USE OF AN <i>IN VIVO</i> TEST SYSTEM TO INVESTIGATE THE ACUTE AND SUB-ACUTE RESPONSES OF THE RAT LUNG TO MINERAL DUSTS

Sykes, S. E.; Morgan, A.; Evans, J. C.; Evans, N.; Holmes, Andrew; Moores, S. R.

doi:10.1093/annhyg/26.5.593

Cited by 25 publications

(3 citation statements)

References 22 publications

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“…Previous studies have demonstrated that changes in bronchoalveolar lavage fluid (BALF) LDH and total protein levels are sensitive indicators of lung injury (10)(11)(12). Increases in LDH, a cytosolic enzyme, are indicative of cytotoxicity, while changes in total protein suggest exudation of plasma proteins, i.e.…”

Section: Pulmoonary Pathologymentioning

confidence: 99%

Toxicity in the Rat of Smoke Produced by Combustion of Aircraft Audio Cable Insulation

Carpenter¹,

Rossi²,

Narayanan³

et al. 1993

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Section: Pulmoonary Pathologymentioning

confidence: 99%

Toxicity in the Rat of Smoke Produced by Combustion of Aircraft Audio Cable Insulation

Carpenter¹,

Rossi²,

Narayanan³

et al. 1993

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“…For cytotoxic materials such as bentonite and noncytotoxic materials (such as titanium dioxide) which are not fibrogenic, the acute inflammatory response of the lung was short-lived, and the free cell population of the lung returned to normal within a few weeks. For quartz, however, which is both cytotoxic and fibrogenic, the influx of PMN was followed by a subacute phase in which the inflammatory response persisted and was even exacerbated over a period of at least three months (4,5). This prolonged inflammatory response is now known to occur both in experimentally induced fibrosis in animal models (6) and in patients with idiopathic pulmonary fibrosis (7).…”

Section: Introductionmentioning

confidence: 99%

The advantages and limitations of an in vivo test system for investigating the cytotoxicity and fibrogenicity of fibrous dusts.

Sykes¹,

Morgan²,

Moores³

et al. 1983

Environ Health Perspect

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The acute response of the rat lung to a range of fibrous materials has been investigated by bronchopulmonary lavage, at dose levels of 0.5 and 1.0 mg, 1 and 7 days after their administration by intratracheal instillation. The materials chosen for study included UICC chrysotile A, amosite, crocidolite and anthophyllite, and samples of S. African "long" amosite and glass fiber. In addition, the subacute response to 1, 2 and 3 mg of chrysotile and amosite has been studied at 50 and 100 days after instillation. In the acute phase at 1 day after instillation, the response to chrysotile was greater than that to any of the other materials, but by 7 days there was no gradation in the response to different dusts. In the subacute phase, cell recoveries were low, and it was not possible to assess the long-term cytotoxic or fibrogenic effects of amosite and chrysotile by analyses of lung washes, even though biochemical and histological methods indicated gross changes in lung pathology.

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“…Numerous studies in rats have shown that an inflammatory and pneumotoxic response develops after acute intratracheal exposure to silica (2)(3)(4). This response is characterized as a rapidly progressive disease associated with extensive epithelial damage and abundant airway debris.…”

mentioning

confidence: 99%

Acute silica toxicity: attenuation by amiodarone-induced pulmonary phospholipidosis.

Antonini

McCloud²,

Reasor³

1994

Environ Health Perspect

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Exposure to the toxic mineral dust silica has been shown to produce an acute inflammatory response in the lungs of both humans and laboratory animals. Coating silica with phospholipids reduces its toxicity when studied with in vitro systems. The drug amiodarone increases phospholipid within the cells, airways, and alveoli of the lungs. This increase in phospholipid is due to amiodarone's ability to inhibit phospholipase activity within alveolar macrophages (AMs) and whole lung. The purpose of this study was to determine whether the amiodarone-induced increase in pulmonary phospholipid would protect the lungs from acute damage caused by the intratracheal instillation of silica. Treatment of male Fischer 344 rats with amiodarone for 14 days caused an increase in phospholipid content in bronchoalveolar lavage fluid and AMs compared to vehicle-treated controls. The rats were then instilled with silica or saline vehicle. At both 1 and 14 days after silica exposure, pulmonary phospholipidosis was associated with a marked reduction in acute silica-induced pulmonary damage as assessed by biochemical parameters in bronchoalveolar lavage fluid, however, the influx of neutrophils into the airspaces was not reduced. Four times more phospholipid was bound to the silica recovered from amiodarone-treated rats compared to controls. The results of these in vivo experiments indicate that pulmonary phospholipidosis attenuates the acute damage associated with the intratracheal instillation of silica in rats. By using an in vitro cell culture system, we demonstrated that, in contrast to control AMs, phospholipidotic AMs were significantly more resistant to the cytotoxicity of surfactant-coated silica.(ABSTRACT TRUNCATED AT 250 WORDS) Images p372-a Figure 1. Figure 2. Figure 3. Figure 4. Figure 5. Figure 6. Figure 7. Figure 8.

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USE OF AN IN VIVO TEST SYSTEM TO INVESTIGATE THE ACUTE AND SUB-ACUTE RESPONSES OF THE RAT LUNG TO MINERAL DUSTS

Cited by 25 publications

References 22 publications

Toxicity in the Rat of Smoke Produced by Combustion of Aircraft Audio Cable Insulation

Toxicity in the Rat of Smoke Produced by Combustion of Aircraft Audio Cable Insulation

The advantages and limitations of an in vivo test system for investigating the cytotoxicity and fibrogenicity of fibrous dusts.

Acute silica toxicity: attenuation by amiodarone-induced pulmonary phospholipidosis.

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