Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A child with hypogammaglobulinemia and intractable diarrhea underwent parenteral alimentation for five months. A clinical syndrome of acrodermatitis enteropathica subsequently developed associated with a depression in thymus-dependent lymphocyte (T cell) numbers, abnormal T-cell mitogen-induced blast transformation, and anergy to skin test antigens. Plasma zinc levels were found to be abnormally low. Zinc therapy resulted in dramatic resolution of the clinical manifestations of acrodermatitis enteropathica. Cell-mediated immune function was also restored to normal, suggesting an important role for zinc and possibly other trace metals in cellular immune responses.
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PMID:Zinc therapy of depressed cellular immunity in acrodermatitis enteropathica. Its correction. 11 58

Stimulated rabbit peritoneal polymorphonuclear leukocyte (PMN) preparations simultaneously produce prostaglandin-like material and mediators that induce metabolic alterations in experimental animals characteristic of the host's responses to inflammation. The alterations observed in rats include responses by: proteins, carbohydrates, hormones, trace metals, and total blood neutrophils. This study demonstrates a possible relationship between prostaglandins and PMN-derived substances that mediate plasma zinc depression, hepatic amino acid uptake, and increased numbers of blood neutrophils. Production of these mediators by stimulated-PMN preparations was prevented by 23 muM indomethacin or 93 muM aspirin. Conversely, morphine (2 mM or less) had no detrimental effect on production of these mediators, although, it consistently stimulated production of a substance stimulating total blood neutrophia. In addition, 2 muM prostaglandin E and F stimulated production of substances mediating hepatic amino acid uptake plasma zinc depression, respectively. At this concentration, neither prostaglandin significantly altered production of substances mediating increased numbers of total blood neutrophils. A partial-nitrogen atmosphere, dibutyryl cyclic analogs of AMP and GMP, or homogenization of the PMN had no effect on mediator production. The inhibitory effect of indomethacin and aspirin also was observed with PMN-homogenastes. These experimental observations suggest that prostaglandin synthesis has a function in production of mediators by stimulated-PMN preparations.
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PMID:Possible relation of prostaglandins to PMN-derived mediators of host metabolic responses to inflammation. 19 Jun 50

Cadmium affects the induction of thymidine and thymidylate kinases in regenerating rat liver. EDTA administered simultaneously with cadmium reverses its inhibitory action on enzyme synthesis, and prevents the depression of thymidine incorporation into DNA observed in cadmium-treated animals. Zinc does not abolish the inhibitory action of cadmium on the synthesis of DNA in regenerating liver, and the incorporation of thymidine into DNA in the testes was inhibited more by intraperitoneal injection of cadmium plus zinc than by injection of cadmium alone. Inhibition of thymidine incorporation into DNA in the liver and testes was proportional to the amount of cadmium administered up to about 2 mg CdCl2/kg body weight, but surprisingly, higher doses of cadmium caused less inhibition.
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PMID:Synthesis of DNA in the liver and testes of cadmium-tested partially hepatectomized rats. 22 99

Detubulation of the untreated fiber decreases the time constant of the action potential's foot (tauf) and increases the maximal rate of rise of the spike (Vmax). Zinc at all concentrations, and regardless of whether the fiber is intact or detubulated, increases tauf and decreases Vmax, and thus seems to decrease Na activation of the fiber. Detubulation was used principally to elucidate the localization and mechanism of the Zn2+-induced retardation of the falling phase of the frog sartorius fiber action potential, which evidently results from a general depression of delayed rectification. At 50 to 1000 mum, Zn2+ not only prolongs repolarization of intact fibers (measured by increase in t0.5, the half-time of the spike's fall), but also produces a marked hump early in this phase. Detubulation of zinc-free fibers reduces t0.5 to about 80% of its intact value, and under Zn2+ treatment t0.5 is increased but only to about 80% of that produced in the inus, detubulation decreases t0.5 in Zn2+-treated fibers not only to about 80% of that produced in the intact fiber, and the falling-phase hump is completely obliterated. Thus, detubulation decreases t0.5 in Zn2+-treated fibers not only by generally eliminating T-tubular participation in action potential generation, but also by subtracting a Zn2+-induced retardation of tubular delayed rectification. Tubular delayed rectification must therefore be an intrinsic feature of normal excitation. These results are further analyzed by means of (i) Stanfield's findings about retardation of delayed rectification by Zn2+ and (ii) Adrian-Peachey's theory of T-tubule participation in action potential generation, which suggests that the Zn2+-evoked repolarization hump signals onset of Zn2+-altered active participation of T-tubules in determining the spike's shape.
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PMID:Detubulation effects on the action of zinc on frog skeletal muscle action potential. 30 43

