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Biomedical subjects

G J Fosmire

Publications and source records attributed to G J Fosmire.

At least 19 recordsLinked to original sources
PubMed2002

Chicken keel cartilage as a source of chondroitin sulfate.

Chondroitin sulfate is used extensively as a treatment for osteoarthritis. This study was conducted to evaluate whether chondroitin sulfate could be isolated from chicken keel cartilage in sufficient quantities and of requisite quality to make it a feasible source of chondroitin sulfate. Proteoglycans were extracted from chicken keel cartilage obtained immediately after slaughter by using 3 M MgCl2 at room temperature. The extract was then dialyzed and digested with papain to remove proteins. Glycosaminoglycans were obtained by ethanol precipitation, lyophilized, and characterized by using gel filtration on Sepharose CL-6B columns. Guanidine-HCI extraction was also used as a control to investigate the efficiency of extraction using MgCl2. Results showed that, from every gram of wet or non-lyophilized keel cartilage, 32.9 +/- 4.8 mg (dry weight) of glycosaminoglycans could be obtained following MgCl2 extraction. Analyses revealed that 75.5 +/- 4.2% of these glycosaminoglycans were chondroitin sulfate. Chromatographic analyses showed a single symmetrical peak, which could be almost entirely removed by prior digestion with chondroitinase ABC, indicating that the material in the peak was in fact chondroitin sulfate. The average molecular weight (also called relative molecular mass, Mr) of the glycosaminoglycans was also estimated (Mr 48,500). Characterization using polyacrylamide or agarose gel electrophoresis showed diffuse bands containing chondroitin sulfate, which could be entirely removed by prior digestion with chondroitinase ABC. This study shows that chicken keel cartilage is a readily available source of chondroitin sulfate.

Animals↗
PubMed1996

Zinc status does not affect aluminum deposition in tissues of rats.

To examine whether zinc deficiency would increase the toxicity of dietary aluminum, weanling, male Sprague-Dawley rats were fed purified diets containing either 2 or 30 mg Zn/kg diet, with or without 500 mg Al/kg diet for 28 d. Individually pair-fed rats were fed the 30 mg Zn/kg diet with or without added aluminum to control for inanition secondary to zinc deficiency. Rats fed the 2 micrograms Zn/kg diet showed evidence of zinc deficiency, including anorexia, growth retardation, and depressed concentrations of zinc in tibias and livers. Zinc deficiency did not significantly increase the concentrations of aluminum in the tibias, livers, kidneys, or regions of the brain examined (cerebrum, cerebellum, midbrain, and hippocampus). Inclusion of aluminum in the diet did not alter aluminum concentrations in the various tissues. Under the conditions of this study, zinc deficiency did not result in greater sensitivity to dietary aluminum exposure.

Aluminum↗
PubMed1995

The impaired growth induced by zinc deficiency in rats is associated with decreased expression of the hepatic insulin-like growth factor I and growth hormone receptor genes.

This study was conducted to determine whether dietary zinc status affects the expression of the insulin-like growth factor I and growth hormone receptor/growth hormone binding protein genes in the liver of growing rats. Weanling male Sprague-Dawley rats were randomly allotted to zinc-deficient, pair-fed or ad libitum-fed dietary treatments and fed diets containing no added zinc for 14 d. Zinc acetate was added to the deionized, distilled water (30 mg/L) provided to pair-fed and ad libitum-fed rats. As expected, zinc deficiency significantly reduced growth rate by 60% and was associated with a significantly lower serum insulin-like growth factor I concentration (46 and 67% lower than pair-fed and ad libitum-fed rats, respectively). The reduction in serum insulin-like growth factor I concentration was associated with a decrease in insulin-like growth factor I gene expression. The abundance of the 7.5-kb insulin-like growth factor I mRNA transcript in zinc-deficient and pair-fed rats was 14 and 31% that of the ad libitum-fed rats. The 0.8-1.2-kb insulin-like growth factor I transcript also was significantly lower in the zinc-deficient and pair-fed rats. In contrast, the abundance of the 1.8-kb insulin-like growth factor I transcript was unaffected by zinc deficiency. The growth hormone receptor mRNA levels of zinc-deficient and pair-fed rats were 17 and 50% and their growth hormone binding protein mRNA levels were 46 and 65% those of the ad libitum-fed rats. In summary, zinc deficiency markedly decreases expression of the insulin-like growth factor I and growth hormone receptor genes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Zinc toxicity.

