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Biomedical subjects

R Boyne

Publications and source records attributed to R Boyne.

At least 19 recordsLinked to original sources
PubMed1995

Role of the promoter in the sensitivity of human thymidine kinase to lack of Zn2+.

Previous studies had indicated that lack of Zn2+ inhibits the expression of thymidine kinase activity and produces a corresponding reduction in the concentration of its mRNA. The present investigations have shown that with human thymidine kinase this is associated with increased binding of a specific protein to the gene's promoter in the region between -55 and -83 bp 5' to the transcription initiation site. A second binding site for the protein is present within the sixth exon of the human thymidine kinase gene.

Animals↗
PubMed1991

Nature of the Zn2+ requirement for DNA synthesis by 3T3 cells.

Transit of 3T3 cells from quiescence to S phase requires an adequate supply of Zn2+ during the second half of the transition. The nature of this requirement has been investigated. Completion of the Zn2(+)-dependent process required ongoing mRNA and protein synthesis but could be accomplished in serum-free medium. Combination of low Zn2+ availability with inhibition of mRNA synthesis by 5,6-dichlororibofuranosylbenzimidazole or of protein synthesis by cycloheximide resulted in the cells almost completely reverting to a quiescent state. The results suggest that Zn2+ is required for the accumulation and maintenance of a protein involved in the progression of untransformed cells into S phase.

Animals↗
PubMed1990

Effects of growth, food intake, and dietary zinc on diadenosine tetraphosphate concentrations in rats.

The nucleotide diadenosine tetraphosphate has been suggested to function as a signal molecule for the initiation of DNA replication. Previous studies have indicated that diadenosine tetraphosphate is synthesized by certain aminoacyl tRNA synthetases and that diversion of AMP from the amino acid-enzyme complex to ATP to form diadenosine tetraphosphate is facilitated by zinc ions. The growth retardation of zinc-deficient rats is associated with specific reduction in DNA replication and also with a potentially growth-limiting decrease in food intake. The possibility has been investigated that in zinc-deficient rats, lack of Zn(2+) restricts diadenosine tetraphosphate synthesis, resulting in a failure to synthesize DNA and in a reduction in growth. The results indicate that the depressed growth potential caused by the reduction in food intake associated with the deficiency was sufficient to lower diadenosine tetraphosphate concentrations significantly in the liver and spleen. However, there was no indication of a specific effect of zinc deficiency on diadenosine tetraphosphate values.

Journal Article↗
PubMed1990

Anaemia and changes in erythrocyte morphology associated with copper and selenium deficiencies and dietary restriction in rats.

Both selenium and copper deficiencies in rats caused morphological changes in erythrocytes but only copper deficiency resulted in anaemia. Similar but less severe morphological changes occurred when rats consuming selenium- and copper-adequate diets had their food intake restricted to that of the copper-deficient animals. Since selenium deficiency did not affect the severity of changes due to copper deficiency this suggests that alterations of erythrocyte morphology may not be entirely due to impaired functions of selenium and copper in cell antioxidant systems. Thus, erythrocyte structure was sensitive to several dietary changes and such alterations are probably independent of the anaemia induced by copper deficiency. This possibility should be considered when changes in erythrocyte morphology are attributed to copper or selenium deficiency in animals which also have a restricted food intake.

Anemia↗
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

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↗
PubMed1978

Changes in leucocyte cytochrome oxidase activity associated with deficiency of copper in laboratory and farm animals.

The cytochrome oxidase activity of circulating leucocytes was investigated by means of a semiquantitative method using blood films. A significant decrease in activity was found in male rats, cattle and sheep that had been deprived of copper. During copper depletion, leucocyte cytochrome oxidase activity declined more slowly than did plasma copper concentration and plasma ferroxidase I activity, and so was less sensitive as a guide to the copper status of the animal.

Animals↗