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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Hypervitaminosis A in the dog

Cho, Doo Youn January 2010 (has links)
Digitized by Kansas Correctional Industries
2

A morphologic study of the effects of hypervitaminosis A on the submandibular salivary gland of the rat a thesis submitted in partial fulfillment ... oral pathology ... /

Regezi, Joseph A. January 1971 (has links)
Thesis (M.S.)--University of Michigan, 1971.
3

A morphologic study of the effects of hypervitaminosis A on the submandibular salivary gland of the rat a thesis submitted in partial fulfillment ... oral pathology ... /

Regezi, Joseph A. January 1971 (has links)
Thesis (M.S.)--University of Michigan, 1971.
4

Study of hypervitaminosis E in the chick

Wong, Fook Chuen January 1970 (has links)
A study was made of the effects of feeding excess vitamin e to chicks. Three groups of experiments were conducted to investigate (1) thyroidal response to excess vitamin e, (2) respiration rate of muscle mitochondria from chicks fed excess vitamin e; and (3) symptoms of hypervitaminosis e. In two separate experiments, chicks were fed normal and excess levels (220 i.u./kg. of diet) of vitamin e and were subjected to temperatures of 14.5 and 31.5°c. the goitrogenic effect of thiouracil on the birds in the different treatments was measured. At both temperatures the thiouracil-treated chicks fed excess vitamin e exhibited a lesser enlargement of the thyroid glands than did chicks receiving a normal level of vitamin e. This finding indicates a reduction in the secretion of thyroid stimulating hormone (tsh) in birds fed excess vitamin e. the level of vitamin e which was fed did not affect the growth rate or feed consumption at either temperature. It, therefore, appears that the metabolic rates of the chicks fed the low and excess levels of vitamin e were similar despite differences in thyroid activity and that tissue respiration in birds fed excess vitamin e can be maintained with a reduced supply or turnover of thyroid hormone. The activity of the thyroid gland itself was studied in response to excess vitamin e in another experiment. Using radioiodine (l¹³¹) as a tracer, it was found that the rates of iodine uptake and release by the thyroid gland were both slower in birds fed excess vitamin e (220 i.u./kg. 0f diet) than in control birds. Because vitamin e acts as a biological antioxidant, it may, in excess amounts, depress the rate of oeiodination of thyroxine in the peripheral tissue at which thyroid hormone is removed from the circulation. As a consequence, the secretion of tsh would be reduced. In order to obtain some indication of cause and effect in the mechanism by which the excess vitamin e affects thyrotropic hormone secretion rate and thyroid activity, the respiration rate of mitochondria isolated from the pectoral muscle of chicks which had been fed excess vitamin e (2200 i.u./kg. 0f diet) was compared with that of the control birds. The results showed a significant reduction in oxygen uptake by the muscle mitochondria of chicks fed the excess amount of vitamin e. The growth rate of the chicks fed the excess level of vitamin e in this experiment was markedly lower than that of the control chicks. It is suggested that the chick may maintain a normal respiration rate when fed excess vitamin e up to a certain level through a reduction in thyroid activity. With a large excess of vitamin e, however, no further compensation is possible. and respiration rate is depressed below normal. Excess vitamin e caused hypoprothrombinemia, indicative of vitamin k-deficiency. Other symptoms noted were a reduction in hematocrit values, reticulocytosis and an abnormally fluid appearance of the bone marrow. Based upon observations of bone calcification, the calcium requirement appeared to be increased in the presence of excess vitamin e. / Land and Food Systems, Faculty of / Graduate
5

