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Biomedical subjects

J R Arthur

Publications and source records attributed to J R Arthur.

At least 91 records · Page 5Linked to original sources
PubMed1988

The influence of dietary history on the production of free radicals in rat liver microsomes.

Free radicals have been trapped in microsomal fractions from rat livers by the use of alpha-(4-pyridyl-l-oxide)-N-tert-butylnitrone (4-POBN) and detected by ESR spectroscopy. Using this technique we have investigated the effects of low dietary concentrations of vitamin E and selenium (Se) on free radical production. When the microsomal fractions were incubated with Fe, ADP and NADPH significantly greater amounts of radicals were initially trapped when rats were deficient in vitamin E (whether combined with Se deficiency or not) than from Se-deficient animals or Se- and vitamin E-supplemented controls. After prolonged incubation (ca. 30-45 mins) the free radicals trapped from the microsomes from the Se-deficient animals rose to amounts comparable to those seen in the vitamin E-deficient microsomes. Over the same period of incubation approximately half this quantity of radicals were trapped in liver microsomes from Se- and vitamin E-supplemented rats. The effects of 4-POBN on the levels of peroxidation in the various microsomal fractions were assessed by measuring the thiobarbituric acid reactive substances (TBARS). The presence of 4-POBN significantly reduced the amounts of TBARS formed on incubation and there was a clear distinction between the groups on the basis of the vitamin E status of their diets.

Animals↗
PubMed1988

Copper deficiency and tissue glutathione concentration in the rat.

Copper deficiency in rats increased renal vein and arterial (heart) plasma GSH concentration by approximately 50%. There was no change in plasma GSSG concentration. Renal vein plasma GSSG/GSH ratio was decreased in copper deficiency, which is consistent with previous reports showing a copper-dependent thiol oxidase activity in the renal basement membrane. No change occurred in arterial plasma GSSG/GSH ratio. Hepatic GSH concentrations were also elevated by 50% in copper deficiency, GSSG concentrations were unaffected, but GSSG/GSH ratio was depressed. Renal and cardiac tissue GSH and GSSG were unaffected by copper deficiency. The decreased SOD activity and GSH-Px activity observed in copper deficiency may contribute to increased hepatic and plasma GSH concentrations.

Animals↗
PubMed1988

Thyroid hormone concentrations in selenium deficient and selenium sufficient cattle.

Selenium deficient calves when compared to selenium supplemented calves had increased plasma thyroxine concentrations and decreased plasma tri-iodothyronine concentrations. These changes in the selenium deficient calves were accompanied by significant increases in plasma urea and creatinine concentrations and decreased plasma alkaline phosphatase activity. The demonstration that low selenium status can cause imbalances in thyroid hormone metabolism may provide an explanation for some of the effects of the deficiency.

Alkaline Phosphatase↗
PubMed1988

Plasma pyruvate kinase activity vs creatine kinase activity as an indicator of the porcine stress syndrome.

Plasma pyruvate kinase (PK) and creatine kinase (CK) activities were increased significantly (P less than 0.001 and P less than 0.05, respectively) in homozygote halothane-reacting pigs (nn), compared with those activities in homozygote nonreacting pigs (NN). Pyruvate kinase activity was less variable within groups than was CK activity, allowing more effective discrimination between nn and NN geno-types. The PK and CK activities in plasma increase with age in halothane-reacting pigs and the nonreacting pigs. Enzyme activities in heterozygote (Nn) nonreacting pigs did not differ significantly (P greater than 0.05) from enzyme activities of homozygote (NN) nonreacting pigs. Although PK was better than CK in identifying stress-susceptible pigs, age-related effects and the failure to identify heterozygotes may restrict the use of plasma PK activity as a diagnostic test for the stress syndrome.

Animals↗
PubMed1987

Inhibition of hepatic deiodination of thyroxine is caused by selenium deficiency in rats.

Selenium (Se) deficiency produced up to a 14-fold decrease in hepatic tri-iodothyronine (T3) production from thyroxine (T4) in vitro. The T3 production rate could not be restored by the addition of a variety of cofactors, nor by the addition of control homogenate. The impairment in hepatic T3 production observed in Se deficiency was reflected in the concentrations of thyroid hormones circulating in plasma, T4 being increased approx. 40% and T3 being decreased by 30%. However, the fall in plasma T3 concentrations was smaller than might be expected in view of the marked decreased in T3 production. Se deficiency had no measurable effect on plasma reverse-tri-iodothyronine concentrations. The data suggest that Se deficiency produces an inhibition of both 5- and 5'-deiodination, consistent with the widely held view that these reactions are catalysed by the same enzyme complex. The mechanism of inhibition appears not be mediated by changes in thiol levels, but a direct role of Se in the activity of the deiodinase complex cannot be excluded.

