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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In our laboratory, the protective and therapeutic effects of surplus dietary iron and ascorbic acid on cadmium toxicity in rats have been studied and in this experiment, an effect of surplus iron and ascorbic acid on lead toxicity was examined. In young rats ingesting a diet containing 500 ppm of lead, growth retardation and anemia were observed. Suplementation of 400 ppm of iron and 1% of ascorbic acid to the lead containing diet prevented the growth depression and anemia and caused reductions of concentrations of lead in the kidney and tibia. Whereas, addition of 50 ppm of cadmium to the lead containing diet aggravated the growth retardation and anemia, but reduced the concentrations of lead in the kidney and tibia. Dietary supplementation of iron to the lead containing diet prevented the growth depression and anemia and reduced the accumulation of lead in the kidney, however the supplementation of ascorbic acid alone did not show any ameliolative effects. Rats were fed the lead containing diet and then transferred to the basal diet with or without iron and ascorbic acid. Recoveries from the growth retardation and anemia were not observed in rats within a week after the transfer to the non-lead diet with or without iron and ascorbic acid. These results suggest that iron prevents the growth depression and anemia in rats ingesting lead by an inhibition of lead asborption.
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PMID:Effect of dietary supplementation of iron and ascorbic acid on lead toxicity in rats. 22 25

The trace metals nickel and platinum, which are not substrates for ferrochelatase and thus do not form heme in biological systems, were found to act similaryl to cobalt, and heme itself, in regulating heme metabolism in liver and kidney. These metals induced heme oxygenase activity in both organs with the peak of induced enzyme activity reached approximately 16 hr after single injections in rats. Both metals caused transient depression of cellular glutathione content followed by increases above normal after 12 hr in liver. Nickel and platinum were more potent inducers of heme oxygenase in kidney than in liver (10-13 times normal versus 5-6 times normal). At high concentrations, they inhibited heme oxygenase [heme, hydrogen-donor:oxygen oxidoreductase (alpha-methene-oxidizing, hydroxylating), EC 1.14.99.3] in vitro. Both were active in regulating heme metabolism only when administered in the ionic form. Complexing of the metals with sulfhydryl agents completely blocked their actions on heme metabolism. Administration of cysteine orally prior to or shortly after administration of the metals had a similar blocking effect. Nickel and platinum produced depression of delta-aminolevulinate synthase [succinyl-CoA:glycine c-succinyltransferase (decarboxylating), EC 2.3.1.37] activity in liver, but neigther inhibited this rate-limiting ennzyme for heme synthesis in vitro. Furthermore, despite the substantial decreases in cellular heme and hemoprotein contents mediated by the metal, production of delta-amimolevulinate synthase did not undergo the compensatory increase that would be expected if there were a direct reciprocal feedback relationship between cellular heme level and synthesis of this enzyme. These findings indicate that it is not necessary for metal ions to be chelated in the porphyrin ring in order to regulate the enzymes of heme synthesis and heme oxidation. Accordingly, it is suggested that the iron atom of heme is the proximately active regulator of delta-aminolevulinate synthase and heme oxygenase--actions generally ascribed to the iron-tetrapyrrole complex itself--and that the tetrapyrrole moiety of the complex functions primarily as a means of transport of the metal to regulatory sites in cells.
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PMID:Regulation of heme pathway enzymes and cellular glutathione content by metals that do not chelate with tetrapyrroles: blockade of metal effects by thiols. 26 10

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

Recent reports demonstrated that the energy-dependent step of vitamin B12 uptake into cells of Escherichia coli rapidly declines after cessation either of the expression of the tonB gene or of general protein synthesis. It is shown here that inhibition of protein synthesis results in the decline, with similar kinetics, of all tonB-dependent processes, including sensitivity to colicins B and Ia, irreversible adsorption of phage phi80, and siderophore-mediated iron uptake. The role of ongoing TonB-dependent reactions on this lability of TonB function was investigated. Ferrichrome and the enterochelin precursor, 2,3-dihydroxybenzoate, caused both a moderate depression of B12 uptake activity in growing cells (reversed upon removal of the siderophore) and an acceleration of the loss of activity following inhibition of protein synthesis by addition of spectinomycin. Strains lacking the tonB-dependent siderophore uptake systems did not show these responses. The results suggest the consumption of tonB product during its action.
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PMID:Outer membrane-dependent transport systems in Escherichia coli: turnover of TonB function. 35 Aug 36

