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)

The effect of varying dietary levels of zinc was evaluated in mice fed T-2 toxin. A semipurified diet was used to produce a low zinc (less than 2 parts per million (ppm], a zinc replete (100 ppm), and a high zinc (2500 ppm) diet. T-2 toxin was added to the three zinc diets at a concentration of 10 ppm. The mice were fed one of the six diets ad libitum for up to 28 days. Mice from each diet were submitted for necropsy after 14 and 28 days and after 14 days zinc absorption and retention was measured in mice from each of the low and replete zinc diets, with and without T-2 toxin. Animals receiving a low zinc diet with T-2 toxin had reduced weight gains. The high zinc diet did not depress growth and did not influence T-2 depression of growth. The diets produced significant hematological changes without evidence of a T-2 toxin - zinc interaction. While zinc absorption was greater in mice fed the low zinc diet than those fed the replete zinc diet, T-2 toxin decreased absorption of zinc in the low zinc group and increased absorption in the replete zinc group. T-2 toxin did not influence the biological half-life of retained zinc in either the low or replete zinc groups. The biological half-life of zinc was significantly increased in the mice fed the low zinc diet relative to the replete zinc diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biointeraction of dietary T-2 toxin and zinc in mice. 650 80

Rhesus monkeys were fed a diet marginally deficient in zinc (4 ppm zinc) throughout pregnancy and were monitored for changes in hematological, biochemical, and immunological parameters. This dietary zinc level was chosen because it did not produce an overt deficiency syndrome when fed for 10 wk to nonpregnant monkeys. Deprived animals were compared to control groups fed a zinc replete (100 ppm) diet ad libitum or on a food restricted (pair fed) basis. Beginning in the 3rd trimester zinc-deprived monkeys exhibited characteristic signs of deficiency including dermatitis, anorexia, and low levels of plasma zinc (less than 65 micrograms/100 ml) and of serum alkaline phosphatase activity. The extent of plasma zinc depression in deficient monkeys was dependent on total food intake; severely anorexic monkeys lost weight but maintained normal plasma zinc levels; monkeys that gained 20 to 30% of their body weight during pregnancy had severely depressed plasma zinc. Plasma vitamin A was reduced in the deprived group while copper, magnesium, and folate levels remained similar to controls. Hematological changes indicative of iron deficiency anemia (reduced packed cell volume, mean corpuscular volume, and Hb) were also seen in severely deficient monkeys. In addition, the peripheral lymphocyte mitogen response was reduced in deficient dams. We conclude that marginal deficiency of dietary zinc can produce significant abnormalities of nutritional status and has the potential for producing serious immunohematological dysfunction during pregnancy.
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PMID:Studies of marginal zinc deprivation in rhesus monkeys. I. Influence on pregnant dams. 669 28

Zinc deficiency was diagnosed in 2 flocks of sheep and a herd of goats. Alopecia and eating of wool were observed. Skin lesions were hyperkeratosis and parakeratosis. Abnormal hoof growth and a closed stance with arched back and bowed hindlimbs were seen. Anorexia, depression, and foot soreness diminished quickly after zinc supplementation. Skin lesions healed and hair and wool growth resumed. A cause for the deficiency could not be established.
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PMID:Zinc deficiency in sheep and goats: three field cases. 673 71

A pronounced and irreversible depression of the erythroid and liver delta-aminolevulinate dehydratase (porphobilinogen synthase; 5-aminolevulinate hydro-lyase, EC 4.2.1.24) activity was observed in rats exposed to trichloroethylene, a widely used solvent. The depression could not be restored after the treatment with dithiothreitol and zinc; however, radioimmunoassay of delta-aminolevulinate dehydratase indicated that trichloroethylene exposure did not essentially decrease the amount of enzyme. The depression of the enzyme activity thus proved to be due not to a reduction in the enzyme amount but to enzyme inhibition. The purified holoenzyme (fully activated delta-aminolevulinate dehydratase with 1 atom zinc per subunit) and apoenzyme (fully activated enzyme with the remaining zinc less than 0.1 atom per subunit) were prepared to investigate the in vitro inhibition of the enzyme by trichloroethylene. Incubation with trichloroethylene did not inhibit the holoenzyme, but inhibited the apoenzyme dose-dependently. Trichloroethylene inhibited the holoenzyme when incubated with the mixed function oxidase system. The in vitro experiments reported here indicate two mechanisms of the enzyme inhibition by trichloroethylene. In the liver of rats exposed to trichloroethylene, cytochrome P-450 concentration and heme saturation of tryptophan pyrrolase (EC 1.13.11.11) are reduced; in addition, the activity of delta-aminolevulinate synthase (EC 2.3.1.37) increased. After exposure to trichloroethylene at 2.14 g/m3, urinary delta-aminolevulinic acid increased to 142% of the control, while the excretion of coproporphyrin was reduced to 19.6% of the control.
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PMID:Inhibition of delta-aminolevulinate dehydratase in trichloroethylene-exposed rats, and the effects on heme regulation. 674 80