Animals↗
PubMed1987

The effects of selenium and copper deficiencies on glutathione S-transferase and glutathione peroxidase in rat liver.

Selenium (Se) deficiency in rats produced significant increases in the activity of hepatic glutathione S-transferase (GST) with 1-chloro-2,4-dinitrobenzene as substrate and in various GST isoenzymes when determined by radioimmunoassay. These changes is GST activity and concentration were associated with Se deficiency that was severe enough to provoke decreases of over 98% in hepatic Se-containing glutathione peroxidase activity (Se-GSHpx). However, decreases in hepatic Se-GSHpx of 60% induced by copper (Cu) deficiency had no effect on GST activity or concentration. Increased GST activity in Se deficiency has previously been postulated to be a compensatory response to loss of Se-GSHpx, since some GSTs have a non-Se-glutathione peroxidase (non-Se-GSHpx) activity. However, the GST isoenzymes determined in this study, GST Yb1Yb1, GST YcYc and GST YaYa, are known to have up to 30-fold differences in non-Se-GSHpx activity, but they were all significantly increased to a similar extent in the Se-deficient rats.

Animals↗
PubMed1987

Effects of changes in dietary zinc, copper and selenium supply and of endotoxin administration on metallothionein I concentrations in blood cells and urine in the rat.

These studies were designed to investigate the effects of low dietary zinc, copper or selenium intake of certain types of stress and of injection of zinc, copper or cadmium on metallothionein I (MT-I) concentrations in the blood and urine of rats. The aim was to establish whether such measurements could be of value in the diagnosis of zinc deficiency. Marginal zinc deficiency rapidly caused a major decrease in MT-I levels in the blood cells and to a lesser extent in urine. Injection of zinc and also of cadmium and copper had the opposite effect and increased MT-I concentrations in both samples, although the effects of zinc on blood cells and urine were relatively transient. The MT-I in the blood cells was associated mainly with the erythrocytes. No changes in blood or urine MT-I levels were found in copper- and selenium-deficient rats. Neither cold stress nor restriction of food intake for 24 h had any significant effect on MT-I levels in the blood cells or urine. Endotoxin injection increased urinary MT-I excretion in both zinc-adequate and zinc-deficient rats but did not affect blood cell MT-I levels in either group of animals. It appears therefore that assay of erythrocyte MT levels could be of particular value in the diagnosis of zinc deficiency, especially when it is accompanied by stress or infection.

Animals↗
PubMed1987

Stimulation of peroxidation in rat liver microsomes by (copper, zinc)-metallothioneins.

The abilities of pig liver (copper, zinc) metallothionein I and rat liver zinc metallothionein II to modify lipid peroxidation in incubations of liver microsomes have been compared with the activities of reduced glutathione, mannitol, quinacrine, EDTA, dimethyl-pyrroline-N-oxide and phenyl-butyl-nitrone. Lipid peroxidation was determined by assay of thiobarbituric acid reactive substance formation in incubations of microsomes with iron/ADP or a mixture of xanthine and xanthine oxidase. Zinc metallothionein II had no effect on the extent of peroxidation in either system but (copper, zinc) metallothionein I caused a stimulation of peroxidation initiated by xanthine and xanthine oxidase, all other compounds tested were inhibitory. Gel exclusion chromatography of incubations of (copper, zinc) metallothionein I with xanthine and xanthine oxidase revealed aggregation of the metalloprotein. This may have exposed copper in a form capable of initiating peroxidation.

Animals↗
PubMed1987

Tissue damage in vitamin E deficient rats is not detected by expired ethane and pentane.

Despite evidence for tissue damage in vitamin E deficient rats, no discernible difference in ethane and pentane production was apparent compared with controls. It is suggested that other sources of hydrocarbons may mask hydrocarbon production from peroxidation of polyunsaturated fatty acid components of cell membranes, or that tissue damage occurs before peroxidation of the polyunsaturated fatty acids.

Animals↗
PubMed1987

Blood antioxidant status and plasma pyruvate kinase activity of halothane-reacting pigs.

Samples of blood were collected (by jugular venipuncture) from 10 homozygote halothane-reacting pigs and 7 homozygote nonreactors. Antioxidant status was assessed by measurement of blood glutathione peroxidase, glucose-6-phosphate dehydrogenase, and superoxide dismutase activities and plasma concentrations of vitamin E. Significant differences in these values were not apparent between halothane-reacting pigs and nonreactors. Halothane-reacting pigs had tissue damage as indicated by significantly increased plasma activities of the enzymes creatine kinase and pyruvate kinase. The latter showed better discrimination between the 2 populations than did creatine kinase and could prove to be a more effective marker for identification of stress-susceptible pigs.

Animals↗
PubMed1986

An in vivo and in vitro study of selenium deficiency and infection in rats.

