[EXPERIMENTAL STUDY OF ESOPHAGEAL TRANSIT IN B COMPLEX AVITAMINOSIS AND C AVITAMINOSIS].
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[Blood coagulation in C avitaminosis. Part II. The change in the prothrombin and thrombotropin concentration and causes of decreased thromboplastin activity of the blood in C avitaminosis in guinea pigs].
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Animals↗
[The ultrastructure of the parietal exocrinocytes of the glandulae propriae in the gastric mucosa in A avitaminosis].
Electron microscopic and morphometric methods were used to study the state of the parietal exocrinocytes of the proper glands of gastric mucosa in dynamics of A avitaminosis. The experiment was performed in 80 albino rats taken from mother's feeding with the initial body mass 40-50 g, divided into 2 groups. In animals of the first group A-avitaminosis was induced by feeding the animals with semisynthetic diet devoid of vitamin A. The 2nd control group was given the same semisynthetic diet but with retinol acetate (45 units a day for each animal). Ultrastructural findings showing the elevated production of hydrochloric acid at early stages of the development of A avitaminosis were obtained: hyperplasia of the internal mitochondrial membrane, dilatation of the intracrystal space and considerable enlargement of the area of secretory membranes of tubulovesicles and microvilli of the intracellular tubules. Deep deficiency of vitamin A disturbs the stability of intracellular membranes and leads to irreversible destructive alterations in the proper gastric glands by the end of the experiment. The facts obtained are of importance for both the understanding of specific nature of secretion of hydrochloric acid and for mechanisms of development of erosion and ulcers of gastric mucosa in A avitaminosis.
Animals↗
[Enzyme activity of thiamine diphosphate biosynthesis and degradation in the mouse liver in the dynamics of B1 avitaminosis development].
Activities of thiamin pyrophosphokinase (TPK EC 2.7.6.2) and thiamin pyrophosphatase (TPPase EC 3.6.1.6) were studied in liver homogenate supernatants obtained from mouse (female, body weight of 21-23 g) in dynamics of B1 avitaminosis. As compared with controls distinct deficiency of thiamin led a decrease in coenzyme thiamin diphosphate (TPP) down to 15% as well as of transketolase activity (TPP-dependent enzyme) down to 35%, especially during the terminal stage of the avitaminosis; the process was accompanied by cyclic alterations in activity of TPK and TPPase. Within 9 and 17 days of the B1 avitaminosis the activity of TPK increased by 62% and 38% and the activity of TPPase--decreased by 30% and 20%, respectively. Alterations in the enzymatic activity appear to be characteristic for adaptation in response to thiamin deficiency.
Animals↗
[Some features of [1-14C] leucine exchange in rat liver during acute oxythiamine avitaminosis].
The leucine content in rat liver and blood serum under acute oxythiamine avitaminosis is decreased. Simultaneously oxythiamine inhibits the activity of alpha-ketoisocaproate dehydrogenase resulting in a decrease of leucine catabolism in the liver. The level of total tRNA in hepatocyte cytosol is lowered, the radioactivity of leucine in aminoacyl-tRNA on the 6th min after injection of [1-14C]leucine is increased approximately 1.5-fold as compared to normal. The radioactivity of leucine in blood serum and aminoacyl-tRNA is directly significantly correlated with the content of leucine incorporated into the proteins, while the level of intracellular [14C]leucine is not correlated with the protein radioactivity (r=-0.154,p greater than 0.5) or with blood serum amino acid radioactivity (r=-0.184, p greater than 0.5). The results obtained thus indicate that 1) in acute oxythiamine avitaminosis when the labelled amino acid is incorporated within 3-6 min the label is "concentrated" in blood serum resulting in increased specific radioactivity of the protein in rat liver; 2) in blood serum leucine is predominantly utilized during protein biosynthesis; 3) acute oxythiamine avitaminosis has no significant effect on protein biosynthesis in rat liver; 4) specific radioactivity of the protein cannot serve as an index of protein synthesis rate.
Animals↗
[Comparative studies of the properties of aldolase isoenzymes A-C in normal rabbit brain and in skeletal muscles from rabbits with E-avitaminosis dystrophy].