Laboratory and epidemiological evidence indicate that the enhanced flux of iron and zinc from the plasma to the storage compartments, such as liver, serves as a protective host response to combat infection. Studies were performed to determine the status of this nonspecific immune response in the diabetic animal, since it is commonly held that the diabetic has an increased incidence and susceptibility to infection. Normal rats and rats previously rendered diabetic by streptozotocin (STZ) were injected with either saline or Escherichia coli endotoxin, and plasma levels of zinc, iron, and copper were monitored 8 hr thereafter. Diabetic rats reduced their plasma zinc and iron levels by 35 and 25%, respectively, in response to endotoxin injection whereas control rats had a 70% decrease in zinc and a 46% depression in iron. Insulin administration to the diabetic rats restored the ability to decrease plasma zinc and iron to the same degree as control rats. Plasma copper did not change in any group. Further investigation suggested that the defect in trace metal response occurred after the secretion of leukocytic endogenous mediator (LEM) in the inflammatory response pathway. It is concluded that STZ-diabetic rats have a diminished ability to decrease plasma zinc and iron in response to endotoxin, and that this defect is due to an ineffective response of target tissues to the effects of leukocytic endogenous mediator. Furthermore, it is postulated that the hyperinsulinemia associated with the stress of infection functions to lower plasma zinc and, possibly, iron, thereby allowing the host to better combat infection.
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PMID:Depressed response of plasma iron and zinc to endotoxin and LEM in STZ-diabetic rat. 684 54

1. It was shown, using a paired-feeding technique, that the growth depression in zinc-deficient chicks was largely caused by the greatly reduced consumption of the deficient diet. 2. Chicks receiving a zinc sulphate solution directly into the crop ate an amount of zinc-deficient diet similar to that of the zinc-deficient diet eaten ty the control chicks; palatability was thus ruled out as the cause of the anorexia. 3. Only chicks receiving the zinc-deficient diet displayed signs of zinc deficiency.
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PMID:The contribution of anorexia to reduced growth in zinc-deficient chickens. 695 21

Thirteen patients maintained on long-term hemodialysis were studied with respect to their serum zinc concentration and T-lymphocyte response to phytohemagglutinin. Six patients demonstrated depression of T-cell mitogen response, while seven patients demonstrated a normal response. The mean serum zinc concentration of the patients with abnormal response was lower than those patients with a normal response (63 +/- 11 versus 75 +/- 14 microgram/di, respectively). There was no significant correlation between an individual's serum zinc concentration and T-cell response (r = 0.16). Five patients whose T-cell responses were depressed were given intravenous zinc chloride during each dialysis run for 6 wk (10 mg intravenous zinc, three times weekly) and were evaluated before and after therapy. All five patients remained anergic to four skin tests antigens. Only one patient (who had the lowest pretreatment serum zinc concentration at 48 micrograms/dl) demonstrated significant improvement in mitogen response after zinc therapy. Although dialysis patients commonly have low serum zinc concentrations and depressed mitogen response, in our patients these two findings were generally unrelated. Additionally, supplemental zinc did not change base-line measurements of T-lymphocyte mitogen response in four of five patients studied.
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PMID:Zinc and T-lymphocyte function in hemodialysis patients. 698 41

Ten male patients requiring maintenance hemodialysis were given zinc in the dialysate (400 micrograms/liter) or placebo in a double-blind crossover experiment. Sexual activity, depression ratings, and hematocrit were unchanged while subjective appreciation of food taste and smell was significantly less during zinc than placebo condition. No patients who were sexually inactive while receiving placebo became sexually active while receiving zinc.
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PMID:Effects of zinc in chronic hemodialysis. 698 19

The concentration of metallothionein (MT) in the liver of the perinatal rat is relatively high at term and 7 days after birth and then decreases to barely detectable levels by day 28. The developmental pattern MT-zinc parallels that of MT. When challenged with a single injection of cadmium chloride, the 26-day-old rat responds with a dose-related increase in hepatic MT which sequesters both cadmium and zinc. When the 5-day-old rat is similarly challenged, induction of MT occurs only at the highest dose tested (6 mg Cd/kg); however, due to the pre-existence of MT in these younger rats, cadmium administered at the lower doses still binds to the MT in a dose-related manner. Despite the induction of MT seen in both age groups following the 6.0 mg/kg dose, exposure to that level of the metal produced death in 30% of the younger animals but in only 4% of the older animals. When cadmium was administered to pregnant rats on day 19 of gestation, it was found to produce a dose-related induction of maternal hepatic MT over the following 48 hr. In contrast, maternal exposure to the metal led to a significant depression of fetal hepatic MT over the same time interval.
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PMID:Role of hepatic metallothionein during perinatal development in the rat. 705 77

Male rats were fed vitamin E-adequate, Torula yeast-based diets for 30 days to assess the influence of dietary selenium (0, 0.1, or 1.0 ppm) on the toxicity of dietary cadmium (0, 30, or 60 ppm). At all selenium levels, increased cadmium intake depressed feed consumption, reduced feed efficiency and lowered body weight gain. In liver, concentrations of cadmium and zinc increased, and iron concentration decreased with increased intake of cadmium. Dietary selenium did not affect concentrations of cadmium, zinc, iron or copper in liver. Blood hemoglobin level declined and relative heart weight (g/100 g body wt) increased with increased intake of cadmium. Increased selenium intake partially alleviated the cadmium-induced depression in blood hemoglobin levels in rats fed diets that contained 30 ppm cadmium, and partially ameliorated the cadmium-induced increase in heart size in rats fed either 30 or 60 ppm cadmium. Hepatic and renal glutathione peroxidase (GSH-Px) activity increased with increased selenium intake. Increased cadmium intake did not affect renal GSH-Px activity. Hepatic GSH-Px activity in rats fed diets that contained 0.1 ppm selenium decreased with increased cadmium intake; however, hepatic GSH-Px activity was not affected by dietary cadmium in rats fed diets that contained 1.0 ppm selenium. Interactions between nontoxic levels of dietary selenium and relatively high levels of dietary cadmium apparently resulted in an antagonism of selenium metabolism by cadmium in some systems, and partial amelioration of cadmium toxicity by selenium in other systems
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PMID:Some metabolic interrelationships between toxic levels of cadmium and nontoxic levels of selenium fed to rats. 707 26


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