Although consequences of zinc deficiency have been recognized for many years, it is only recently that attention has been directed to the potential consequences of excessive zinc intake. This is a review of the literature on manifestations of toxicity at several levels of zinc intake. Zinc is considered to be relatively nontoxic, particularly if taken orally. However, manifestations of overt toxicity symptoms (nausea, vomiting, epigastric pain, lethargy, and fatigue) will occur with extremely high zinc intakes. At low intakes, but at amounts well in excess of the Recommended Dietary Allowance (RDA) (100-300 mg Zn/d vs an RDA of 15 mg Zn/d), evidence of induced copper deficiency with attendant symptoms of anemia and neutropenia, as well as impaired immune function and adverse effects on the ratio of low-density-lipoprotein to high-density-lipoprotein (LDL/HDL) cholesterol have been reported. Even lower levels of zinc supplementation, closer in amount to the RDA, have been suggested to interfere with the utilization of copper and iron and to adversely affect HDL cholesterol concentrations. Individuals using zinc supplements should be aware of the possible complications attendant to their use.

Adult↗
PubMed1986

Zinc deficiency affects the composition of the rat adrenal gland.

The response of the adrenal gland to zinc deficiency was examined in male weanling rats. In comparison with decapsulated adrenals from ad libitum fed controls, glands from zinc deficient rats had greater relative weight (mg/g body wt), DNA concentration, and total lipid and cholesterol concentrations as well as a smaller protein/DNA ratio. Several of these differences (protein/DNA and cholesterol concentration) could be attributed to the inanition accompanying zinc deficiency, as zinc deficient values were similar to those of pair fed controls. Values for total DNA and protein concentration were similar for all groups. Electron micrographs of the zona fasciculata showed a small number of lipid droplets in the adrenals from ad libitum fed controls, an increase in lipid droplets from pair fed controls, and an even more striking increase in lipid droplets from the zinc deficient adrenals. The increased adrenal lipid composition in the zinc deficient group may be secondary to enhanced steroidogenesis or a zinc deficiency-induced defect of lipid metabolism.

Adrenal Glands↗
PubMed1985

Effects of marginal zinc deficiency on subclinical lead toxicity in the rat neonate.

Influence of maternal dietary zinc intake on tissue distribution of lead and zinc in neonatal rats administered lead acetate by gavage during lactation was examined. Milk from dams fed a marginally deficient diet (6 micrograms Zn/g diet) contained a lower zinc concentration at the beginning of lactation than did that from control dams (30 micrograms Zn/g diet); no differences were seen by d 11 of lactation. Dams fed the deficient diet had lower plasma zinc values in comparison with pair-fed or ad libitum-fed dams and lower femur zinc concentration in comparison with pair-fed dams. Pups suckling marginally deficient dams had lower concentrations of zinc in plasma, femurs and kidneys although hippocampal and cerebellar zinc were unaltered. Body weights of pups from marginally zinc-deficient dams were lower than those from ad libitum-fed dams, but similar to those from pair-fed dams. Lead ingestion had no effect on body weight. Marginally zinc-deficient pups had greater lead accumulation in blood, femurs, hippocampi and cerebella, but not kidney, than did zinc-adequate pups. Marginal zinc deficiency during lactation increases the body lead burden of suckling rats, an effect not attributable to increased transfer of lead into milk in response to suboptimal maternal zinc status.

Animals↗
PubMed1984

Alterations in the postnatal development of the cerebellar cortex due to zinc deficiency. II. Impaired maturation of Purkinje cells.

