Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002874 (aplastic anemia)
 5,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver iron and copper concentrations were estimated in 395 patients undergoing hepatological examination. Relations to clinical, morphological and laboratory data were evaluated. Liver iron concentrations were not significantly different in chronic hepatitis of viral, toxic or immunological origin. Liver iron levels exceeding 100 mg/100 g dry liver tissue (normal range up to 300 mg/100 g) were only found in idiopathic hemochromatosis (n = 8), in a patient with prophyria cutanea tarda and in a multiple transfused patient who suffered from aplastic anemia. Liver copper content was significantly increased in primary biliary cirrhosis compared to chronic hepatitis of other origin. Apart from untreated Wilson's disease (n = 3) copper levels higher than 25 mg/100 g dry liver tissue (normal range up to 6 mg/100 g) were measured in chronic active hepatitis B (n = 2), primary biliary cirrhosis (n = 9) and in chronic hepatitis of uncertain origin (n = 3). Therefore excess accumulation of copper in the liver was typical of Wilson's disease but less diagnostic than severely elevated liver iron stores of idiopathic hemochromatosis.
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PMID:[Significance of the iron and copper content of the liver for the differential diagnosis of chronic liver diseases]. 223 66

The major components of untreated wood--cellulose, hemicellulose, and lignin--have not been implicated as toxicants, but extractive substances, especially in heartwood, can be toxic. Decay-resistant woods are more likely to contain irritants or sensitizers than nondurable woods. Short-term exposures to certain wood dusts may result in asthma, conjunctivitis, rhinitis, or allergic dermatitis, but long-term effects may include nasal cancer and Hodgkin's disease. Some thermophilic microorganisms found in wood are human pathogens, and septic splinters (chromomycosis) and inhalation of ascomycete spores from stored wood chips have been implicated in human illnesses. Reconstituted wood can contain formaldehyde resins, which pose health risks in enclosed humid areas. Pentachlorophenol (PCP)-treated wood is particularly toxic--short-term exposures to PCP-treating solutions can lead to aplastic anemia and mortality, while diseases such as Hodgkin's disease are associated with long-term exposures. Since much commercial lumber is dipped in PCP, the separation of the chronic effects of wood dust from PCP exposure is difficult. Chromated copper arsenate (CCA)- and ammoniacal copper arsenite (ACA)-treated wood may leach arsenic. CCA-treated wood is potentially safer, since it contains the pentavalent arsenic, which is a common constituent in the environment. ACA contains the trivalent arsenic, which is more toxic.
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PMID:Health hazards of natural and introduced chemical components of boatbuilding woods. 390 39

Reduction of the nitro group of chloramphenicol (CAP) gives rise to more highly reactive intermediates which may in involved in the aplastic anemia associated with CAP use. One such intermediate, nitroso-chloramphenicol (NO-CAP), has been found to be a potent agent for mediating degradation of isolated DNA. In a reaction mixture containing 100 microM NO-CAP, 100 microM CuCl2, and 5 mM NADH, 7 micrograms of Escherichia coli [3H]DNA was completely degraded to acid-soluble fragments in 30 min. Damage to DNA was in the form of single-stranded scissions. The requirement for copper was specific, and copper chelating reagents blocked the degradation. The need for a reducing agent could be met equally well by NADH or NADPH, but not by sulfhydryl reagents such as glutathione, dithiothreitol and 2-mercaptoethanol. Oxygen was also necessary for the NO-CAP mediated DNA damage, with reduced forms of oxygen participating in the reaction. A role for H2O2 was indicated by the inhibition of the degradation seen when catalase was included in the mixture. Hydroxyl radicals are known to be produced in the reaction of H2O2 with certain transition metals. Scavangers of hydroxyl radicals also inhibited strand-scission, suggesting that the radicals may be the primary agents in DNA degradation. The importance of the nitroso moiety of NO-CAP was evidenced by the lack of DNA damage seen when NO-CAP was replaced by CAP under the conditions tested.
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PMID:Degradation of isolated deoxyribonucleic acid mediated by nitroso-chloramphenicol. Possible role in chloramphenicol-induced aplastic anemia. 712 41

The toxic effects of environmental factors at work places on the hematopoietic and immune systems are of basic importance due to the time of exposure, lasting on average 8 hours daily during one week. Porphyrinurias and porphyrias have been observed after exposure to hexachlorobenzene, chlorinated dibenzodioxins, polychlorinated biphenyls, polybrominated biphenyls, vinyl chloride and lead. Aplastic anemia may occur after exposure to benzene, pesticides, arsenic, cadmium and copper compounds. Megaloblastic anemia has been noted in subjects exposed to arsenic, chlordane, benzene and nitrous oxide. Methemoglobinemia is induced by aromatic nitro and amino compounds. Hemolytic reactions caused by arsenic, methyl chloride, naphthalene, lead, cadmium and mercury compounds represent a separate problem. Immunodeficiencies resulting in decreased antitumor and antiinfectious immunity have been reported in subjects exposed to asbestos, ozone, dimethylsulphoxide, vinilidene chloride, and benzene homologues. Lymphocytopenia may be induced by manganese, lead, toluene and industrial noise. Neutropenia was marked after exposure to carbon disulphide, arsenic compounds, benzene and electromagnetic fields. Only a few reports concern the lymphocyte T3, T4 and T8 subpopulations. Electromagnetic fields (microwaves) cause an imbalance of that subpopulation, consisting of a decrease in the T8 cell count. The neutrophil enzymes, such as myeloperoxidase and alkaline phosphatase, decrease in their activity after exposure to polychlorinated biphenyls, carbon disulphide, chlorobenzene and DDT. A majority of agents cited include genotoxic effects reflected in chromosome aberrations and increased sister chromatid exchange and abnormal unscheduled DNA synthesis. Leukemia or lymphoma risk is increased after exposure to pesticides, electromagnetic fields, benzene and irradiation.
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PMID:Immunotoxic and hematotoxic effects of occupational exposures. 817 62

