Silica induced

Guoping C, FanP, Jingxi S, Xiaoping L, Shiqin J, YuriL 1997 Purification and characterization of a silica-induced lavage protein with fibroblast growth-promoting activity. J Cell Biochem 67 257-264... 

Srivastava, K. D. et al. Crucial role of interleukin-1 beta and nitric oxide synthase in silica-induced inflammation and apoptosis in mice. Am. J. Respir. Crit Care Med 165, 527, 2002. 

Scheme 23 Helical silica-induced highly enantioselective asymmetric autocatalysis of chiral pyrimidyl alkanol...

F. Kozin, B. Millstein, G. Mandel, and N. Mandel, Silica induced membranolysis a study of different structural forms of crystalline and amorphous silica and the effects os protein adsorption, J. Colloid Interface Sci. 88, 326-337 (1982). 

Mandel, G. and Mandel, N., The structure of crystalline Si02, In Silica and Silica-Induced Lung Diseases, Castranova, V., Vallyathan, V., and Wallace, W.E., Eds., CRC Press, Boca Raton, FL, 1996, p. 63. 

Holian A, Uthman MO, Goltsova T, et al. 1997. Asbestos and silica-induced changes in human alveolar macrophage phenotype. Environ Health Perspect Suppl 105 1139-1142. 

Shi X., Ding M., Chen F., Wang L., Rojanasakul Y., Vallyathan V., and Castranova V. (2001) Reactive oxygen species and molecular mechanisms of silica-induced lung injury. J. Environ. Pathol. Toxicol. Oncol. 20(suppl. 1), 85-93. 

Iyer R, Hamilton RF, Li L, Holian A. Silica-induced apoptosis mediated via scavenger receptor in human alveolar macrophages. Toxicol AppI Pharmacol 1996 141 84-92. 

Suzuki, N., Horiuchi, T., Ohta, K., Yamaguchi, M., Ueda, T., Takizawa, H., Hirai, K., Shiga, J., Ito, K. and Miyamoto, T. (1993). Mast cells are essential for the full development of silica-induced pulmonary inflammation a study with mast cell-deficient mice. Am. J. Respir. Cell Mol. Biol. 9, 475-483. 

Piguet, P.F., CoUart, M.A., Grau, G.E., Sappino, A.P. and VassaUi, P. (1990). Requirement of tumour necrosis factor for development of silica-induced pulmonary fibrosis. Nature. 344, 245-247. 

DiMatteo M, Reasor MJ. Modulation of silica-induced pulmonary toxicity hy dexamethasone-containing liposomes. Toxicol Appl Pharmacol 142(2) 411-421, 1997. 

Increased cytokine production may also play a role in silica-induced autoimmune vascular disease. Adhesion molecule expression is elevated on vascular endothelial cells in response to TNF-a and IL-1. Adhesion molecules such as endothelial leukocyte adhesion molecule-1 (ELAM-1) and intercellular adhesion molecule-1 (ICAM-1) recruit inflammatory cells to specific sites on the vascular endothelium, and it has been hypothesized that vascular pathology following silica exposure may be the result of this interaction (Nowack et al., 1998). IFN-y is expressed at elevated levels by lymphocytes in silicotic thoracic lymph nodes and may be responsible for the long-lasting inducible nitric oxide synthase (iNOS) expression in these tissues (Friedetzky et al., 2002). The increase in IFN-y may also cause a shift towards a dominant Thl response, contributing to the maintenance of a chronic inflammatory state in silica-containing lymph nodes (Gam et al., 2000). 

In vitro studies also provide important evidence that silica s properties as an adjuvant may be relevant in silica-induced autoimmunity. Incubation of silica and silicate with isolated human T cells caused polyclonal lymphocyte activation, which in vivo could lead to a breakdown of tolerance via nonspecific stimulation of autoreactive T cell clones (Ueki et al., 1994). 

Molecular Mechanisms of Asbestos- and Silica-Induced Lung Cancer... 

FIGURE 4.1 Mechanisms of asbestos-and silica-induced cancer. 

The notion of the silica-induced necrotic cell death was far earlier than that of the apoptotic induction by silica. In CFY rats, silica-induced necrosis occurred in a relatively earlier period of postinstillation, between 12 to 72h. In mice, necrotic epithelial cell death occurred within 24h of silica instillation." Driscoll et al. " reported that necrosis induced by silica was in a prolonged marmer. The necrosis, as indicated by the presence... 

