Effect of asbestos on lipid peroxidation in the red cells.

Gabor, Silvia; Anca, Z

doi:10.1136/oem.32.1.39

Cited by 10 publications

(5 citation statements)

References 13 publications

(13 reference statements)

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supporting

confidence: 79%

Selenium Effects on the Cytotoxicity and Lung Fibrosis Induced by Silica

S¹,

Ciugudeanu²,

Botoc³

et al. 1986

Acta Pharmacologica et Toxicologica

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The initial event after inhalation of quartz particles is their damaging effect on macrophages, which represent hte most critical cells involved in the pathogenesis of silicotic fibrosis (1,ll). Our previous studies (4,5,6,7,8,9), documented also by other authors (2,3,10,14) provided support for the assumption that lipid peroxidation may be one of the quartz cytotoxic mechanisms in cells and lung tissue. There is evidence that a cooperative antioxidative defense system located within the biological structures can protect against cellular peroxidative damage (12,13). As selenium is intimately linked with the antioxidative system, the present paper was conducted to investigate the in vitro and in vivo effects of this trace element on the quartz induced cytotoxic damage in macrophages and pulmonary fibrosis.Guinea pig peritoneal macrophages were incubated with quartz standard dust (Ddrentruper) of 3 1-1 size and selenium (Na SeO 5H 0). The criteria for the assessment of cell membrane intggris; mgasurements were made on cell ciability (erythrosin exclusion), adherence, migration, lactate dehydrogenase (LDH) and acid phosphatase (AP). The peroxidative damage was estimated by lipid peroxide release (TBA-reaction), glutathione peroxidase (GSH-px) and superoxide dismutase (SOD) activities.Experiments in vivo were performed on rats divided into 4 groups: 1.control, intratracheally instilled with lml saline; 2 . selenite-supplemented (1 ppm) in drinking water for 90 days; 3. quartz intratracheally instilled with a single dose of 30 mg dust; .slenite-supplemented and quartz-trated rats. The animals were killed at 60 days after dust administration. Wet lung and lymph node weights, lipid, phospholipid and hydroxiproline content of the lungs were determined in order to estimate the in vivo fibrosis proliferation. Fig. 1, 2 and 3, reporting the in vitro results, give evidence of selenium protection against quartz cytotoxic action on cell viability, adhesiveness, migration, LDH and AP release. When selenium was added to cell cultures the antioxidant enzyme activities, GHS-ps and SOD, as well as lipid peroxide levels restored to the control cell values.

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“…

…”

supporting

confidence: 79%

Selenium Effects on the Cytotoxicity and Lung Fibrosis Induced by Silica

S¹,

Ciugudeanu²,

Botoc³

et al. 1986

Acta Pharmacologica et Toxicologica

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“…In previous studies asbestos has been shown to induce lipid peroxidation with red blood cells (Gabor & Anca, 1975), phospholipid emulsions (Weitzman & Weitberg, 1985) and isolated microsomes (Gulumian et at., 1983). Others have shown the iron component of crocidolite fibres can catalyse the generation of hydroxyl radicals from hydrogen peroxide (Weitzman & Graceffa, 1984).…”

Section: Discussionmentioning

confidence: 99%

The role of catalytic iron in asbestos induced lipid peroxidation and DNA-strand breakage in C3H10T1/2 cells

Turver

Brown²

1987

Br J Cancer

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Summary The involvement of catalytic iron in the vitro activities of crocidolite asbestos has been investigated. Exposure of C3HlOT1 cells to either the UICC crocidolite standard reference sample or a non fibrous (milled) derivative resulted in an increase of thiobarbituric acid reactive substances. This catalytic activity was inhibited by pretreatment with the iron chelator desferrioxamine. The effect of this activity on cellular DNA was measured in an assay based on the production of DNA-strand breaks. Increased levels of DNA-strand breaks were detected in cultures treated with both the milled and UICC crocidolite. Inclusion of desferrioxamine with the asbestos inhibited DNA-strand breakage. It is concluded the catalytic iron present on the dust is capable of damaging both lipid and DNA and that this could be an important mechanism in asbestos pathogenicity.

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“…Gabor and Anca (54) first demonstrated that asbestos can initiate lipid peroxidation in a cell model of red blood cells. Gulumian et al (55,56) showed that crocidolite asbestos enhanced lipid peroxidation in rat lungs and liver microsomes.…”

Section: Eaizymesmentioning

confidence: 99%

The Role of Oxygen Free Radicals in Occupational and Environmental Lung Diseases

Vallyathan¹,

Shi²

1997

Environmental Health Perspectives

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Oxygen free radicals and their metabolites, collectively described as reactive oxygen species (ROS), have been implicated in the pathogenesis of many diseases. The pulmonary system is particularly vulnerable to ROS-induced injury because of its continuous exposure to toxic pollutants from a wide variety of sources in the ambient air. Additionally, lungs are exposed systemically to ROS generated from xenobiotic compounds and endogenous sources. This review describes the sources of endogenous and exogenous ROS generation in the lung. Special emphasis is given to major sources of ROS in occupational and environmental exposures to asbestos, crystalline silica, coal, chromium, herbicides, bleomycin, and cigarette smoke. ROS-induced lung injury at different target levels may contribute to similar patterns of cell injury and alterations at the molecular level by initiation, propagation, and autocatalytic chain reactions. Intracellular signalling, activation and inactivation of enzymes, stimulation, secretion, and release of proinflammatory cytokines, chemokines, and nuclear factor activation and alterations are also common events. Understanding the interactions of these intricate mechanistic events is important in the prevention and amelioration of lung injury that results from acute and chronic exposures to toxins in ambient air. Environ Health Perspect 1 05(Suppl 1 :1 65-177 (1997)

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Effect of asbestos on lipid peroxidation in the red cells.

Cited by 10 publications

References 13 publications

Selenium Effects on the Cytotoxicity and Lung Fibrosis Induced by Silica

Selenium Effects on the Cytotoxicity and Lung Fibrosis Induced by Silica

The role of catalytic iron in asbestos induced lipid peroxidation and DNA-strand breakage in C3H10T1/2 cells

The Role of Oxygen Free Radicals in Occupational and Environmental Lung Diseases

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