Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This contribution presents data from the literature as well as our own results concerning the mechanisms of hepatic encephalopathy (HE). 1. Blood chemistry: In patients with liver cirrhosis, the plasma levels of ammonia, phenylalanine, tyrosine, phenolic acids, and octopamine correlated with the stages of HE. Methionine and free tryptophan concentrations were increased only in stages 2-4. Further, branched chain amino acids were below the normal range. Experimental findings in animals elucidated some mechanisms of these changes. 2. Effects of administered substances: With ammonia, methionine, methanethiol, tryptophan, phenolic substances, and fatty acids central nervous disturbances were observed. 3. Interactions: Anemia, methanethiol, and fatty acids favored ammonia toxicity. Alkalosis diminished cerebral symptoms. 4. Neurotransmitters: HE was accompanied by an enhanced turnover of serotonin and by increased amounts of false neurotransmitters (like octopamine) in the brain. 5. Oxydative brain metabolism: Disorders of cerebral oxygen and glucose utilization were mainly documented in cases of long term HE with EEG alterations. 6. Structural changes of the brain: Most of them are irreversible.
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PMID:[Pathogenesis of hepatic encephalopathy (author's transl)]. 1 66

Experiments were conducted to determine the effects of feeding diets low in protein, glycine, or tryptophan on iron metabolism in the growing chick. Three-day-old chicks, which were fed the experimental diets to 2 weeks of age, were given orally a solution of 59FeSO4 in order to determine the percentage of iron absorbed and excreted (determined by the fecal recovery method) and iron utilized and stored (determined by the radioactivity retained per unit liver, gastrocnemius muscle, and whole blood) 7 days post dose administration. The feeding of diets low in protein (5.4%, 8.5%, or 10.8%) or tryptophan (0.12%) but adequate in iron to growing chicks caused: a marked reduction in growth, rate of erthropoiesis, and percentage iron absorption; an excessive increase in iron deposited in the liver and muscle, and percentage iron collected in the excreta; and anemia which was attributed to the deficiency of protein or tryptophan respectively, in the diets fed. The feeding of diets low in glycine (0.33%) but adequate in iron caused: a marked reduction in growth and percentage iron, absorption, and a transitory increase in percentage of iron excreted without causing anemia or affecting the distribution of absorbed iron in liver, muscle and blood. The total plasma protein concentration was reduced in protein deficient chicks, but was not affected by a tryptophan or glycine deficiency.
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PMID:Effects of dietary protein, glycine, and tryptophan on iron metabolism in the growing chick. 83 77

A summary of the effects of contraceptive pills on vitamins in the b lood is presented. The significant increase of Vitamin-A in the plasma of contraceptive users is believed to be a result of the increase of bet alipoprotein, which binds chiefly to Vitamin-A. Although high concentrations of Vitamin-A have caused teratogenicity in test animals, the increase found in humans using contraceptive pills is not high enough to cause risk. A lowering of Vitamin-B6 (pyridoxin) levels has occurred with the use of contraceptive pills. This can cause alteration in the metabolism of tryptophan, which could cause depression in pill users. The lack of pyridoxine can also increase the production of xanthuric acid which binds with insulin, resulting in a decreased glucose tolerance. A decrease in folic acid in pill users has also been observed, caused by some effect of the pill on the folate deconjugate. The Vitamin-B12 level is also lowered for unascertainable reasons related to the decrease in folic acid. No anemia occurs in spite of the lowered Vitamin-B complex levels in the blood. A lack in Vitamin-C in users of pills containing estrogens is possibly effected by a corresponding increase between estrogens and ceruloplasmin, a protein active in the oxidation of ascorbic acid. This lack of Vitamin-C has had no clinical significance thus far.
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PMID:[P-pills and vitamins]. 114 66

