Toxicity of cadmium oxide installed into the rat lung. II. Inflammatory responses in broncho-alveolar lavage fluid

Hirano, Seishiro; Tsukamoto, Naomi; Higo, Sachiko; Suzuki, Kazuo

doi:10.1016/0300-483x(89)90172-8

Cited by 25 publications

(5 citation statements)

References 25 publications

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“…For example, the earliest stages of Cd-induced lung injury primarily involve the disruption of the alveolar septum and the leakage of fluid and solutes into the alveoli (Bus et al, 1978;Pearson and Prozialeck, 2001). However, these early stages of injury are soon followed by the influx and activation of leukocytes and the release of inflammatory mediators that facilitate the inflammatory processes responsible for subsequent pulmonary injury and fibrosis (Bell et al, 2000;Driscoll et al, 1992;Frankel et al, 1991;Hirano et al, 1989).…”

Section: Pulmonary Injurymentioning

confidence: 96%

The vascular endothelium as a target of cadmium toxicity

2006

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Section: Pulmonary Injurymentioning

confidence: 96%

The vascular endothelium as a target of cadmium toxicity

2006

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“…At 90 tg/m3, CdS was less toxic than CdO dust, and the toxicity of the soluble CdSO4 was between the toxicities of these poorly soluble compounds (109). Other studies found the soluble CdCl2 and the poorly soluble CdO either equally toxic (83) or CdO more toxic to the lung than CdCl2 (112,116,117). Both the mortality of rats (109) and pulmonary toxicity in hamsters (115) indicated that, in agreement with its higher bioavailability (112), CdO is more toxic than CdS.…”

Section: Animal Experimentsmentioning

confidence: 96%

Epidemiological and Experimental Aspects of Metal Carcinogenesis: Physicochemical Properties, Kinetics, and the Active Species

Magós¹

1991

Environmental Health Perspectives

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The carcinogenic properties ofselected metals and their compounds are reviewed to provide a useful reference for existing knowedge on relationships between physical and chemical forms, kinetics and carcnogenic potental and between epqiemiology, bioassays, and short-term testL Exteive consideation is given to arsenic, berl, cadmium, chromium, lead, and nickel. Other metas such as antimony, cobalt, copper, iron, man selnium, and zinc are discussed briefly.

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“…These compounds were either radiolabeled or not, soluble or insoluble, with varying valence states, and the mass of the exposure ranged widely. Despite these variabilities, all forms of metals demonstrated some translocation out of the lung [39,40,43,44].…”

Section: Mechanisms For App-induced Vasocons-trictionmentioning

confidence: 99%

“…These studies mostly used rats as model and delivered metals by either inhalation or instillation. Numerous metal compounds have been employed [38] [ [39][40][41][42]. These compounds were either radiolabeled or not, soluble or insoluble, with varying valence states, and the mass of the exposure ranged widely.…”

Section: Mechanisms For App-induced Vasocons-trictionmentioning

confidence: 99%

Vascular Effects of Ambient Pollutant Particles and Metals

Huang

Ghio²

2006

CVP

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Exposure to ambient pollutant particle (APP) is associated with increased cardiovascular morbidity and mortality. Recent evidence indicates that APP-induced vasoconstriction may be an important mechanism. APP constricts systemic arteries and increases blood pressure in human. APP decreases the diameter of pulmonary arterioles in animals. Intratracheal instillation of APP increases pulmonary artery resistance in isolated buffer-perfused lungs, and APP constricts isolated arterial rings. APP-induced vasoconstriction may be secondary to the release of inflammatory mediators from lung cells, which then activate vascular endothelial and smooth muscle cells. The vasoconstriction may also be caused by alterations in autonomic nervous system balance. Some soluble metals (e.g., vanadium) can produce acute vasoconstriction in in vitro and in vivo systems, and contribute to the systemic health effects of APP since they can more easily permeate the alveolar-capillary membrane than the whole particle. Both APP and its associated metals have been shown to enhance the release of endothelin 1 and reactive oxygen species, activate epithelial growth factor receptor and mitogen-activated protein kinases, and inhibit nitric oxide vasodilator activity. The vasoactive properties of APP and metals raised the possibility that patients with vascular diseases may be more susceptible to APP-induced adverse health effects, and that people who are regularly exposed to high amount of metals, e.g., vanadium contained in certain dietary and muscle-building regimens or in the air of boiler making plants, may have increased risk for vascular diseases. Understanding how metals induce vasoconstriction may lead to the development of novel vasodilator therapies for vascular diseases.

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Toxicity of cadmium oxide installed into the rat lung. II. Inflammatory responses in broncho-alveolar lavage fluid

Cited by 25 publications

References 25 publications

The vascular endothelium as a target of cadmium toxicity

The vascular endothelium as a target of cadmium toxicity

Epidemiological and Experimental Aspects of Metal Carcinogenesis: Physicochemical Properties, Kinetics, and the Active Species

Vascular Effects of Ambient Pollutant Particles and Metals

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