Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this investigation was to throw light on the biological behavior and metabolic regulation of hepatic enzymes of the nonoxidative branch of the pentose phosphate pathway. The activities of transaldolase (EC 2.2.1.2) and trasketolase (EC 2.2.1.1) Were compared in biological conditions that involve modulation of gene expression such as in starvation, in differentiation, after partial hepatectomy, and in a spectrum of hepatomas of different growth rates. The enzyme activities were determined under optimal kinetic conditions by spectrophotometric methods in the 100,000 X g supernatant fluids prepared from tissue homogenates. The kinetic properties of transaldolase and transketolase were similar in normal liver and in rapidly growing hepatoma 3924A. For transaldolase, apparent Km values of 0.13 mM (normal liver) and 0.17 mM (hepatoma) were observed for erythrose 4-phosphate and of 0.30 to 0.35 mM for fructose 6-phosphate. The pH optima in liver and hepatoma were at approximately 6.9 to 7.2. For the transketolase substrates, ribose 5-phosphate and xylulose 5-phosphate, the apparent Km values were 0.3 and 0.5 mM, respectively, in both liver and hepatoma. A broad pH optimum around 7.6 was observed in both tissues. In organ distribution studies, enzyme activities were measured in liver, intestinal mucosa, thymus, kidney, spleen, brain, adipose tissue, lung, heart, and skeletal muscle. Taking the specific activity of liver as 100%, transaldolase activity was the highest in intestinal mucosa (316%) and in thymus (219%); it was the lowest in heart (53%) and in skeletal muscle (21%). Transketolase activity was highest in kidney (155%) and lowest in heart (26%) and skeletal muscle (23%). Starvation decreased transaldolase and transketolase activities in 6 days to 69 and 74%, respectively, of those of the liver of the normal, fed rat. This was in the same range as the decrease in the protein concentration (66%y. In the liver tumors, transaldolase activity was increased 1.5- to 3.4-fold over the activities observed in normal control rat liver. Transketolase activity showed no relationship to tumor proliferation rate. In the regenerating liver at 24 hr after partial hepatectomy, the activity of both pentose phosphate pathway enzymes was in the same range as that of the sham-operated controls. In differentiation at the postnatal age of 5, 12, 23, and 32 days, hepatic transaldolase activities were 33, 44, 55, and 72%, respectively, of the activities observed in the 60-day-old, adult male rat. During the same period, transketolase activ-ties were 18, 21, 26, and 55% of the activities observed in liver of adult rat. The demonstration of increased transaldolase activity in hepatomas, irrespective of the degree of tumor malignancy, differentiation, or growth rate, suggests that the reprogramming of gene expression in malignant transformation is linked with an increase in the expression of this pentose phosphate pathway enzyme...
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PMID:Behavior of transaldolase (EC 2.2.1.2) and transketolase (EC 2.2.1.1) Activities in normal, neoplastic, differentiating, and regenerating liver. 1 80

The behavior of the rate-limiting enzyme of purine catabolism, xanthine oxidase (EC 1.2.3.2); was examined in normal liver, in 17 hepatomas of different growth rates, and in rapidly growing differentiating and regenerating liver. Xanthine oxidase activity was measured in the supernatant fluid prepared by centrifugation of 5% homogenates at 100,000 X g for 30 min. There was no uricase activity in the supernatant fluid. The affinity of xanthine oxidase to xanthine was similar in normal liver and in slow- and rapidly growing hepatomas (Km=6 to 8 muM), and theoptimum pH was 8.0; at pH 7.4, the activity was 80% of that at the pH optimum. A standard assay was worked out for the liver and hepatoma systems; the enzyme activity was linear during 60-min incubation and proportionate with amounts of protein added over a range of 0.5 to 3.0 mg. Xanthine oxidase specific activity was 9 times higher in small intestine than in liver. Activities in lung, spleen, kidney, heart, testes, and thymus were 67, 59, 21, 19, 8, and 8%, and in skeletal muscle, brain, and bone marrow activities were 5% of that of the liver. In regenerating liver, xanthine oxidase activity was not changed from that of the liver of sham-operated controls up to 96 hr after operation. The activity of the average differentiating liver cell was less than 5% of that of adult liver during the first week after birth. At postnatal ages of 18, 25, 30 and 40 days, the activity rose to 18, 46, 76, and 94%, respectively, of that of the adult liver. In starvation, hepatic xanthine oxidase activity per cell was preferentially depleted as compared to the decline in protein concentration. Upon refeeding, the enzymatic activity was restored more slowly than the protein content. Since xanthine oxidase activity was decreased in all examined hepatomas, including the slowest-growing, well-differentiated neoplasms, the altered activity of this enzyme appears to be.linked with neoplastic transformatiobosyl 1-pyrophosphate amidotransferase (EC 2.4.2.14), was increassed in the hepatomas, the reprogramming of gene expression results in an imbalance that favors the synthetic over the catabolic potential. This enzymatic imbalance should confer selective advantages to the cancer cells.
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PMID:Imbalance of purine metabolism in hepatomas of different growth rates as expressed in behavior of xanthine oxidase (EC 1.2.3.2). 18 29

