Platon J. Collipp

Selenium in Premature Infants

Premature infants have a lower selenium concentration in serum than full-term infants and children. The selenium concentration goes down quickly in infants treated for respiratory distress syndrome without supplementation. One premature infant with bronchopulmonary dysplasia had persistently low concentrations of selenium. Vitamin E supplements did not affect the serum selenium concentration in healthy premature infants. Supplementation with 3 microgram/kg of selenium in parenteral fluids prevented the fall in the concentration seen in other infants not supplemented. Premature infants and especially those treated with oxygen may warrant selenium supplementation to the parenteral nutrition solution. Vitamin E supplements alone are apparently not sufficient to prevent selenium deficiency and potential oxygen toxicity.

Effect of Oral Zinc Supplements on Growth, Hormonal Levels, and Zinc in Healthy Short Children

13 short children aged 7-13 years who had a retarded bone age and low hair zinc concentration (under 140 micrograms/g) were treated with oral zinc supplements for a year. There was a significant increase in the growth rate in the children whose hair zinc concentration increased. Growth hormone, testosterone and somatomedin C also increased after oral zinc supplementation. Data from 755 short healthy children who have attended our Growth Clinic are presented which describe their hair and serum zinc concentration at different ages. The data indicate a decline in hair zinc concentration after birth with a gradual increase at age 4-6 years, finally reaching adult normal levels after adolescence.

Zinc Deficiency: Improvement in Growth and Growth Hormone Levels with Oral Zinc Therapy

A 14-year-old girl and a 13-year-old boy were found to be growth hormone deficient by insulin-arginine stimulation tests, and were also found to be zinc deficient. When oral zinc replacement was given, they both had a significant increase in growth rate which continued for at least 2 years, and subsequent growth hormone tests were normal.

Growth hormone and liver mitochondria: Effects on cytochromes and some enzymes

Abstract The effects of hypophysectomy and subsequent growth hormone treatment on liver mitochondrial levels of cytochromes, flavoprotein, cytochrome oxidase and NADH oxidase were studied in rats. Hypophysectomy lowered cytochrome a , a 3 , b , c , and c 1 , concentrations and cytochrome oxidase activity. On the other hand, flavoprotein concentration and NADH oxidase activity were increased. Administration of either human or bovine growth hormone restored the cytochrome levels. Cytochrome oxidase activity was also increased but did not reach its original level. Only the bovine hormone exerted a lowering effect on flavoprotein and NADH oxidase activities. These and other results suggest that growth hormone influences mitochondrial electron transport.

Growth and Ultimate Height of Children with Asthma

Except that the male/female ratio among the asthmatic children was 3: 1, all groups were similar with respect to age, race, national origin, family income, and parental height. The tendency to have an allergy is known to be a hereditary characteristic. The parents of the children in this study were surveyed for a history of asthma. Only six of the 59 allergic and six of the 69 control children had

Hormones and liver mitochondria: Effects of growth hormone and thyroxine on respiration, fluorescence of 1-anilino-8-naphthalene sulfonate and enzyme activities of complex I and II of submitochondrial particles

Abstract The effects of hypophysectomy and subsequent administration of bovine growth hormone (0.1 IU/100 g body wt) and l -thyroxine (5 μg/100 g body wt) on respiration, energization-dependent fluorescence of 1-anilino-8-naphthalene sulfonate, NADH dehydrogenase, energy-independent nicotinamide nucleotide transhydrogenase, and succinate dehydrogenase activities were investigated in submitochondrial particles of rat liver. Hormones were injected daily for 7 days. Hypophysectomy decreased the respiratory rate with NADH or succinate and the activities of the three enzymes. Administration of growth hormone increased the respiration but showed selectivity toward NADH. Thyroxine increased the respiration more than growth hormone did with both substrates. Growth hormone increased the activities of NADH dehydrogenase and transhydrogenase whereas thyroxine increased the activity of only succinate dehydrogenase. After growth hormone treatment transhydrogenase activity was increased to about three times that of controls which may have significance in some processes mediated either directly or permissively by growth hormone. When both hormones were injected together, there was a significant decrease in the thyroxine-dependent rise in respiration on succinate as well as the growth hormone-dependent rise in enzyme activities. Fluorescence yield of 1-anilino-8-naphthalene sulfonate in unenergized submitochondrial particles remained unchanged independent of the hormonal status. Energization with succinate or NADH increased the fluorescence yield by about 2–20 times. Several parameters of energizationdependent fluorescence were decreased after hypophysectomy. In restoring these parameters, growth hormone and thyroxine showed specificity toward the energization substrate NADH and succinate, respectively. From the present results we conclude that (a) growth hormone and thyroxine regulate mitochondrial activity by affecting different segments of the respiratory chain, namely Complex I and Complex II, respectively, and (b) growth hormone and thyroxine exert moderating effects on one another.