Investigations on hypervitaminosis E in rats

Macdonald, Ian Bruce January 1979 (has links)
In view of the fact that some fat soluble vitamins are toxic in large doses to experimental animals and man, this study was initiated to investigate the long-term effects of low, moderate and high levels of dietary vitamin E on various metabolic parameters in the rat. Six groups of female Wistar rats (50 g) were fed for as long as 16 months the basal vitamin E-free diet with supplements ranging from 0 to 25»000 IU vitamin E (DL-a-tocopheryl acetate) per kilogram diet. The levels of vitamin E chosen were 0, 25, 250, 2,500, 10,000 and 25,000 IU/kg diet; 0 representing vitamin E-free, 25 representing moderate level and 250 to 25»000 representing large doses. All nutrients in the basal diet except vitamin E were adequate. The focus of this study was on the effects of large doses of dietary vitamin E on: (l) the hematological indices such as hematocrit and hemoglobin levels, prothrombin time and erythrocyte hemolysis at 9, 12 and 16 months of treatment; (2) urinary creatine and creatinine levels at 11 months of treatment; (3) body weight and various organ weights at 8 and 16 months of treatment; (4) femoral parameters such as ash content, and calcium and phosphate concentrations of bone at 8 and 16 months of treatment; and (5) the levels of a-tocopherol, vitamin A, total lipids, and cholesterol in liver and plasma at 8 and 16 months of treatment. Rats fed 10,000 and 25.000 IU vitamin E/kg diet for 8 and 16 months had significantly reduced body weights in comparison to those receiving the moderate level of vitamin E. The depressing effect of excess dietary vitamin E on body weight was not as marked as that of vitamin E deficiency. There was little difference between the moderate and high vitamin E supplemented groups with respect to the weights of liver, uterus and kidney. However, high levels of dietary vitamin E increased the relative heart weights after 8 months and the spleen weights after 16 months. Hemoglobin and hematocrit values were not influenced by excessive amounts of vitamin E after 9 or 12 months of treatment. At 16 months however, the hematocrit values of rats fed 10,000 and 25,000 IU vitamin E/kg diet were increased significantly over those of rats fed 25 IU/kg diet. The prothrombin time was reduced in rats treated with excess dietary vitamin E for 12 and 16 months. Only vitamin E deficiency, but not excess vitamin E, was associated with increased membrane fragility of erythrocytes. In rats subjected to excess vitamin E for 16 months the ash content of bone was decreased. High levels of dietary vitamin E increased the plasma alkaline phosphatase activity after 16 months of treatment. These results indicate that there may be increased mineral turnover in bones of rats fed high levels of vitamin E for prolonged periods. Urinary levels of creatine and creatinine were not affected by high levels of dietary vitamin E. However, in the vitamin E deficient rats, the creatine excretion increased while the creatinine excretion decreased, resulting in a very high ratio of creatine/creatinine in urine. The α-tocopherol stored in liver rose significantly with increasing dietary vitamin E. A logarithmic relation was demonstrated between liver α-tocopherol concentration and dietary levels of vitamin E. The total α-tocopherol in whole liver of rats fed the different levels of vitamin E for 16 months was approximately double that in rats treated for 8 months. A curvilinear relationship between plasma tocopherol and the logarithm of dietary vitamin E was found in rats treated for 8 and 16 months. Total lipids in liver increased significantly with increasing dietary vitamin E in rats treated for 8 months, but not in rats treated for 16 months. There was little difference in liver cholesterol concentration between the moderately supplemented and highly supplemented groups. Increasing dietary vitamin E significantly lowered plasma total lipids and cholesterol in rats treated for 16 months. A quantitative examination of the data showed that the reduction in plasma total lipids was not simply a reflection of the cholesterol levels, and suggests that a high dietary level of vitamin E affected one or more of the constituents of the total lipids (phospholipids and/or triglycerides) other than cholesterol. From the findings of this long-term study, it appears that high levels of dietary vitamin E result in biochemical changes in some aspects of metabolism in rats. Some of the changes worth recognition are the depression in body weight, increase in relative spleen and heart weights, decrease in ash content of bones with concurrent increase in plasma alkaline phosphatase activity, increased hematocrit value and fatty liver in rats treated for 8 months. A logarithmic relationship was observed between dietary levels of vitamin E and the concentrations of this vitamin in liver and plasma. The results of this study suggest that excess vitamin E over prolonged periods of time have some harmful effects in rats. / Land and Food Systems, Faculty of / Graduate
6

A study of the bovine electrocardiogram in hypervitaminosis D and traumatic pericarditis /

Smith, Charles Roger January 1953 (has links)
No description available.
7

Liver injury in hypervitaminosis A: Evidence for activation of Kupffer cell function.

Sim, Wai-Lum Winnie. January 1988 (has links)
The most important and novel finding of this work was enhanced liver Kupffer cell phagocytic and metabolic function by hypervitaminosis A. An animal model of hypervitaminosis A was developed in male Sprague-Dawley rats gavaged with 250,000 I.U. retinol/Kg body weight/day for 3 weeks. Presence of hypervitaminosis A was indicated by characteristic changes in the fur coat, presence of brittle bones and spontaneous fractures and a significant increase in plasma and liver concentrations of retinyl palmitate while retinol levels remained the same as in controls. Hypervitaminosis A did not cause severe liver abnormalities as reflected by normal plasma glutamate pyruvate transaminase activity and bilirubin. Hepatic blood flow and portal pressure were also normal. Liver microsomal cytochrome P-450 was decreased while malondialdehyde, a by-product of lipid peroxidation, was increased by the Vitamin A treatment. Examination of liver tissue by light microscopy showed no signs of liver cell injury. The main change was a marked increase in size of the fat or Vitamin A storing cells. Although hypervitaminosis A itself did not cause severe liver damage, pretreatment with high doses of Vitamin A severely potentiated liver injury by known hepatotoxicants such as carbon tetrachloride, endotoxin and acetaminophen. The potentiation of hepatotoxicity was determined by activity of glutamate pyruvate transaminase in plasma as well as by histological examination of liver tissue. Measurement of clearance from blood of indocyanine green and ⁹⁹ᵐTc-disofenin indicated this hepatocyte function was normal. Kupffer cell phagocytic function was enhanced in hypervitaminosis A as determined by clearance from blood of ⁹⁹ᵐTc-sulfur colloid. In vitro, there was also evidence that treatment with high doses of Vitamin A activated or enhanced Kupffer cell function. Kupffer cells from control and Vitamin A treated rats were isolated by enzymatic dispersion, purified by centrifugal elutriation, and placed in culture. Activation was indicated by (1) increased phagocytosis of ⁵¹Cr-labeled opsonized sheep red blood cells (2) enhanced release of superoxide anion and (3) enhanced production of tumor cytolytic factor by Kupffer cells from Vitamin A treated rats. Stimulation of Kupffer cell function in hypervitaminosis A seemed to be via lymphokines produced by lymphocytes in response to the excess Vitamin A. We propose that activated Kupffer cells may play an important role in liver injury in hypervitaminosis A.
8

EFFECTS OF HYPERVITAMINOSIS A ON THE ERYTHROCYTE MEMBRANE.

Sim, Wai-Lum Winnie. January 1983 (has links)
No description available.
9

Pathogenesis of vitamin A-induced exencephaly in mice

Theodosis, Dennise Theodosia. January 1974 (has links)
No description available.
10

Pathogenesis of vitamin A-induced exencephaly in mice

Theodosis, Dennise Theodosia. January 1974 (has links)
No description available.

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