The effect of 24 and 48 hours of food and water deprivation on ascorbic acid, liver, leukocyte counts and internal lymphoid organ weights of crossbred chicks was examined. Starvation caused an increase in plasma ascorbic acid level, a significant decrease in leucocyte count in peripheral blood, significant loss in body weight and a profound loss in liver, bursa of fabricius, spleen and thymus weights. Deprived chicks were I.V. injected with Escherichia coli dead bacteria and sheep red blood cells at different times before and after onset of deprivation. Blood samples were taken 3, 6, and 12 days thereafter. A lower antibody titer was found on the 6th day post vaccination in the groups where deprivation started on the day before or on the day of vaccination.
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PMID:The effect of starvation on antibody production of chicks. 34 87

The effects of starvation on the cellular immune response of C58/Wm mice to syngeneic malignant lymphoid cells (1b cells) were studied. Mice were starved 1-3 days before or after immunization. The capacity of starved animals to survive immunization was used to quantify immunosuppression. When starvation bracketed immunization by -1 to +1 days, only 2 of 23 mice survived primary immunization, compared with 100% survival for nonstarved controls. A 2-day period of starvation +1 to +7 days after primary immunization reduced survival about 30%. For a test of the effect of starvation on the secondary immune response, mice were immunized, starved 2 days, and then challenged with viable lb cells. When mice were starved from -3 to +1 days before or after challenge, there was a 25-45% decrease in survival. Starvation caused a disproportionate depletion of lymphoid tissue elements. The proportional loss in the weight of the spleen and thymus was essentially twice as great as the loss in total body weight. The peripheral blood leukocyte count was reduced by about 20% when mice were starved 1 day and by approximately 50% when they were starved 2 days. When mice were starved 1-2 days, the differential leukocyte count did not shift and there was no significant change in the number of blood erythrocytes or in the hematocrit. Starvation for 2 days caused a 65-70% reduction in the number of viable mononuclear spleen cells. Starvation for 3 days caused about 90% reduction. Adoptive cell transfer experiments showed that the immunocompetence of individual spleen immunocytes was not reduced by starvation.
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PMID:Immune mechanisms in leukemia: suppression of cellular immunity by starvation. 118 12

During a three-day fast, followed by four days of refeeding, the content of the multicatalytic proteinase as well as hydrolyzing activity towards Suc-Leu-Leu-Val-Tyr-7-amino-4-methylocoumarin (SLLVT-MCA) was measured in various rat tissues. When compared with normal rats, the MCP content, as determined by immunochemical techniques, was unchanged over the entire experimental period in the three tissues examined: gastrocnemius muscle, thymus and testis. By contrast, a differential response was observed in the three tissues with respect to specific and total SLLVT-MCA splitting activity: for thymus and testis, these values were again unchanged, whereas in gastrocnemius muscle, both specific and total enzyme activity fell by almost 70% on day three of fasting but returned to control values on day four of refeeding. This change in activity was not due to the accumulation or degradation of a specific proteinase inhibitor. Data demonstrate that, in association with the insulin-deficient state of starvation, the activity of the multicatalytic proteinase shows an adaptive behaviour which becomes manifest in some but not in other tissues.
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PMID:Tissue-specific changes of multicatalytic proteinase activity in the fasted rat. 184 9

Activity of lysosomal proteinases cathepsins A, B, C, D, H and L was studied in liver, kidney, spleen, thymus, heart, skeletal muscle and brain tissues of rats, maintained on full value diet, on a diet free of proteins and on the diet enriched with methionine. Distinctly dissimilar reactions of thiol-dependent proteinases was detected in liver, heart tissues and skeletal muscles as compared with the reaction of cathepsins A and D; activity of cathepsins B, H and L was decreased 1.5-2-fold in the animal groups maintained on diets both free of proteins and enriched with methionine. The data obtained suggest that concentration of endogenous inhibitors of lysosomal thiol-dependent proteinases rather than content of SH-groups in tissues was responsible for alterations of their activity under conditions of protein starvation.
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PMID:[Lysosomal hydrolases of various rat organs in the process of cell nutrition]. 223 32

The mechanism and cellular targets of mononuclear cell depletion were investigated in strains of mice susceptible or resistant to lethal infection with a virulent street rabies virus (SRV). Significant depletion was evident in the thymus of all infected animals at approximately 5 days postinfection and subsequently involved the spleen and lymph nodes in mice developing clinical signs of rabies. Immunofluorescent analyses of lymphocyte subsets in depleted spleens revealed that cell losses were non-selective since the relative proportions of K+, Thy-1+, Lyt-1+, and Lyt-2+ cells remained unchanged. Diminished expression of I-A membrane glycoproteins on spleen lymphocytes was noted, however, perhaps reflecting reduced availability of I-A-inducing lymphokines. Adrenal hormone toxicity was identified as the cause of mononuclear cell depletion in that mice adrenalectomized before SRV infection showed no evidence of lymphoid depletion. The failure of adrenalectomy to alter anti-rabies antibody responses or SRV lethality also indicates that involution of the lymphoid system is a consequence and not a cause of genetically controlled host susceptibility to SRV. The mechanism of adrenal gland stimulation in rabies-infected mice appears to involve a virus-induced dysfunction in the pituitary gland rather than a stress response to paralysis-induced starvation, based on results of kinetic studies on weight loss, appetite depression, and paralysis in these animals and previous reports of pituitary infection during rabies disease. The relationship of these observations to current theories on rabies virus pathogenicity is discussed.
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PMID:Murine susceptibility to street rabies virus is unrelated to induction of host lymphoid depletion. 232 81