Zinc deficiency during the first 3 postnatal weeks retarded the maturation of Purkinje cells. The dendrites of the Purkinje cells of 21-day-old zinc-deficient (ZD) rats were reduced in size and had fewer branches. Somatic processes were found in 24% of the Purkinje cells of ZD animals. Only 3% of the Purkinje cells of normal animals had somatic processes. A basal polysomal mass in the Purkinje cells of 21-day-old ZD rats indicated that zinc deficiency impaired the cytoplasmic maturation of Purkinje cells. The development of the glial envestment of the dendrites and the maturation of climbing fibers also were retarded. Pair-fed controls were studied to control for the effects of inanition in the ZD dams. In the pups of pair-fed dams, undernutrition slightly impaired the growth of the dendrites but produced few qualitative changes in the maturation of the soma and climbing fibers. Somatic processes were found on 10% of the Purkinje cells of pair-fed animals. Thus, the findings in the ZD animals were not only caused by the decreased maternal food consumption but by zinc deficiency. The retarded maturation of Purkinje cells was related to the altered metabolism of Purkinje cells and to effects secondary to decreased numbers of parallel fibers.

Aging↗
PubMed1983

Alterations in the postnatal development of the cerebellar cortex due to zinc deficiency. I. Impaired acquisition of granule cells.

The effects of zinc deficiency on cerebellar development were investigated in suckling rats. In 21-day-old zinc-deficient rats the cerebellum as well as the whole brain was reduced in size. The cerebellar cortex was underdeveloped and showed a persistence of the external granule cell layer, a reduction in the thickness of molecular layer and a decrease in the area of the internal granule cell layer. Lobular variations were present. Along the posterior superior fissure there was approximately a 60% reduction in the number of granule cells and in the number of granule cells per Purkinje cell. It was suggested that the reduction in the number of granule cells was predominantly the result of impaired cell proliferation in the external granule cell layer. Comparisons with undernourished, pair-fed pups indicated that the effects of zinc deficiency could not be mediated totally through the reduced food consumption experienced by zinc deficient dams.

Animals↗
PubMed1982

Taste acuity, plasma zinc levels, and weight loss during radiotherapy: a study of relationships.

Thirty-five patients who were to undergo radiotherapy and 13 normal subjects were evaluated with taste questionnaires, taste acuity tests, and plasma zinc analyses. The studies were repeated on the patients in the fifth week of radiotherapy. The mean taste thresholds for NaCl (salt), sucrose (sweet), HCl (sour), and urea (bitter) were elevated and the plasma zinc levels were lower (77.2 +/- 11.8 vs. 94.6 +/- 30.1 g/100 ml, p = 0.055) for the patients than for the controls. However, there was not a significant correlation between the taste thresholds and plasma zinc levels at any time. The mean weight loss experienced by the 14 patients who reported subjective taste alteration in the fifth week was 3.1 kg versus 0.1 kg (p = 0.005) for those who did not report taste alteration. The data suggest that alterations in taste acuity, but not plasma zinc levels, are associated with weight loss during radiotherapy.

Adult↗
PubMed1981

Effect of zinc deficiency on appetite and plasma amino acid concentrations in the rat.

1. Levels of zinc in liver and plasma of the Zn-depleted rats fluctuated with the feeding cycle and were significantly higher at the bottom than at the top of the cycle. As Zn deficiency became more severe fluctuations in plasma Zn diminished. Concentrations of Zn in liver, in contrast to levels in plasma and femur, were not markedly lowered by day 15. 2. In contrast to ad lib-fed (AL) and overnight-fasted (OF) controls, some pair-fed (PF) controls had elevated levels of Zn in liver and plasma. 3. Intakes of water and food were significantly correlated in Zn-deficient rats. Packed cell volumes were significantly higher for Zn-depleted than for AL and PF rats. 4. Food intakes and plasma glucose concentrations were related in AL, OF and PF control rats but not in Zn-deficient rats. 5. At day 15 of Zn deficiency the order of total plasma amino acid concentrations in the groups of rats was AL greater than Zn-deficient greater than OF greater than PF. Many of the differences between the AL and OF groups for individual plasma amino acids also appeared in the Zn-deficient group at the top and bottom of the feeding cycle. Differences in individual amino acid concentrations at the top and bottom of the feeding cycle tended to be opposite in the PF and the Zn-deficient group. Levels of tyrosine and tryptophan in plasma were correlated (P less than 0.05) with the cyclic feeding pattern of the Zn-deficient group; however, the ratios tryptophan or tyrosine: sum of other large neutral amino acids did not correlate significantly with the eating habits of Zn-deficient rats.

