Mechanisms of carcinogenesis by crystalline silica in relation to oxygen radicals.

Saffiotti, Umberto; Daniel, Lambert N.; Mao, Yan; Shi, Xianglin; Williams, A. Olufemi; Kaighn, M. Edward

doi:10.1289/ehp.94102s10159

Cited by 35 publications

(16 citation statements)

References 11 publications

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“…Earlier studies reported increased TGFP expression in rats with experimental silicosis Saffiotti et al, 1994). Our studies using the silicainjury model showed increased staining of TGFP ( Fig.…”

Section: Discussionsupporting

confidence: 69%

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Induction of interleukin‐1/and interleukin‐8 mRNAs and proteins by TGFβ1 in rat lung alveolar epithelial cells

Kumar¹,

Rabadi²,

Sigurdson³

et al. 1996

J. Cell. Physiol.

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The transforming growth factor-p (TGF-P) has been shown to increase in lung injury and in fibrotic states of the lung. In the current study, we sought to investigate whether TGFP, induced the expression of I L -l a and IL-8 in rat alveolar epithelial cells. We evaluated TGFP, , IL-1 a, and IL-8 expression by irnmunofluorescence in silica-injured and saline-treated control rat lungs. Antibodies to IL-1 a, 11-8, and TGFP, showed intense staining in silica-injured lungs as compared to saline-instilled lungs. Primary isolated type II cells from silica-injured lungs showed increased expression of I L -l a as compared to saline-instilled lungs. To evaluate the effects of TGFPl, we treated an immortalized rat type II cell-derived cell line (LM5) with 100 pg/ml of TGFP, in serum-free medium for 0-24 hours and analyzed the expression of IL-1 a and IL-8 mRNAs and proteins using semiquantitative RT-PCR, Northern blot analysis, Western blot analysis, and immunohistochemistry. Densitometric analysis of Northern blots showed modest constitutive expression of IL-1 a gene in untreated control LM5 cells. TGFP, treatment resulted in an increase in IL-1 a rnRNA, that reached maximum levels @-fold) by 2 hours and remained elevated for 4-1 6 hours, with a subsequent decline by 24 hours. Similarly, Northern blot and RT-PCR analysis demonstrated that TGFP, treatment resulted in maximum induction of IL-8 mRNA (6-8.5-fold) within 1 -4 hours. The levels remained elevated for up to 24 hours afterwards. Western blot analysis results further confirmed the expression of both I L -l a and IL-8 proteins by LM5 cells. TGFP, treatment resulted in increased expression of both IL-1 a and IL-8 proteins. lmmunofluorescence studies demonstrated increased staining of I L -l a by TGFP, as compared to untreated cells. These results suggest that TGFP, may regulate I L -l a and IL-8 expression in alveolar epithelial cells and contribute to polyrnorphonuclear leukocyte recruitment and lung injury in clinical states with increased TGFP,. o 1996 WiIey-Liss, Inc. Zitnik, 1992; Zhang et al., 1993; Vanhee et al., 1995; Rolfe et al., 1991). Progression to fibrosis has been associated with ongoing expression o f inflammatory cytokines that modulate fibroblast and epithelial cell proliferation and extra cellular m a t r i x (ECM) deposition (Raghu et al., 1989; Khalil et al., 1991, 1994; Piguet e t al., 1990; McGowan, 1992). TGFP has been shown to increase in pulmonary fibrotic states (Raghow et al., 1989; Broekelmann et al.

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Section: Discussionsupporting

confidence: 69%

“…Increased spontaneous production of IL-6, IL-8, and TNF-a has also been shown in silicosis and coal workers' pneumoconiosis (Vanhee et al, 1995). TGFP, was localized by immunocytochemistry in rat alveolar type I1 cells adjacent to silicotic granulomas Saffiotti et al, 1994).…”

mentioning

confidence: 99%

Induction of interleukin‐1/and interleukin‐8 mRNAs and proteins by TGFβ1 in rat lung alveolar epithelial cells

Kumar¹,

Rabadi²,

Sigurdson³

et al. 1996

J. Cell. Physiol.

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“…Continued silica exposure leads to an alteration in macrophage function. There is release of inflammatory cytokines, for example, IL-1, free radicals, and growth factors [3, 4]. This stimulates collagen synthesis and production of antibodies against collagen.…”

Section: Discussionmentioning

confidence: 99%

Bilateral Spontaneous Pneumothorax in Chronic Silicosis: A Case Report

Mishra

Jacob

Basu

et al. 2014

Case Reports in Pathology

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Silicosis is an occupational lung disease caused by inhalation of crystalline silica. People working in occupations like sandblasting, surface drilling, tunneling, silica flour milling, ceramic making, and so forth are predisposed to develop silicosis. Crystalline forms of silica are more fibrogenic than the amorphous forms, highlighting the importance of the physical form in pathogenesis. Lung biopsy is rarely performed for the diagnosis of silicosis as it can easily be detected by occupational history and radiological features. Patients with silicosis can develop complications like tuberculosis, lung cancer, progressive massive fibrosis, cor pulmonale, broncholithiasis, or tracheobronchial compression by lymph nodes. Pleural involvement in silicosis is rare. Spontaneous pneumothorax is a pleural complication that can develop in such patients. Usually in silicosis pneumothorax is unilateral. We hereby report the lung biopsy findings and discuss the mechanism of pneumothorax development in a case of chronic silicosis who, later on died during the course of the disease.

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“…ROS-mediated single- and double-strand DNA breaks, DNA adduct formation, and/or transformation of bronchial epithelial cells into mesenchymal cells have been described (Lenaz, 2012). DNA damage and neoplastic transformation of the airways have been reported in the lungs of animals exposed to crystalline silica or sulfurmustard (Malaviya et al, 2010; Saffiotti et al, 1994). Lung macrophages and epithelial cells also exhibit DNA damage following exposure to ozone (Sunil et al, 2012), an effect inhibited by pretreatment with vitamin E (Cheng et al, 2003), indicating an association between oxidative stress and DNA damage.…”

Section: Pulmonary Toxicants and Oxidative Stressmentioning

confidence: 99%

Oxidative stress-induced autophagy: Role in pulmonary toxicity

Malaviya

Laskin

2014

Toxicology and Applied Pharmacology

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Autophagy is an evolutionarily conserved catabolic process important in regulating the turnover of essential proteins and in elimination of damaged organelles and protein aggregates. Autophagy is observed in the lung in response to oxidative stress generated as a consequence of exposure to environmental toxicants. Whether autophagy plays role in promoting cell survival or cytotoxicity is unclear. In this article recent findings on oxidative stress-induced autophagy in the lung are reviewed; potential mechanisms initiating autophagy are also discussed. A better understanding of autophagy and its role in pulmonary toxicity may lead to the development of new strategies to treat lung injury associated with oxidative stress.

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Mechanisms of carcinogenesis by crystalline silica in relation to oxygen radicals.

Cited by 35 publications

References 11 publications

Induction of interleukin‐1/and interleukin‐8 mRNAs and proteins by TGFβ1 in rat lung alveolar epithelial cells

Induction of interleukin‐1/and interleukin‐8 mRNAs and proteins by TGFβ1 in rat lung alveolar epithelial cells

Bilateral Spontaneous Pneumothorax in Chronic Silicosis: A Case Report

Oxidative stress-induced autophagy: Role in pulmonary toxicity

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