Distribution of 3H-acetyl human growth hormone in subcellular fractions of rat liver

Abstract 3 H-Acetyl human growth hormone ( 3 H-HGH) (∼60 μg) was injected intravenously into hypophysectomized rats. Radioactivity appeared in all the subcellular fractions of liver as early as 2 minutes after the injection. Until 10 minutes postinjection virtually all of the tissue radioactivity was precipitable with trichloroacetic acid, whereas at 20 and 40 minutes after injection all of the radioactivity was soluble in trichloroacetic acid. Liver uptake (cpm/mg protein) peaked at about 20 minutes postinjection. The appearance of radioactivity in the crude nuclear fraction closely followed that of the whole homogenate. Radioactivity in the microsomal and mitochlondrial fractions was highest at the early time periods (up to 10 minutes) and then declined progressively. The radioactivity in the final supernatant or cytoplasmic fraction increased slowly, peaked at 20 minutes, and remained the highest. Pretreatment with unlabeled or 14 C-labeled HGH significantly reduced the mitochondrial and microsomal uptake of 3 H-HGH. In contrast with these results, when 3 H-HGH was added in vitro just before homogenization and fractionation of liver, most of the radioactivity (77%) appeared in the cytoplasmic fraction. These results are interpreted to mean that the appearance of 3 H-HGH in the particulate fractions at these early time periods may have functional significance, and that important initial binding sites of growth hormone in the liver cell may be mitochondria and microsomes.

Effects of growth hormone on respiration and ATPase activity of rat liver and heart mitochondria.

Abstract The effects of hypophysectomy on respiration and ATPase activity of mitochondria of rat heart and liver were investigated. Hypophysectomy decreased significantly the rate of State 3 respiration and ATPase activity of liver but not of heart mitochondria. Heart cytochrome oxidase activity was also not affected. ADP:O and respiratory control ratios were not affected. Administration of bovine growth hormone (bGH) to hypophysectomized rats partially restored the rate of respiration and ATPase activity of liver mitochondria. However, hypophysectomy decreased heart mitochondrial protein synthesis as measured by in vivo and in vitro incorporation of radioactive leucine, but did not affect the in vitro uptake of the amino acid. Administration of bGH restored the incorporation capacity to the normal level. Similar effects on liver mitochondrial protein synthesis have already been reported. These data suggest that the effects of growth hormone on mitochondrial function may vary with the two tissues.

Growth hormone receptors in lymphocytes of growth hormone-deficient children

Human growth hormone was injected intravenously into 18 growth hormone-deficient children and growth hormone binding sites in lymphocytes were investigated. Fresh circulating lymphocytes had a low initial value for the binding of growth hormone to solubilized receptors (3.45 +/- 1.46%) but after growth hormone injection, the binding rapidly increased to 14.8 +/- 4.2% at 2 1/2 h and 8.7 +/- 1.8% at 5 h. The sharp increase in binding is due to increase in the number of binding sites. Two control children who received chorionic gonadotropin had no change in lymphocyte growth hormone receptors. The methodological differences between the present study and previous attempts to identify human growth receptors in lymphocytes were (1) lymphocytes were separated and disrupted with Triton X-100 as quickly as possible (to avoid error from receptor leaking out of the cell) and (2) the receptors were assayed at 2 1/2 h after growth hormone administration (previous studies were 12-24 h later). One possible explanation for the data is that growth hormone receptor from liver is taken up by lymphocytes and rapidly released again, thus, contributing to the hormonal receptor economy in humans.

Growth hormone and rat liver mitochondria: effects on urea cycle enzymes.

Abstract Effects of hypophysectomy and subsequent growth hormone administration on mitochondrial enzymes of the urea cycle were investigated in rat liver. Hypophysectomy increased the activities of the two mitochondrial enzymes, carbamyl phosphate synthetase and ornithine transcarbamylase but not of the cytosolic enzyme, argininosuccinate synthetase. The activity of mitochondrial phosphate dependent glutaminase was not affected. Administration of bovine growth hormone (100 μg/100 g body weight) for two weeks decreased the activities of carbamyl phosphate synthetase and ornithine transcarbamylase almost to the normal level. These results suggest a specific effect of growth hormone on mitochondrial enzymes of the urea cycle and serve to explain the increased urea formation in hypopituitarism.