Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera from cancer patients specifically suppressed phosphofructokinase (fructose-6-phosphate kinase [PFK], EC 2.7.1.11), a rate-limiting enzyme in the glycolysis pathway. Among 418 cancerous sera, 68.7% evidence suppression; there was no organ specificity. Among 42 sera from early gastric cancer patients, 29 (69.0%) were positive, as were advanced gastric cancer, 14/19 (73.3%) pancreas cancer, and 75/101 (74.3%) lung cancer sera. In contrast 6/50 (12.0%) sera from patients with gastroduodenal ulcer, 3/23 (13.0%) with myoma uteri, and 0/6 with lung tuberculosis were positive. Patients with diabetes mellitus and those receiving steroid hormone therapy showed strong positive suppression. Comparative studies using other tumor markers (immunosuppressive acid protein, carcinoembryonic antigen, alpha-fetoprotein, beta 2-microglobulin, and ferritin) and the same sera used from PFK assay showed that the PFK method was two to three times more sensitive. Sephadex G-200 column chromatography revealed that the PFK-suppressive activity was retained in the postalbumin fraction. The PFK method may represent a promising new cancer screening method.
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PMID:A new cancer marker: a possible cancer screening method based on the suppression of phosphofructokinase by sera from cancer patients. 293 46

Trypanosoma brucei EATRO 110 infection in deer mice (Peromyscus maniculatus) produced anemia in 15 of 42 mice between postinoculation days 14 and 70. The infected anemic (IA) mice had significantly higher reticulocyte counts (P less than 0.025), spleen (P less than 0.001) and liver (P less than 0.005) weights, and higher parasitemia than did infected nonanemic (INA) mice. gamma-Globulin concentrations of infected mice were markedly increased, and values for INA mice were 10% higher than values for IA mice. Erythrocyte hexokinase, glucose-6-phosphate dehydrogenase, glutathione peroxidase, glutathione reductase, and pyruvate kinase activities were increased in infected mice, whereas phosphofructokinase was only slightly decreased in infected mice. Seemingly, development of anemia was not related to defects in erythrocyte metabolism. Serum iron values of infected mice were similar to those of controls. Storage iron (hemosiderin and ferritin) concentrations were increased in the spleen and to a lesser extent in the liver. The activity of superoxide dismutase, an enzyme that favors conversion of easily mobilized soluble ferritin to poorly mobilized insoluble hemosiderin, was decreased per unit weight of the enlarged spleen, although total activity was increased. The superoxide dismutase activity per unit weight of liver was not altered in infected mice although total liver activities were increased. These findings, as well as the marked reticulocytosis, indicate that lack of iron supply does not have a part in precipitating the anemia of T brucei infection. Leukocytosis was present in infected animals and was associated with lymphocytosis, eosinopenia, basophilia, and monocytosis; these changes were more marked in IA than in INA mice.
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PMID:Pathogenesis of Trypanosoma brucei infection in deer mice (Peromyscus maniculatus): hematologic, erythrocyte biochemical, and iron metabolic aspects. 686 60

Embryonic dysmorphogenesis has been blocked by antioxidant treatment in vivo and in vitro, suggesting that embryonic excess of reactive oxygen species (ROS) has a role in the teratogenic process of diabetic pregnancy. We report that the basal levels of ROS in dispersed rat embryonic cells in vitro, as determined by fluorescence of dichlorofluorescein (DCF), were not different in cells from control and diabetic pregnancy at day 10 or 12. Beta-hydroxybutyrate (beta-HB) and succinic acid monomethyl ester both augmented DCF fluorescence in cells from day 12 embryos of normal and diabetic rats but not from day 10 embryos. Cells of day 10 and day 12 embryos from normal and diabetic rats responded to increasing glucose concentrations with a dosage-dependent alleviation of DCF fluorescence. Day 10 embryonic cells exhibited high glucose utilization rates and high pentose phosphate shunt rates, but low mitochondrial oxidation rates. Moreover, in vitro culture of embryos between gestational days 9 and 10 in the presence of 20% oxygen induced an increased and glucose-sensitive oxidation of glucose compared with embryos not cultured in vitro. At gestation day 12, however, pentose phosphate shunt rates showed a decrease, whereas the mitochondrial beta-HB oxidation rates were increased compared with those at gestation day 10. This was paralleled by a lower expression of glucose 6-phosphate dehydrogenase- and phosphofructokinase-mRNA levels at day 12 than at day 10. On the other hand, H-ferritin mRNA expression at day 12 was high compared with day 10. None of the mRNA species investigated were affected by the diabetic state of the mother. It was concluded that beta-HB-induced stimulation of mitochondrial oxidative events may lead to the generation of ROS at gestational day 12, but probably not at day 10, when only a minute amount of mitochondrial activity occurs. Thus our results do not support the notion of diabetes-induced mitochondrial oxidative stress before the development of a placental supply of oxygen.
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PMID:Beta-hydroxybutyrate increases reactive oxygen species in late but not in early postimplantation embryonic cells in vitro. 951 22