A literature review of the effect of oral contraceptive (o.c.) use on various metabolic processes is presented. Several studies show an adverse effect of o.c. use on subclinical diabetes and on patients with manifest insulin-independent diabetes. Some researchers have found a beneficial effect of o.c. use on older diabetics. It has not been determined whether the estrogen or gestagen component of o.c.s is responsible for this decrease in glucose tolerance, nor has the mechanism for this effect been discovered. Changes in various plasma protein concentrations have been observed during o.c. use, which affect the blood coagulation and the blood pressure regulation systems. The estrogen component appears to be responsible for the increase in the serum triglyceride concentration during o.c. use; the mechanism is still unknown. Some studies indicate that o.c. use causes an increase in serum cholesterol levels, which could promote gall stone formation. An increase in Vitamin A concentration has been observed during o.c. use. Riboflavin, folic acid, vitamin B 12, and ascorbic acid levels have been shown to decrease during o.c. use. A decrease in pyridoxin levels during o.c. use indicates an increased metabolism of tryptophan to nicotinic acid robosyl-5-phosphate. This would cause a decrease in serotonin production, which could be a cause of the depression experienced by some o.c. users. An increase in the plasma copper and caeruloplasmin levels during o.c. use is apparently due to the estrogen component. An increase in transferrin and the serum iron levels have been observed during o.c. use. Contradictory findings are reported concerning the plasma concentration of zinc.
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PMID:[Metabolic studies under administration of oral contraceptives. A review]. 34 1

Data are presented to show that ingestion of cadmium chloride by rats at low levels leads to alteration of zinc metabolism in the liver, even though the formation of metallothionein is not evident. A dose-response relationship between amount of cadmium ingested and degree of perturbation of zinc metabolism in liver was found. Oral cadmium was shown to cause emphysema and reduce pulmonary function in male rats; the effect was less severe or delayed in onset if dietary zinc concentration was high. Interference with copper and iron metabolism was shown to occur in rats given low levels of cadmium orally. Depression of copper and iron metabolism of the rat fetus was found to occur when dams received very low doses of cadmium during gestation, even though very little cadmium passed the placental barrier.
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PMID:Some effects of oral ingestion of cadmium on zinc, copper, and iron metabolism. 48 54

Nickel toxicity was studied in young chicks fed a semi-purified diet. Dietary nickel concentrations of 300 mg/kg and higher resulted in significant reduction in growth rate. Mortality and anemia were observed in chicks receiving 1100 mg/kg nickel. Dietary nickel content of 300 mg/kg resulted in a significant increase in kidney nickel content while higher dietary levels were required to affect the nickel content of other body tissues. Supplementation of nickel toxic diets (500 mg/kg) with 100 mg/kg of cobalt, iron, copper, and zinc did not alleviate the symptoms of nickel toxicity or consistently affect tissue nickel accumulation. The addition of cobalt resulted in a further depression in growth rate when added to the nickel toxic diet. However, subsequent studies showed that this was due to the toxicity of cobalt and no evidence was found for an interaction between these two elements. The lack of interaction of nickel with copper, iron, and zinc is in contrast to the results observed by other investigators at low dietary concentrations of nickel.
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PMID:Studies on nickel metabolism: interaction with other mineral elements. 51 46