Kang, J.L., Pack, I.S., Hong, S.M., Lee, H.S., and Castranova, V., Silica induces nuclear factor-kappa B activation through tyrosine phosphorylation of I kappa B-alpha in RAW264.7 macrophages, Toxicol Appl. Pharmacol, 169, 59-65, 2000. 

Desaki, M., Takizawa, H., Kasama, T., Kobayashi, K., Morita, Y., and Yamamoto, K., Nuclear factor-kappa b activation in silica-induced interleukin 8 production by human bronchial epithelial cells. Cytokine, 12, 1257-1260, 2000. 

Chen, F., Lu, Y., Kuhn, D.C., Maki, M., Shi, X., Sun, S.C., and Demers, L.M., Calpain contributes to silica-induced I kappa B-alpha degradation and nuclear factor-kappa B activation, Arch. Biochem. Biophys., 342, 383-388, 1997. 

Sarih, M., Souvannavong, V., Brown, S.C., and Adam, A., Silica induces apoptosis in macrophages and the release of interleukin-1 alpha and interleukin-1 beta, J. Leukoc. Biol, 54, 407-413,1993. 

Leigh, J., Wang, H., Bonin, A., Peters, M., and Ruan, X., Silica-induced apoptosis in alveolar and granulomatous cells in vivo. Environ. Health Perspect, 105 (Suppl. 5), 1241-1245, 1997. 

Deshpande, A., Narayanan, P.K., and Lehnert, B.E., Silica-induced generation of extracellular factor(s) increases reactive oxygen species in human bronchial epithelial cells, Toxicol Sci., 67,... 

Shen, H.M., Zhang, Z., Zhang, Q.F., and Ong, C.N., Reactive oxygen species and caspase activation mediate silica-induced apoptosis in alveolar macrophages. Am. J. Physiol. Lung Cell. Mol. Physiol, 280, LI0-17, 2001. 

Van Dyke, K., Antonini, J.M., Wu, L., Ye, Z., and Reasor, M.J., The inhibition of silica-induced lung inflammation by dexamethasone as measured by bronchoalveolar lavage fluid parameters and peroxynitrite-dependent chemiluminescence, Hgenf5 Hcn on, 41,44 9, 1994. 

Claudio, E., Segade, F., Wrobel, K., Ramos, S., and Lazo, P.S., Activation of murine macrophages by sihca particles in vitro is a process independent of silica-induced cell death. 

Figure 11 Vibrational spectral changes in a. 6 ym anatase film on silica-induced by high-energy pulsed laser irradiation.

It has been reported recently that flux and even selectivity of PMP and PTMSP can be enhanced by the addition of nanoparticles (285, 286]. Merkel et al. [285] added fumed sihca to PMP and observed a simultaneous increase of butane flux and butane/methane selectivity. This unusual behavior was explained by fumed-silica-induced disruption of polymer chain packing and an accompanying increase in the size of free volume elements through which molecular transport occurs. Gomes et al. [286] incorporated nanosized sihca particles by a sol-gel technique into PTMSP and found also for this polymer a simultaneous increase in flux and selectivity. It has to be studied, if physical aging of the polyacetylenes is reduced by the addition of nanoparticles. 

Premasekharan, G., Nguyen, K., Contreras, J., Ramon, V., Leppert, V. J., and Forman, H. J. 2011. Iron-mediated lipid peroxidation and hpid raft disruption in low-dose silica-induced macrophage cytokine production. Free adic iQl M 51,1184—1194. 

Fig. 1. Silica can activate various cell types involved in the pathophysiology of systemic sclerosis (SSc). Macrophages activated by silica in vitro liberate the same cytokines and growth factors known to be active in the pathophysiology of idiopathic SSc. Microvascular endothelium is involved in silica-induced as well as idiopathic SSc with similar activation patterns in vitro and in vivo. Dermal fibroblasts are affected by silica in vitro, and fibroblasts are the cells producing large amounts of extracellular matrix in vivo. In vitro, the synthesizing capacity of fibroblasts depends greatly on culture conditions. All these effects are based on our in vitro experiments with silica shown in italic. These effects are similar to pathophysiological events known from idiopathic SSc...

Obviously, the endothelial cell damage occurs early, before systemic symptoms appear. This is suggested by the observation that Raynaud s phenomenon often precedes SSc and by elevated levels of von Willebrand factor and circulating immune complexes not only in silica-induced SSc, but also in healthy silica-exposed miners. 

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