Bone marrow fragments from 10 patients with a megaloblastic anaemia due to vitamin B12 or folate deficiency were studied by electron microscopy and electron microscope autoradiography. A proportion of the erythroblasts showed ultrastructural abnormalities. Some of the cells containing autophagic vacuoles, large siderosomes, iron-laden mitochondria, irregularly shaped nuclei, membrane-bound nuclear clefts, or incomplete nuclear membranes were found to be capable of DNA, RNA and protein synthesis. Other cells showed advanced degenerative changes such as the distension of the perinuclear space, the clumping of cytoplasmic organelles near the nucleus and a reduction in the electron density and ribosome content of the cytoplasm. Most of these grossly abnormal cells suffered from either a marked depression or an arrest in protein and RNA synthesis, and were presumably destined for phagocytosis by reticulum cells.
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PMID:Electron microscope and high resolution autoradiographic studies of megaloblastic erythropoiesis. 40 60

Chick growth assays were used to evaluate the efficacy and toxicity of the L- and D-isomers of N-acetylmethionine when fed as a source of methionine in crystalline amino acid diets. In agreement with earlier rat studies employing intact protein diets, N-acetyl-L-methionine had a methionine-sparing value of 100% and N-acetyl-D-methionine a value of zero. The former was also observed to be fully effective as a methionine supplement when added to a methionine-deficient diet containing equal protein contributions from soybean, casein and gelatin. Isosulfurous levels of excess L-methionine or N-acetyl-L-methionine were equally growth depressing, but L-methionine elevated spleen iron deposition to a greater extent than N-acetyl-L-methionine. N-acetyl-D-methionine in excess depressed growth only slightly, due entirely to a depression in voluntary food intake, and no evidence of splenic hemosiderosis was observed from this addition.
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PMID:Efficacy of the D- and L-isomers of N-acetylmethionine for chicks fed diets containing either crystalline amino acids or intact protein. 44 54

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

The protective and curative effects of high levels of dietary iron and ascorbic acid on moderately long-term toxicity in rats were examined. In rats fed a diet containing 500 ppm of lead for 56 days, growth retardation, reduction of food consumption, anemia, hypertrophy of the kidney and accumulation of lead in the bone and kidney were observed, however, activities of alkaline phosphatase and GOT in the plasma did not change. Addition of 400 ppm of iron and 1% of ascorbic acid to the lead containing diet prevented the growth depression, reduction of food consumption, anemia and decreased the accumulation of lead in tissues. When these compounds were added to the lead containing diet for 18 days after feeding the lead diet alone for 38 days, almost no curative effects on lead toxicity were observed. In contrast to cadmium toxicity, dietary iron and ascorbic acid have no curative effect on established lead toxicity.
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PMID:Effectiveness of dietary iron and ascorbic acid in the prevention and cure of moderately long-term lead toxicity in rats. 50 45

Recently developed techniques for the investigation of iron kinetics were used to study the disturbance of iron metabolism in 19 untreated patients with Hodgkin's diseases (HD). The erythroid abnormality in newly diagnosed HD appears to be confined to those patients with systemic symptoms of weight loss, night sweats and fever, and consists of depression of marrow erythroid activity. These patients had a significnatly lower haemoglobin and serum iron concentration and a higher serum ferritin concentration, both when compared to normal subjects and to those patients with HD who lacked systemic symptoms. Ineffective erythropoiesis and red-cell destruction were not significantly increased. The present findings, confirm that HD patients with systemic symptoms have a depression of erythropoiesis, and that in these patients the marrow fails to respond to the stimulus of mild anaemia.
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PMID:Erythropoiesis and iron metabolism in Hodgkin's disease. 50 65

The mechanism regulating the formation of the globin-chains of hemoglobin is unknown. We have examined the formation of the alpha-, beta- and gamma-chains during the first 6 months in 10 healthy infants. Immediately after birth the ratio between rates of synthesis of alpha- and non-alpha-chains was 0.94 +/- 0.16. At 6 weeks the ratio was alpha/gamma + beta = 1.22 +/- 0.29. After oral therapy with iron (2 mg/kg) between ages 3 and 6 months the ratio alpha/gamma + beta became 0.92 +/- 0.14. Whether the imbalance at 6 weeks is due to a depression of alpha-chain synthesis or to a stimulation of gamma-chain and beta-chain synthesis remains unclear. Possibly in infants without iron therapy the gamma-chain synthesis is stimulated as was suggested by the comparison of the gamma/beta ratios in infants with and without iron therapy.
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PMID:[The effect of iron on globin chain synthesis during the first six months of extrauterine life (author's transl)]. 51 75


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