This article reviews the pathophysiologic concept that superoxide and hydrogen peroxide, generated by activated leukocytes, together with low-molecular-weight chelate iron derived from fecal sources and from denatured hemoglobin, amplify the inflammatory response and subsequent mucosal damage in patients with active episodes of ulcerative colitis. The putative pathogenic mechanisms reviewed are as follows: (1) Dietary iron is concentrated in fecal material owing to normally limited iron absorption. (2) Mucosal bleeding, characteristic of ulcerative colitis, as well as supplemental oral iron therapy for chronic anemia, further conspire to maintain or elevate mucosal iron concentration in colitis. (3) Fenton chemistry, driven especially by leukocyte-generated superoxide and hydrogen peroxide, leads to formation of hydroxyl radicals. (4) The resultant oxidative stress leads to the extension and propagation of crypt abscesses, either through direct membrane disruption by lipid peroxidation or through generation of secondary toxic oxidants such as chloramines. (5) Chemotactic products of lipid peroxidation, including 4-hydroxynonenal, provide positive feedback to accelerate this inflammatory/oxidative process, leading to acute exacerbations of the disease. (6) Other oxidized products, such as oxidized tryptophan metabolites, created by free radical mechanisms in or near the mucosa, may act as carcinogens or tumor promotors that contribute to the exceedingly high incidence of colon carcinoma in patients suffering from chronic ulcerative colitis. In this way, self-sustaining cycles of oxidant formation may amplify flare-ups of inflammation and mucosal injury in ulcerative colitis. This concept, if proved correct by subsequent research, would provide a rationale for several novel clinical approaches to the management of ulcerative colitis, including use of SOD mimetics, iron chelators, and chain-breaking antioxidants.
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PMID:Oxygen radicals in ulcerative colitis. 135 59

The carcinogenic tryptophan pyrolysis products, 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) and 3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2), have been measured in plasma and red blood cells (RBC) of patients with uremia and normal subjects by using a high-performance liquid chromatography (HPLC) method. In both uremic patients and normal subjects, these carcinogens have been detected in RBC as well as plasma. Trp-P-1 and Trp-P-2 levels in plasma of uremic patients were significantly higher than those of normal subjects. Moreover, these carcinogen levels in RBC (per hemoglobin) were significantly elevated in uremic patients in spite of the presence of severe anemia. These results suggest that patients with uremia are continuously exposed to higher levels of these carcinogens as compared with normal subjects. Our data also support the idea that these carcinogens in plasma and RBC are suitable for monitoring exposure levels in humans.
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PMID:Elevation of levels of carcinogenic tryptophan pyrolysis products in plasma and red blood cells of patients with uremia. 154 Oct 61

The case of a female child with a unique generalized congenital dyschromia is reported. She had hypopimented skin, with hypomelanosis and hypomelanocytosis, and many pigmented macules, which consisted of epidermal and dermal hypermelanosis without hypermelanocytosis. Biochemical investigations revealed normal catecholamine metabolism but abnormal tryptophan metabolism, including a decrease in blood serotonin and melatonin. A slight platelet storage pool disease was demonstrated, and a recurrent megaloblastic folate-related anemia occurred. The possible relationship between the pigmentary disease and the biochemical abnormalities is discussed. We suggest that this case represents a previously undescribed association of dyschromia, erythrocyte, platelet, and tryptophan metabolism abnormalities.
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PMID:Congenital dyschromia with erythrocyte, platelet, and tryptophan metabolism abnormalities. 318 92

Two groups of three German shepherd dogs each were inoculated with Leishmania chagasi or Leishmania donovani amastigotes and the infection was followed for 82 days. The dogs developed a persistent infection, became thin, and developed splenomegaly and lymphadenomegaly by 55 days after inoculation. All dogs developed a normocytic, normochromic anemia of increasing severity. Thrombocytopenia and leukopenia occasionally occurred. Blood tryptophan levels were decreased significantly in infected dogs. Increased total serum protein, with hypergammaglobulinemia and hypoalbuminemia, was present in all dogs to various degrees. There was a marked increase in gamma globulins, with smaller increases in alpha and beta globulins. Many of the clinicopathologic changes observed in these dogs were similar to the disease as it occurs in man. The German shepherd dog may be a useful laboratory model for the study of visceral leishmaniasis.
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PMID:Visceral leishmaniasis in the German shepherd dog. I. Infection, clinical disease, and clinical pathology. 671 Aug 16

