PubMed Health⌕ Search

Biomedical subjects

R E Burch

Publications and source records attributed to R E Burch.

At least 19 recordsLinked to original sources
PubMed1984

Effects of zinc deficiency on ethanol metabolism and alcohol and aldehyde dehydrogenase activities.

Alcohol dehydrogenase, low Km and high Km mitochondrial and microsomal aldehyde dehydrogenase, and in vivo ethanol elimination rates were determined in five groups of male Sprague-Dawley rats given liquid diets, as follows: control (C), control plus 5% ethanol (CE), pair-fed control and zinc-deficient (PC-ZnD), zinc-deficient (ZnD), and zinc-deficient plus 5% ethanol (ZnDE). Rats fed CE had decreased liver and serum zinc content. The animals given ZnD diets had an even more dramatic decrease in their tissue zinc concentrations and displayed marked growth retardation. The in vivo blood ethanol elimination rate was increased in animals fed ethanol, and this increase was accompanied by increased alcohol and aldehyde dehydrogenase activities. There was a significant decrease in the ethanol elimination rate in rats given ZnD and ZnDE diets. Alcohol dehydrogenase activities in rats with deficient zinc levels also were decreased, and there were no changes in acetaldehyde dehydrogenase activities. Our results suggest that the metabolism of ethanol to acetaldehyde is impaired in zinc deficiency, but acetaldehyde to acetate conversion appears normal.

Alcohol Dehydrogenase↗
PubMed1983

Impaired ethanol metabolism with advancing age.

Ethanol metabolism as a function of age was assessed in male Sprague-Dawley rats. The ethanol metabolic rates decreased linearly with advancing age. It was also observed that a linear decrease in hepatic alcohol dehydrogenase activity occurred as a function of age. The decreased enzyme activity could be the biochemical mechanism underlying changes in ethanol metabolism. Impaired ethanol metabolism may produce increased pharmacologic effects in older subjects due to increased blood ethanol levels.

Aging↗
PubMed1980

Enhanced lipid peroxidation in liver microsomes of zinc-deficient rats.

The clinical association of decreased serum and hepatic zinc in patients with cirrhosis of the liver presumably arising from excess ethanol ingestion prompted a study of the activities of zinc and alcohol in experimental animals. The purpose of this study was to determine the effect of zinc deficiency upon lipid peroxidation in the liver. The effect of ethanol and zinc deficiency on lipid peroxidation was also evaluated. Rats were used in the experimental design, one group received a control diet, and one was maintained on a zinc-deficient diet. One-half of each group also received 3.85 g ethanol per kilogram body weight daily. Lipid peroxidation in vivo was determined by estimation of diene conjugation of microsomal lipids. The in vitro lipid peroxidation potential was measured by the generation of malonic dialdehyde by enzymatic as well as nonenzymatic reactions. Analysis of this data indicated that increased hepatic microsomal lipid peroxidation was associated with zinc deficiency whether using in vivo or in vitro indices of measurement. Review of the data from individual animals indicated that the lowest levels of serum zinc were associated with increased hepatic content of phospholipids. The degree of lipid peroxidation in the zinc deficient animals was not increased by ingestion of alcohol.

Animals↗
PubMed1979

Trace elements in human nutrition.

Clinical recognition of the role of trace elements in human nutrition is increasing. Heretofore, many clinicians felt that the development of deficiency states was not likely except in very extreme conditions because the presence of trace elements in nature was so ubiquitous. The increased use of total parenteral nutrition seems to have made this viewpoint untenable. The recognition of additional genetic diseases of trace element metabolism such as Menkes' kinky hair syndrome and acrodermatitis enteropathica has also served to focus clinical attention on trace elements. As time passes, no doubt, additional diseases of trace element metabolism will be recognized.

Aging↗
PubMed1979

Serum levels of selenium, calcium, copper magnesium, manganese and zinc in various human diseases.

Serum selenium as well as serum zinc, copper, magnesium, calcium and manganese were investigated in a control group of adult males and in 11 groups of patients in various disease states. Not only the change of each trace element but also the possible association between elements was studied in the various groups. All patients were fasting when sampled and studied only after the acute phase of the disease was corrected. Trace metal determinations were performed by atomic absorption spectrophometry (Mg, Ca, Cu, Zn) and by neutron activation analysis (Se, Mn). All patients showed low serum zinc when compared to controls. Cirrhotic patients had a low serum selenium level as well as low calcium, magnesium and zinc. Emphysemia and cancer patients had an elevated serum copper concentration while copper and manganese levels were elevated in congestive heart failure, infection and pschoses. To our knowledge this is the first time low serum selenium values have been demonstrated to be associated with the low serum zinc, calcium and magnesium levels found in cirrhotic patients.

