Biomedical subjects

T L Blalock

Publications and source records attributed to T L Blalock.

6 recordsLinked to original sources

PubMed1988

Metallothionein gene expression in rats: tissue-specific regulation by dietary copper and zinc.

Regulation of metallothionein gene expression by dietary zinc and copper was examined in rat liver, kidney, intestine and brain using a 3 X 3 factorial design. Purified diets containing 5, 30 and 180 mg Zn/kg and 1, 6 and 36 mg Cu/kg were fed for 2 wk. Serum concentrations of copper and zinc were lower at the lowest intakes of either metal than at normal or supplemental levels. Kidney metallothionein levels were proportional to dietary zinc, being 50% less in the 5 mg Zn/kg group than in those fed the highest zinc intake. Metallothionein mRNA was measured by dot blot hybridization to a 32P-labeled oligonucleotide DNA probe representing the terminal 5' sequence of the metallothionein gene. In kidney the number of metallothionein mRNA molecules per cell increased four- to five-fold (from 4 to 29 molecules per cell) with increasing dietary zinc. A less pronounced effect on metallothionein mRNA was observed in response to dietary copper. At the lowest copper intake level and highest intake of zinc intestinal metallothionein mRNA was sevenfold greater than in any other group. Liver and brain did not respond appreciably to the dietary levels of copper and zinc that were fed. Chromatography showed that copper and zinc content of renal metallothionein was directly related to the dietary levels fed. In kidney, both metallothionein-1 and -2 genes were expressed.

Administration, Oral↗

PubMed1987

Metallothionein.

Early research on metallothionein centered on aspects related to a detoxification role. As our understanding of the complex endocrine control that regulates metallothionein gene expression increases, a wider appreciation of a functional role(s) is emerging. Medical implications of control of metallothionein turnover include diagnosis of specific diseases and regulation of its expression as a host defense component.

Binding Sites↗

PubMed1984

Humoral immunity in chicks experiencing marginal vitamin B-6 deficiency.

An economical vitamin B-6-deficient ration that was palatable to broiler chickens was prepared and fed to 1-day-old chicks. The experimental ration was a typical soy-glucose ration. Vitamin B-6 was removed by washing the soybean meal with water. Microbiological analysis revealed that the washed ration contained 0.45 mg vitamin B-6 per kilogram. Experimental rations were formulated to contain 0.5, 1.0 and 3.0 mg supplemental pyridoxine x HCl per kilogram of ration. These supplemental levels produced the following total pyridoxine concentrations in the diet: 0.95, 1.48 and 3.18 mg pyridoxine x HCl activity per kilogram of diet. Chicks were grown to 7 weeks of age and characteristic vitamin B-6 deficiency signs were quantitated and/or observed. Notable signs in chicks receiving 0.5 mg added vitamin B-6 were increased mortality, decreased body weight gain and increased incidence of abnormal leg conformation. The humoral immune system of broiler chicks that were moderately deficient in vitamin B-6 was investigated. Marginal pyridoxine deficiency caused significant reduction in antibody levels to sheep red blood cells (SRBC) and relative levels of IgM and IgG during the peak and degradation phases of the primary response. During the hyperimmune response total anti-SRBC levels were not affected; however, relative levels of IgM and IgG were lowered.

Animals↗

PubMed1984

Hematology of chicks experiencing marginal vitamin B6 deficiency.

An economical vitamin B6-deficient ration, which was palatable to broiler chickens, was prepared and fed to 1-day-old broiler chicks. The experimental ration was a glucose-soybean meal diet. Vitamin B6 was removed by washing the soybean meal with water. Microbiological analysis revealed that the washed ration contained .45 mg vitamin B6 activity/kg. Experimental rations were formulated to contain .5, 1.0, and 3.0 mg added pyridoxine HCl/kg of ration. These supplemental levels produced total pyridoxine concentrations, as assayed, of .95, 1.48, and 3.18 mg pyridoxine HCl activity/kg of diet. Chicks were grown to 7 weeks of age and characteristic B6 deficiency traits, including increased mortality, decreased body weight gain, and increased incidence of abnormal leg conformation, were quantitated or observed. An extensive hematological evaluation at 4 weeks of age indicated that this marginal B6 deficiency resulted in increased erythrocyte numbers, decreased mean corpuscular hemoglobin levels, and increased erythrocyte fragility. No changes in hematocrits, total hemoglobin level, intracellular hemoglobin concentration, or reticulocyte number were found. These results indicate that anemia did not occur in broilers experiencing a moderate vitamin B6 deficiency. The hematological condition is described as microcytic, normochromic polycythemia.

Animals↗

PubMedDate not supplied

Studies on the role of iron in zinc toxicity in chicks.

The interaction of dietary iron and zinc was studied in chicks. Zinc was found to be more toxic in iron-deficient animals than iron-supplemented animals as measured by hemoglobin concentrations and growth. Analyses of the kidney and liver for iron and zinc were carried out. As the level of iron was increased from 0-1000 ppm supplementation, the concentration of liver zinc increased. The organ levels of iron were decreased as the dietary zinc levels were increased from 0-5000 ppm. Radioisotope studies using 65Zn revealed that the iron content of the diet did not affect absorption of zinc. Administration of the isotope, either in an intestinal segment or intravenously, resulted in more zinc being taken up by the liver in the iron supplemented animals. This was especially noted when the ratio of the isotope in liver to that in the blood was compared. Gel chromatography of kidney and liver homogenates revealed that iron deficiency resulted in less zinc being eluted in a volume characteristic of metallothionein compared to homogenates of organs from iron supplemented animals. The results indicate that iron-supplemented animals have a greater capacity for sequestering zinc on metallothionein than do iron-deficient animals. Conversely, iron-deficient chicks were more susceptible to the effects of zinc toxicity than are iron-adequate chicks.

Anemia, Hypochromic↗

PubMedDate not supplied

Studies on the role of iron in the reversal of cadmium toxicity in chicks.

Studies were conducted to determine the effect of dietary iron (Fe) levels ranging from a deficiency to an excess on the toxicity of cadmium (Cd) in chicks. In Fe-deficient animals, cadmium was found to be more toxic than in Fe supplemented animals as measured by growth. The liver Cd burdens were increased significantly in the presence of dietary Fe supplementation, and there was a significant Cd-Fe interaction in the Cd concentration of the kidney, indicating that iron deficiency increased the concentration of Cd in the kidneys of those chicks receiving this element. Cd tended to reduce the Fe concentration in both the liver and kidney. The absorption of Cd as measured by the amount of 109Cd that disappeared from an isolated duodenal segment in one h was not affected by the Fe content of the diet, but the amount of isotope appearing in the liver compared to the amount present in the blood was increased in the Fe supplemented chicks. Separation of the Cd binding ligands by column chromatography revealed that more of the Cd in the liver, but not the kidney, was associated with ligands which eluted in a column volume that contained metallothionein in those chicks receiving Fe than in the livers from Fe deficient animals. The inverse relationship between the amount of Cd bound to the metallothionein containing fraction and toxicity may be related causally.

Anemia, Hypochromic↗