Weanling Wistar-strain female rats were fed a normal or an iron-deficient diet for 8 weeks and oral contraceptive steroids (OCS) were added for the last 4 weeks. Hemoglobin content, serum iron and zinc levels, liver iron levels, and tryptophan pyrrolase activities, and liver, kidney, and brain zinc levels and alkaline phosphatase activities were determined. Compared to control rats given the normal diet (N group), elevated liver zinc levels and tryptophan pyrrolase activity were found in rats fed the normal diet containing OCS ( + S group), but other parameters did not alter. In rats fed the iron-deficient diet alone (D group), only liver zinc levels were significantly higher, while other parameters were in general lower than those in the N group. In rats fed the iron-deficient diet containing OCS (D + S group), all hematological values, tissue mineral contents with the exception of liver zinc levels, and liver tryptophan pyrrolase and kidney alkaline phosphatase activities were lowered, compared to the N or N + S group. However, compared to the D group, the values of most parameters in the D + S group did not differ significantly, apart from an increase in serum zinc levels. These observations suggest that OCS does not greatly influence the various changes caused by iron-deficient anemia.
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PMID:Oral contraceptive steroids: effects on iron and zinc levels and on tryptophan pyrrolase and alkaline phosphatase activities in tissues of iron-deficient anemic rats. 738 13

A niacin-deficient purified amino acid diet that contained adequate (40 mg/kg) or deficient (10 or 15 mg/kg) iron was used to assess the growth promoting efficacy of tryptophan as a niacin precursor. Basal diets contained 1400 mg/kg tryptophan, a level that was established as meeting the requirement for tryptophan per se in diets containing excess nicotinic acid. Chicks fed the iron-deficient diets had markedly lower hemoglobin concentrations than those fed the iron-adequate diets. Regardless of iron level, chicks exhibited linear growth responses to either nicotinic acid or tryptophan supplementation. Using multiple-linear regression of weight gain on supplemental tryptophan or nicotinic acid intake, the efficiency (wt:wt) of tryptophan conversion to niacin activity (i.e., tryptophan slope divided by nicotinic acid slope) was a mean of 1.77% (56:1) for chicks fed the iron-deficient diet. This was significantly (P < 0.05) lower than the 2.39% (42:1) efficiency calculated for chicks fed the iron-adequate diet. Thus, iron deficiency reduced tryptophan utilization (for NAD synthesis) but had no effect on nicotinic acid utilization. The results suggest that pellagra in populations having endemic anemia and protein-energy malnutrition may be due not only to inadequate intakes of bioavailable niacin but also to inadequate intakes of bioavailable iron.
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PMID:Iron deficiency reduces the efficacy of tryptophan as a niacin precursor. 812 Jun 64

The gene coding for the major core protein (p26) of the lentivirus equine infectious anemia virus (EIAV) was cloned from EIAV infected serum, expressed in E. coli, and the resultant protein purified to electrophoretic homogeneity. The protein was expressed in a soluble form and was purified by conventional protein separation methods. When analyzed by SDS-PAGE, under both reducing and non-reducing conditions, the purified protein migrated as a 26 kDa monomer. Recombinant p26 (rp26), therefore, does not contain any intermolecular disulfide bond. Gel filtration chromatography also indicated that the protein occurs as a monomer in solution. Labeling of free sulphydryl groups with [1-14C]iodoacetamide suggests that none of the three cysteine residues of rp26 is involved in intramolecular disulfide bonds. The circular dichroism spectrum of rp26 was consistent with the following assignment of secondary structure elements: 51% a-helix, 15% beta-turn, and 34% aperiodic. Fluorescencespectroscopy revealed that the three tryptophan residues in rp26 occupy two different environments. These data support the conclusion that the recombinant protein is folded into an ordered and probably native conformation. Immunoblotting and enzyme immunoassay with EIAV infected sera demonstrated that recombinant p26 protein may be useful for diagnostic purposes.
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PMID:Cloning, expression, purification, and characterization of the major core protein (p26) from equine infectious anemia virus. 916


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