Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six South African White miners were studied with the 2-g L-tryptophan load test and tracer doses of L-tryptophan-7a-14C, L-kynurenine-keto-14C and hydroxy-L-kynurenine-keto-14C. The breath 14CO2 and 14 urinary metabolities were measured. When they were compared with a previous study of American women with scleroderma, similar 14CO2 and tryptophan metabolite excretion patterns were observed in the data from the miners. The labelled quinolinic acid excretion was more significantly elevated in the South African miners' urine than in the urine of the American women. The data from both studies suggest that some patients with scleroderma have an altered step in the tryptophan metabolic pathway after hydroxy-anthranilic acid. What relationship exists between the induction of pulmonary silicosis and the subsequent development of scleroderma, requires additional human studies.
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PMID:Metabolism of 14C-labelled L-tryptophan, L-kynurenine and hydroxy-L-kynurenine in miners with scleroderma. 84 60

Scleroderma-like diseases can be induced by a number of chemical compounds, such as plastics, solvents and drugs. Contaminated rapeseed oil was the cause of the toxic oil syndrome and L-tryptophan induces the so-called eosinophilia-myalgia-syndrome. On the other hand, paraffin and silicon can trigger so-called adjuvant disease, while long-term exposure to silica can lead to idiopathic scleroderma (associated with silicosis in some cases). In addition to the clinical features, some pathogenetic data in the literature, such as genetic factors (HLA, chromosomal anomalies, enzyme deficiencies) and the metabolism of chlorinated ethylenes via reactive epoxide intermediate products, and our own findings are reported. Silica-induced scleroderma cannot be distinguished from the idiopathic form by epidemiological, clinical or immunological studies or by parameters referring to the blood vessels or collagen metabolism. In cell culture studies it has been shown that macrophages/monocytes release IL1, IL6 and TNF after ingestion of silica, which affects fibroblasts, T-helper cells and endothelial cells. Comparative results from the silicosis literature are reported. Finally, the possibly stimulating role of ionizing irradiation (uranium mining) in favouring the development of scleroderma is discussed.
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PMID:[Chemically-induced scleroderma]. 150 11

Workers in denim sandblasting are at a high risk of developing silicosis, an occupational lung disease caused by inhaling crystalline silica dust. The development and progress of silicosis is associated with the activation of the immune system and oxidative stress. In the former, interferon-gamma induces both neopterin release and the enzyme indoleamine [2, 3]-dioxygenase (IDO) in various cells. The determination of the kynurenine-to-tryptophan ratio and neopterin concentration has proven to be an efficient method to monitor the activation status of IDO and cellular immunity. The present study aimed to investigate whether occupational silica exposure leads to any alterations in neopterin levels, tryptophan degradation, and activities of superoxide dismutase (SOD) and catalase (CAT), agents in the antioxidant defense system. Fifty-five male denim sandblasting workers and twenty-two healthy men as controls were included. Mean neopterin and kynurenine levels, kynurenine-to-tryptophan ratio, and SOD activity were higher in subjects with silicosis compared to non-exposed controls (all, p<0.05). Neopterin levels and kynurenine-totryptophan ratios were positively correlated (p<0.05); however, no correlation was observed between length of employment and the measured parameters. Some of the measured parameters were significantly affected by the severity of the pathology. Our results suggest that silica exposure activates the cellular immune response. The increased neopterin levels and tryptophan degradation confirm the possibility of their use as an indicator of cellular immune response.
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PMID:Immunomodulation and oxidative stress in denim sandblasting workers: changes caused by silica exposure. 2408 52