Thymosin alpha 1 (T alpha 1), the N-terminal 28-amino acid fragment of prothymosin alpha (ProT alpha), and ProT alpha, although originally isolated from whole thymus extracts, are also present in nonthymic cells and tissues. We used an ELISA with an antibody raised against T alpha 1 to investigate the relationship between intracellular levels of thymosin immunoreactive peptide(s) (TIP) and cell proliferation in a rat small intestinal IEC-6 cell line. Increasing TIP levels were observed during cell proliferation, which decreased when proliferation was halted by cellular contact inhibition. Serum feeding of cells previously rendered quiescent by serum starvation resulted in a significant increase in TIP within 1 hr. Conversely, serum starvation decreased TIP levels within 1 hr. Peak TIP levels appeared after 3 hr of serum incubation, while maximum [3H]thymidine incorporation was noted after 9 hr, suggesting maximum TIP concentrations in the G1 phase of the proliferative cycle. Immunoelectron microscopy demonstrated an association of TIP with condensed nuclear chromatin. These results support a relation of intracellular TIP levels to IEC-6 cell proliferation and also a nuclear site of action. HPLC analysis of cellular homogenates from proliferating IEC-6 cells revealed a peak of immune reactivity that elutes in the position of T alpha 1.
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PMID:Cellular levels of thymosin immunoreactive peptides are linked to proliferative events: evidence for a nuclear site of action. 237 91

To asses the possible roles of the two active forms of mouse DNA polymerase alpha: primase--DNA-polymerase alpha complex (DNA replicase) and DNA polymerase alpha free from primase activity (7.3S polymerase), in nuclear DNA replication the correlation of their activity levels with the rate of nuclear DNA replication was determined and a comparison made of their catalytic properties. The experiments using either C3H2K cells, synchronized by serum starvation, or Ehrlich culture cells, arrested at the S phase by aphidicolin, showed DNA replicase to increase in cells in the S phase to at least six times that of the G0-phase cells but 7.3S polymerase to increase but slightly in this phase. This increase in DNA replicase activity most likely resulted from synthesis of a new enzyme, as shown by experiments using a specific monoclonal antibody, aphidicolin and cycloheximide. Not only with respect to the presence or absence of primase activity, but in other points as well the catalytic properties of these two forms were found to differ; DNA replicase preferred the activated calf thymus DNA with wide gaps of about 100 nucleotides long as a template-primer, while the optimal gap size for 7.3S polymerase was 40-50 nucleotides long. Size analysis of the products synthesized on M13 single-stranded circular DNA with a single 17-nucleotide primer by DNA replicase and 7.3S polymerase suggested the ability of DNA replicase to overcome a secondary structure formed in single-stranded DNA to be greater than that of 7.3S polymerase.
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PMID:Activity levels of mouse DNA polymerase alpha-primase complex (DNA replicase) and DNA polymerase alpha, free from primase activity in synchronized cells, and a comparison of their catalytic properties. 308 93

The relationship between thymic atrophy and plasma corticosterone levels was examined in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-treated, pair-fed and ad libitum-fed male Sprague-Dawley rats given a usually lethal (125 micrograms/kg) or non-lethal (25 micrograms/kg) dose of TCDD. At both dosages, corticosterone levels in TCDD-treated animals begun to rise as early as day 4 after treatment. At later time points corticosterone levels were 5-7 times higher in rats given the non-lethal dose, and 6-10 times higher in rats administered the lethal dose than the levels observed in ad libitum-fed controls. Corticosterone levels in control rats pair-fed to the lethal dose group (as a result of the severe reduction in feed intake) were similarly elevated as in TCDD-treated rats but this was not the case in pair-fed rats of the non-lethal TCDD dosage (due to an essentially unchanged feed intake). At both dosages, relative thymus weights of TCDD-treated rats started decreasing by day 4 and continued to decline for the most part of the study. Relative thymus weights of rats pair-fed to the non-lethal TCDD dosage were not different from ad libitum-fed rats. However, the decrease in relative thymus weights of rats pair-fed to the lethal TCDD dosage paralleled that of TCDD-treated rats with an apparent 8-day lag period. Morphologically, the thymus as well as the adrenal revealed differential changes in TCDD-treated rats from those observable in pair-fed rats. These results suggest that either TCDD exerts a direct effect on the thymus and the adrenals or it causes an additional stress (e.g., a metabolic stress) over and above the starvation stress, which may be responsible for the differential morphological changes in these glands.
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PMID:Elevated plasma corticosterone levels and histopathology of the adrenals and thymuses in 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated rats. 320 74


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