Adult↗
PubMed1979

Trace element composition of ascitic fluid.

The relationship between trace elements in the serum and ascites of the cirrhotic patient was investigated because there is an interchange of protein, particularly albumin, between serum and ascitic fluid. To study this relationship, serum and ascitic fluid were obtained from 13 patients with biopsy-proved Laennec's cirrhosis. The trace element content of the ascitic fluid studied was less (22% to 73%) than that in serum. Protein fractions were all decreased in ascitic fluid compared with serum. Levels of zinc, calcium, copper, selenium in ascitic fluid correlated well with the ascitic fluid protein fractions. Thus, the trace element composition of ascitic fluid differed appreciably from that of serum, and seemed to correlate with the protein composition of the ascitic fluid in the case of zinc, copper, calcium, and selenium.

Aged↗
PubMed1978

Decreased taste and smell acuity in cirrhosis.

The sensory modalities of taste and smell were evaluated in eight patients with cirrhosis that was proved by biopsy specimens and in 13 control subjects. Additionally, the following serum levels were determined in these same subjects: zinc, copper, magnesium, calcium, manganese, and selenium. Fourteen concentrations each of sucrose, sodium chloride, urea, and hydrochloric acid were used to evaluate taste acuity. Smell was evaluated with 11 concentrations each of nitrobenzene, thiophene, and pyridine. These studies show that decreased acuity of taste and smell occurred in conjunction with cirrhosis in the patients who were tested. There were no trace element abnormalities that consistently correlated with decreased acuity in perception of the individual test substances.

Adult↗
PubMed1976

Trace element contamination of intravenous solutions.

The trace element content of various intravenous solutions was investigated, using atomic absorption and neutron activation analysis methods. The variable content of zinc, calcium, and magnesium led us to seek a source of contamination. Quantities of zinc ranging from 10.75 mug to 132 mug were leached from the rubber stoppers when placed in 0.1N nitric acid for a period of 96 hours. Calcium and magnesium were also leached from the stoppers, but in lesser amounts.

Calcium↗
PubMed1975

Serum and tissue enzyme activity and trace-element content in response to zinc deficiency in the pig.

Zinc deficiency is associated with poor growth and development. It has been postulated that a deficiency of the various zinc metalloenzymes results from the lack of dietary zinc. From present study, an examination of some aspects of this postulate, we conclude the following about zinc deficiency in pigs: (1) Of the tissues studied, it results im diminished zinc content only in liver, kidney, and pancreas. (2) It is associated with tissue abnormalities of various trace elements other than zinc. (3) Histochemical enzyme assays are satisfactory for qualitative but not quantitative determination of zinc metalloenzymes. (4) Deficiency of various tissue zinc metalloenzymes is difficult to demonstrate, even in severe zinc deficiency. (5) It is associated with decreased activity of hepatic leucine aminopeptidase and ornithine transcarbamylase, and decreased serum cholesterol concentrations. Our findings are consistent with the postulate that alterations in a number of trace elements may occur in the entity called zinc deficiency.

Animals↗
PubMed1975

Tissue trace element and enzyme content in pigs fed a low manganese diet. I. Arelationship between manganese and selenium.

Pigs received a diet containing 0.59 p.p.m. Mn. Control pigs received the samequantity of the same diet which was supplemented with 22 p.p.m. of Mn. At the end of6 weeks, pigs fed the low Mn diet had a diminution in tissue Mn levels as well as a diminution in tissue Se content. Tissue levels of Zn, Cu, Ca, and Mg were notaffected by the dietary regimen. Indicative of the fact that experimental animals were probably Mn-deficient was a statistically significant decrease in hepatic arginaseactivity that could be enhanced by the addition of Mn. These studies represent the first experimental evidence that there may be a specific interaction between tissue Se and Mn. Tissue Se levels were decreased to a statistically significant degree in all tissues studied except the kidney in the Mn-deficient animals.

Alkaline Phosphatase↗