Selenium deficiency in rats impairs the ability of neutrophils and peritoneal macrophages to kill Candida albicans organisms in vitro. In contrast, killing of Salmonella typhimurium and Staphylococcus aureus organisms is unaffected by the deficiency. Survival of rats after intraperitoneal injection of 8 X 10(7) S. aureus organisms was not affected by Se deficiency, but a 5-fold increase in the dose (4 X 10(8) S. aureus organisms) led to a significantly greater mortality in the Se deficient rats.

Animals↗
PubMed1986

Effects of dietary copper, cadmium, iron, molybdenum and manganese on selenium utilization by the rat.

The possible antagonistic effects of different dietary concentrations of copper (1.3-200 mg/kg), cadmium (1-5 mg/kg), iron (20-500 mg/kg), molybdenum (0.3-50 mg/kg) and manganese (0.2-200 mg/kg) on selenium utilization by the rat were studied by the measurement of the absorption and organ distribution of dietary selenium as [75Se]selenite and by effects on organ glutathione peroxidase (GSH-Px: EC 1.11.1.9) activity. Although a high concentration of copper (200 mg/kg) in the diet did not alter the percentage absorption and total-body retention of doses of 75SeO3(2)- by rats, after such treatment tissue 75Se distribution was changed and was lower total selenium in some tissues. After copper treatment (200 mg/kg diet) GSH-Px activity of liver, testis, kidney and whole blood was also lower. Dietary cadmium, iron, molybdenum and manganese at the concentrations investigated had no significant effects on selenium metabolism. Thus it is unlikely that copper, cadmium, iron, molybdenum and manganese at normal dietary concentrations will have a major effect on selenium metabolism in the rat, especially if adequate amounts of selenium are being consumed.

Absorption↗
PubMed1986

The response of selenium-deficient mice to Candida albicans infection.

The effects of selenium deficiency on the responses to Candida albicans infection were examined in mice. When selenium-deficient and selenium-supplemented mice were given i.v. injections of 0.1 ml suspensions of 1 X 10(5) or 5 X 10(4) C. albicans in 0.9% sterile saline, deaths in the selenium-deficient animals started after 2.5-3.5 d compared with 7-8.5 d in the selenium-supplemented animals. Further studies demonstrated that 3 d after an i.v. injection of 1 X 10(5) C. albicans, significantly more of the microorganisms were found in the kidneys (P less than 0.001), livers (P less than 0.025) and spleens (P less than 0.01) of the selenium-deficient mice compared with the same organs of selenium-supplemented animals. Selenium deficiency was also demonstrated to impair the ability of mouse neutrophils to kill C. albicans in in vitro tests. The possible relationships of this defect in function to decreased resistance to C. albicans infection is discussed.

Animals↗
PubMed1986

Effects of molybdenum or iron induced copper deficiency on the viability and function of neutrophils from cattle.

Neutrophils from cattle with copper deficiency induced by molybdenum (0.052 mmol molybdenum kg-1 diet) or iron (8.95 mmol iron kg-1 diet) had an impaired ability to kill ingested Candida albicans and were less viable than those from copper-supplemented cattle in in vitro tests of function. Restricted intake (80 per cent of ad libitum) of a copper-adequate diet by cattle also decreased neutrophil candidacidal activity and viability. Additionally, the ingestion of C albicans by neutrophils was impaired by the molybdenum or iron treatments but not by restricted food intake. The changes in neutrophil function and the severity of copper deficiency, in biochemical terms, induced by the molybdenum or iron treatments were greater than those induced by diets of low copper content.

Animals↗
PubMed1985

Superoxide dismutase and glutathione peroxidase activities in neutrophils from selenium deficient and copper deficient cattle.

Oxygen consumption and the activities of the selenoenzyme glutathione peroxidase, and of the hexose monophosphate shunt were lower than normal in neutrophils from Se deficient cattle. However, these activities and the activity of Cu/zinc superoxide dismutase were unaffected in neutrophils from Cu deficient cattle. These results are discussed with reference to impaired neutrophil microbicidal activity previously demonstrated to result from Se or Cu deficiency in cattle.

Animals↗
PubMed1984

Blood selenium content and glutathione peroxidase activity in children with cystic fibrosis, coeliac disease, asthma, and epilepsy.

Long-term selenium status in children from the North-East of Scotland was estimated using whole blood selenium content (BSe) and glutathione peroxidase activity (BGSH-Px). BSe was significantly lower than the reference range in children with cystic fibrosis, coeliac disease and in older patients with phenylketonuria. Whereas BGSH-Px of all the children with coeliac disease and those with cystic fibrosis aged over 6 years matched the reference range, it was reduced in younger patients with cystic fibrosis and in children with dietetically treated phenylketonuria. No child had clinical features of selenium deficiency. BSe in treated epileptics and asthmatics conformed to the reference range, but BGSH-Px in both groups was increased significantly; this was most evident in those receiving corticosteroid preparations.

Adolescent↗