Oral contraceptive (OC) use has been associated with 50 different metabolic changes but few women require increased amounts of nutrients to prevent deficiencies. Plasma triglyceride levels are markedly increased by OCs, but no consistent changes have been found in plasma cholesterol, fatty acids, or phospholipids. Small elevations in blood glucose and plasma insulin levels result from OC use, and plasma albumin is decreased and the alpha and beta globulins and fibrinogen are increased. Women on the pill show slight increases in the urinary excretion of some of the amino acids and decreases in some of the blood amino acids. Tryptophan metabolism is altered by OC use; changes in parameters of Vitamin-B6 metabolism are seen and Vitamin-B6 is used as a cofactor for several enzymes in the tryptophan pathway. At the beginning of OC use the retention of dietary nitrogen increases, and weight gain may result. The estrogens in OCs reduce plasma calcium, phosphorus, and magnesium. Most studies demonstrate an increase in serum iron and copper and a decrease in plasma zinc. Studies have also found an increase in plasma levels of Vitamin-A and a decrease of carotene, Vitamin-E, ascorbic acid, folacin, Vitamin-B12, and Vitamin-B6. 20% of OC users have enlarged cervical and vaginal cells as a result of abnormal folacin metabolism. The abnormality is corrected by oral folacin supplementation. Some women respond to OC treatment with biochemical signs of Vitamin-B6 deficiency and depression. These women should receive 20-40 mg Vitamin-B6 as a supplement.
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PMID:Nutrition during oral contraceptive treatment. 58 16

Although an effective vaccine exists to protect against VEE, not all persons who may be exposed to this disease are likely to be vaccinated. The disease most often presents as a short febrile illness but the convalescence period may be protracted, and death due to encephalitis does occur in a small percentage of those infected. Knowledge of the metabolic alterations which occur during VEE may materially aid in its treatment. Use of the V-198 strain of VEE in the rat produces a uniform model in which to study metabolic alterations. Changes that occur early in the disease include viremia, neutrophilia, a decrease in plasma zinc and transferrin, and increased amino acid uptake into liver. Plasma zinc depression persists into the later stage of the disease, but to a lesser degree. Increases in plasma copper and seromucoid occur late in the disease, concurrent with the development of pronounced encephalitis. Hypoalbuminemia and decreased ketonemia occur during both the early and late stages of the disease. Taken together, these metabolic alterations appear to chronicle the development of VEE in the rat. If these metabolic alterations can be linked to specific pathogenic processes, they may be useful as prognostic indicators, in formulating supportive therapy, and as monitors of potential antiviral therapy.
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PMID:Host metabolic alterations during Venezuelan equine encephalitis in the rat. 62 26

Glycogen-stimulated rabbit peritoneal exudate cells (polymorphonuclear leukocytes, PMN) produce prostaglandins (PG) and substances which induce alterations (mediators) in experimental animals characteristic of host metabolic responses to infection and other acute inflammatory stresses. The effect of Zn2+ on mediator production and PG synthesis was examined because: Zn homeostasis is perturbed during infection, Zn is known to regulate some cellular functions, and there appears to be an interrelationship between PG synthesis and mediator production. Using exudate cells, 2 mM Zn2+ caused complete inhibition of in vitro PG synthesis as assessed by conversion of [1-14C] arachidonic acid into PG. This concentration of Zn2+ also inhibited production of substances mediating plasma Zn depression, hepatic amino acid "uptake", fever, and neutrophil release from bone marrow. Conversely, Zn2+ did not inhibit in vivo metabolic responses to these mediators. Zn-pretreatment of rabbits or simultaneous injection of Zn2+ and crude PMN-derived pyrogenic activity resulted in prolongation of fever. It is suggested that this action of Zn2+ may be attributed to either stabilization of cyclic AMP through inhibition of phosphodiesterase or a Zn-mediator interaction which stabilizes crude endogenous pyrogen. The potential physiological significance of these results includes: possible potentiation of the host's defense mechanisms by Zn2+ and its utilization for prolongation of fever to determine its effect on potentially temperature-dependent host defense mechanisms.
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PMID:In vitro and in vivo actions of zinc ion affecting cellular substances which influence host metabolic responses to inflammation. 64 Nov 11


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