved. The knockdown of NFAT3 by its specific small interfering RNA significantly attenuated the silica-induced TNF-alpha transcription. This study demonstrated that silica was able to activate NFAT in an O(2)(-).-dependent manner, which was required for TNF-alpha induction.

Animals↗
PubMed2005

Involvement of protein kinase C in crystalline silica-induced activation of the MAP kinase and AP-1 pathway.

Crystalline silica has long been well established as a fibrogenic agent, and recent evidence has implicated it as a potential human carcinogen. However, the mechanisms of silica-induced disease development and progression are not well understood. Our previous studies demonstrated that crystalline silica is able to activate activator protein-1 (AP-1) through mitogen-activated protein kinase (MAPK) pathways. The present study investigates the possible involvement of protein kinase C (PKC) in silica-induced activation of the MAPK/AP-1 signal transduction pathway. Treatment of mouse epidermal cells (JB6 cell line) with freshly fractured silica stimulated translocation of PKCalpha and PKCepsilon from the cytosol to the membrane and activated AP-1 transcription activity. Pretreatment of cells with PKC inhibitors, including RO-32-0432, calphostin C, and bisindolylmaleimide I, inhibited silica-induced AP-1 activation and phosphorylation of ERKs and p38 kinase. These inhibitory effects by PKC inhibitors were dose dependent. Furthermore, overexpression of dominant negative mutant (DNM) of PKCalpha or PKCepsilon markedly blocked AP-1 activation as well as phosphorylation of ERKs and p38 kinase induced by freshly fractured silica. These results demonstrate that PKCalpha and PKCepsilon are essential in silica-induced AP-1 activation through the MAP kinase (ERKs and p38 kinases) pathway.

Animals↗