Exposure of humans and experimental animals to benzene has been shown to result in hematotoxicity such as pancytopenia, aplastic anemia, and leukemia. The oxidative activation of the benzene metabolite, hydroquinone (HQ), in the bone marrow to the electrophilic benzoquinone (BQ) has been suggested to play an important role in benzene-induced hematotoxicity. Since the interaction of several xenobiotics with copper has been shown to result in their metabolism, in this study we have investigated the role of copper in the oxidation of HQ and HQ-induced toxicity to mice bone marrow stromal cells, target cells of HQ in the bone marrow. In phosphate-buffered saline, HQ underwent autoxidation slowly to BQ, while the presence of Cu(II) ions (1, 2.5, 5, 10, 50 microM) strongly accelerated the oxidation of HQ to BQ in a concentration-dependent manner. Reaction of HQ with Cu(II) was also accompanied by the reduction of Cu(II) to Cu(I), the utilization of O2, and the concomitant generation of H2O2. The oxidation of HQ by Cu(II) could be blocked by the Cu(I)-specific chelator bathocuproinedisulfonic acid (BCS), particularly when the ratio of BCS to Cu(II) was 4:1. By observing the kinetics of the reactions derived from mixing 100 microM HQ and 100 microM Cu(II), it was found that all of the Cu(II) was reduced to Cu(I) within 5 s, followed by consumption of O2 and the generation of BQ, which reached maximum levels at 4 min after mixing HQ and Cu(II). In addition, oxidation of HQ by Cu(II) also generated chemiluminescence. In the presence of myeloperoxidase, Cu(II)-mediated oxidation of HQ was increased. Addition of Cu(II) to primary bone marrow stromal cell cultures significantly enhanced HQ-induced cytotoxicity. The enhanced cytotoxicity of HQ by Cu(II) could be completely prevented by adding BCS, glutathione (GSH), or dithiothreitol but not by catalase. Supplementation of stromal cells with 20 microM BCS in the absence of exogenously added Cu(II) significantly abated HQ-induced cellular GSH depletion and cytotoxicity, suggesting a possible involvement of endogenous copper in the activation of HQ. The above results indicate that Cu(II) strongly induces the oxidation of HQ and as such may be a factor involved in the oxidative activation and toxicity of HQ in target cells.
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PMID:Oxidation of hydroquinone by copper: chemical mechanism and biological effects. 842 68

Mean serum zinc and copper levels were measured in pediatric patients with idiopathic aplastic anemia. Zinc levels were significantly lower in patients compared to controls and correlated with severity of disease. Serum copper levels were significantly higher in patients. There was no correlation with severity of disease. Cu/Zn ratio also correlated with severity of disease.
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PMID:Serum zinc and copper levels in aplastic anemia. 2279 94

Pancytopenia is a health condition in which there is a reduction in the amount of leucocytes, erythrocytes and thrombocytes. If more than one of the blood cells is low then the condition is called as bicytopenia. The pancytopenic condition is observed in treatment of diseased conditions like thalassemia and hepatitis C. Iatrogenically pancytopenia is caused by some antibiotics and anti-HCV drugs. Medical conditions like aplastic anaemia, lymphoma, copper deficiency, and so forth can also cause pancytopenia. Pancytopenia can in turn decrease the immunity of the person and thereby can be fatal. Current therapies for pancytopenia include bone marrow stimulant drugs, blood transfusion and bone marrow transplant. The current therapies are very excruciating and have long-term side-effects. Therefore, treating these condition using herbal drugs is very important. Herbs like wheatgrass, papaya leaves and garlic are effective in treating single lineage cytopenias. The present review is focused on the potential effects of natural herbs for the treatment of pancytopenia.
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PMID:Herbal approach in the treatment of pancytopenia. 2819 48

Clinical copper deficiency is now more frequently recognized. Hematologically, it can present as anemia (microcytic, normocytic, or macrocytic) and neutropenia. Thrombocytopenia is relatively rare. Neurologically, it can manifest as myelopathy and peripheral neuropathy simulating subacute combined degeneration. Bone marrow findings can mimic myelodysplasia resulting in occasional inappropriate referral for bone marrow transplantation. Other conditions with similar presentations include infections, drug toxicity, autoimmunity, B12 deficiency, folate deficiency, myelodysplastic syndrome, aplastic anemia, and lymphoma with bone marrow involvement. Hematological, but not neurological, manifestations respond promptly to copper replacement, making early diagnosis essential for good outcome. Common risk factors for copper deficiency are foregut surgery, dietary deficiency, enteropathies with malabsorption, and prolonged intravenous nutrition (total parenteral nutrition). We present a unique case of copper deficiency, with no apparent known risk factors.
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PMID:Copper deficiency, a new triad: anemia, leucopenia, and myeloneuropathy. 2904 59