Amino Acids↗
PubMed1981

Plasma zinc in hypertension/toxemia and other reproductive variables in adolescent pregnancy.

A study was conducted at Charity Hospital, New Orleans, among 272 adolescent pregnant women to ascertain the relationship of pregnancy outcome to plasma zinc level measured once at the time of enrollment. Regression analyses were performed on zinc status versus parameters concerning success of pregnancy corrected for gestational stage at specimen collection. Analysis of variance was performed on groups according to presence or absence of complications, with analyses of covariance used to analyze dichotomous groups. Low, though widely variable, plasma zinc levels were found (mean = 58 +/- 12.6 micrograms/dl). Zinc values differed significantly by gestational stage at collection, the regression coefficient indicating a decline of 0.07 micrograms/dl/day. Plasma zinc level correlated significantly with Hb, red blood cells, ferritin, and folic acid. As to course of pregnancy, women experiencing hypertension/toxemia were found to have significantly lower plasma zinc level. Among infants displaying congenital defects at birth those with undescended testes and metatarsus varus were delivered by mothers whose plasma zinc was well below the mean for the group. These findings indicate the need to investigate the influence of dietary patterns and zinc intake on maternal plasma zinc level and pregnancy outcome, further delineating the role of zinc in human reproduction, particularly hypertension of pregnancy.

Adolescent↗
PubMed1980

Nitrogen retention during late gestation in the rat in response to marginal zinc intake.

This study was conducted to characterize nitrogen retention in response to marginal dietary zinc during gestation. Long-Evans rats were randomly assigned to one of two dietary groups on day 1 of gestation. The dams were fed a basal diet supplemented with either restricted or control levels of zinc. Feces and urine were collected for 24 h on day 20 of pregnancy, and their nitrogen and zinc contents were determined. Urinary and fecal nitrogen excretions were similar for zinc-restricted and control dams, whereas fecal zinc excretions were depressed by feeding the zinc-restricted diet. Mean zinc and nitrogen retentions were negative for the zinc-restricted and positive for the control groups. Multiple stepwise regression analysis showed that nitrogen retention on day 20 depended on both dietary nitrogen and zinc intakes. Zinc-restricted offspring weighed 12% less and the maternal plasma zinc concentrations were reduced by 66% when compared with the control group values on day 22. Marginal dietary zinc and the associated anorexia limited fetal growth without causing excessive nitrogen excretion or severe weight loss.

Animals↗
PubMed1977

Maternal and fetal response to various suboptimal levels of zinc intake during gestation in the rat.

Some effects of various degrees of zinc deprivation during pregnancy have been examined in dams and offspring. After mating, the dams were fed a biotin enriched, 20% sprayed egg white diet which contained less than 1 ppm zinc. Zinc was provided in the drinking water at one of the following concentrations: 1, 2, 3, 5, 11, or 25 mg/liter. Pups were taken by cesarean section on day 22 of gestation. The dams given insufficient zinc became anorexic, particularly during the latter third of gestation. Anorexia occurred earlier and was most severe at the lowest levels of zinc intake. The decreased food consumption resulted in energy deprivation and at the lowest levels of zinc intake, in protein insufficiency. The total weight gain and rate of weight deposition in the dams were both functions of the level of zinc provided. Fetal growth and extent of zinc deposition into the fetuses were both related to the amount of zinc provided. The responses of dams and fetuses to the extent of zinc deprivation were not equivalent, however. It appeared that there was a sparing of fetal growth at the expense of the dam at very low levels of zinc intake. Conversely, at higher, but still suboptimal levels of zinc, the fetuses still experienced growth retardation although the dams attained a normal weight deposition during gestation.

Animals↗