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[Genetic polymorphism of tumor necrosis factor-alpha in patients with chronic benzene poisoning].
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OBJECTIVE
To study the relationship between genetic polymorphism of tumor necrosis factor-alpha (TNF-alpha, sites at -238 nt and -308 nt) and susceptibility to chronic benzene poisoning.
METHODS
The polymorphism of TNF-alpha gene were detected by nested polymerase chain reaction-restriction fragment
Increased production of tumor necrosis factor-alpha by bone marrow leukocytes following benzene treatment of mice.
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Hematopoiesis is regulated by cytokines released from bone marrow stromal cells and mature leukocytes. Recent studies have identified these cells as targets for benzene-induced hematotoxicity. In the present studies we analyzed the effects of benzene treatment of mice on the production of
Chlorine-induced extensive tracheobronchial necrosis concomitantly benzene-induced pancytopenia presented with severe pneumonia.
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We report a case of 25-year-old woman with severe tracheobronchial necrosis caused by chlorine released from a mixture household cleaning agents. She subsequently exposed benzene while she was fixing the seats with benzene containing gum. The case was found interesting with its history, delayed
Induction of apoptosis by benzene metabolites in HL60 and CD34+ human bone marrow progenitor cells.
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Two cell types, HL60 human promyelocytic leukemia cells and CD34+ human bone marrow progenitor cells, were used as model systems to explore a possible role for apoptosis in the myelotoxicity of the phenolic metabolites of benzene. HL60 cells were treated with either phenol, catechol, hydroquinone,
Chest wall necrosis and empyema resulting from attempting suicide by injection of petroleum into the pleural cavity.
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Hydrocarbon poisoning such as that of benzene and petroleum usually occurs accidentally by inhalation or ingestion of these cytotoxic chemical compounds. Intravenous or subcutaneous injection of petroleum compounds with intent of suicide or abuse is an extraordinary event that can result in local
The effect of occlusive and unocclusive exposure to xylene and benzene on skin irritation and molecular responses in hairless rats.
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Aromatic hydrocarbons readily penetrate the skin on dermal exposure, leading to irritation, inflammation and cytotoxicity. The effects of short-term occlusive and long-term unocclusive dermal exposure to benzene and xylene on the skin irritation response (transepidermal water loss (TEWL), skin
Tumor necrosis factor-alpha production enhancing activity of substituted 3'-methylthalidomide: influence of substituents at the phthaloyl moiety on the activity and stereoselectivity.
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The synthesis and tumor necrosis factor (TNF)-alpha production enhancing activity of substituted 3'-methylthalidomides on human leukemia cell line HL-60 stimulated with 12-O-tetradecanoyl-phorbol 13-acetate (TPA) are described. Though the introduction of an electron-donating amino group at the
Hydroquinone, a reactive metabolite of benzene, reduces macrophage-mediated immune responses.
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Hydroquinone is a toxic compound and a major benzene metabolite. We report that it strongly inhibits the activation of macrophages and associated cells. Thus, it suppressed the production of proinflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-3, IL-6, IL-10,
A method for in vitro culture of rat Zymbal gland: use in mechanistic studies of benzene carcinogenesis in combination with 32P-postlabeling.
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Zymbal glands were excised bilaterally from the ear ducts of female Sprague-Dawley rats (three/group), minced into approximately four fragments per gland, and transferred into a microtiter plate containing 1.5 mL per well of Waymouth's tissue culture medium supplemented with fetal calf serum,
Histopathological alterations in hepatopancreas of Gafrarium divaricatum exposed to xylene, benzene and gear oil-WSF.
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Gafrarium divaricatum were exposed to xylene (4.25 and 8.50 mg l(-1)), benzene (4.35 and 8.70 mg l(-1)) and gear oil-WSF (1 and 2%) for 30 days. Chronic exposure of clams to the pollutants resulted in loss of bubbling epithelium, reduction in cytoplasm volume and density, fusion of cell membranes
Bone marrow morphology in patients with neutropenia due to chronic exposure to organic solvents (benzene): early lesions.
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The authors present the histological and cytological features of bone marrow (BM) in 152 employees from the steel plant of Cubatão (S. Paulo-Brazil) who presented with neutropenia, due to chronic exposure to benzene and its homologues. All patients were male. Mean age was 35 years. At the time of
Early increase in cyclin-D1 expression and accelerated entry of mouse hepatocytes into S phase after administration of the mitogen 1, 4-Bis[2-(3,5-Dichloropyridyloxy)] benzene.
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We have previously demonstrated that hepatocyte proliferation induced by the mitogen 1,4-bis[2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP) is independent of changes in cytokines, immediate early genes, and transcription factors that are considered to be necessary for regeneration of the liver after
Depletion of WRN enhances DNA damage in HeLa cells exposed to the benzene metabolite, hydroquinone.
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Werner syndrome is a progeroid disorder caused by mutations of the WRN gene. The encoded WRN protein belongs to the family of RecQ helicases that plays a role in the maintenance of genomic stability. Single nucleotide polymorphisms in WRN have been associated with an increased risk for some cancers
The TNF-alpha 238A polymorphism is associated with susceptibility to persistent bone marrow dysplasia following chronic exposure to benzene.
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Chronic exposure to benzene can result in transient hematotoxicity (benzene poisoning, BP) or persistent bone marrow pathology including dysplasia and/or acute myeloid leukemia. We recently described a persistent bone marrow dysplasia with unique dysplastic and inflammatory features developing in
Rhabdomyolysis with acute tubular necrosis following occupational inhalation of thinners.
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Thinners are mixtures of organic solvents commonly containing toluene, xylene, acetone, hexane, benzene and methyl isobutyl ketone. This report describes a case of rhabdomyolysis with acute tubular necrosis and renal failure, most likely attributable to toluene, following occupational exposure to
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