By means of fructose-1,6-diphosphate selective elution of aldolase isoenzymic forms from the phosphocellulose column the izoenzyme AC3 was isolated preparatively from the muscles rabbits with experimental E-avitaminosis muscular dystrophy. The specific activity of aldolase A4 and AC3 with pathology differs from that at normal state by fructose-1,6-diphosphate and fructose-1-monophosphate. As to the electrophoretic activity the isoenzymes A4 and AC3 are similar to the same isoforms at normal state. The values of the Michaelis constants and maximal rate are determined for aldolases A4, AC3 and C4 at normal state and for A4 and AC3 with E-avitaminosis. Differences in these parameters are found relative to two substrates for A4 aldolase and AC3-hybrid at normal state and with dystrophy.
Animals↗
[Morphological characteristics of enterocyte proliferation and differentiation processes in avitaminosis A].
A significant decrease in the total number of mitotically dividing cells (per 1 crypt), especially in the lower portions of the intestine, was observed in rats with avitaminosis A. The levelling of differences in the number of goblet cells in the upper and lower portions of the intestine was also recorded in the animals with avitaminosis A. The investigations conducted have evidenced retinol participation in differentiation and, to a lesser extent, in proliferation of epitheliocytes of the rat small intestine.
Animals↗
[Effect of avitaminosis B6 in mice on the function of the T-lymphocytes in vitro].
The influence of different degrees of avitaminosis B6 in mice on the cytolytic activity of T-lymphocytes measured by the amount of Na2Cr51O4 released from the lysed target cells was studied on a model of primary immune response in a mixed lymphocyte culture in vitro. Keeping of the animals for 3 weeks on pyridoxine-free diet failed to influence the capacity of lymphocytes to proliferate in vitro and their cytolytic activity. In animals on pyridoxine-free diet for 45 days the amount of pyridoxal 5(1)-phosphate in the spleen decreased by 55% in comparison with control. Lymphocytes obtained from these animals and cultivated in vitro had a markedly decreased capacity to 3H-thymidine incorporation into DNA in response to alloantigen. The cytolytic activity of these lymphocytes also diminished. The capacity of various pyridoxine forms to restore T-lymphocyte functions disturbed by avitaminosis B6 was studied.
Animals↗
[Changes in chemical composition, biosynthesis and structure of secretion of intermediate area of chicken stomach with A-avitaminosis].
In the intermediate area of the chicken stomach with A-avitaminosis the amount of the secretion increases and its chemical composition changes sharply: the content of water, lipids, hexolamines and suphates lowers. By means of 14-C-acetate, 35S-methionine and 35S-sulphate it is established that renewal of the secretion is inhibited. The electron-microscopic examinations showed that the secret is homogenous in normalcy but with A-avitaminosis it acquires a honeycomb structure, its physicochemical properties being changed: it becomes rigid, cuticle-like. As a result there appear deep cracks reaching mucosa, which lead to formation of erosions and ulcers. An assumption is advanced that the initial disturbances of the secretion might be not related to protein component (as the ratio of amino acids in it's almost unchanged) and depend on the carbohydrate and lipid components. The hypothesis of de Luc et al. as to the transport and intermediatory function of vitamin A in biosynthesis of glycosamineglycanes, glycolipids and glycolipoproteins is questioned. Vitamin A may take part in these processes but not as an intermediator of metabolic systems but as the level of biological structures (for instance, the Golgi apparatus and others) which organize these systems and coordinate their function.
Animals↗
[The ultrastructure of the main exocrinocytes in the glands proper of the gastric mucosa in A avitaminosis].
The electron microscopic and morphometrical methods were used to study the ultrastructural organization of main exocrinocytes of the proper glands of the mucous membrane of the stomach of rats under conditions of A-avitaminosis. Deficiency of vitamin A causes dystrophic alterations of main exocrinocytes. The fragmentation, degranulation and considerable dilatation of cisterns of the granular endoplasmic reticulum, destruction of the Golgi complex membranes, disturbance of the membranous organization of secretory vacuoles were observed. A conclusion is made of disturbances of the protein-synthesizing function of main exocrinocytes under conditions of A-avitaminosis.
Animals↗
Avitaminosis K and the lack of heart lesions in poultry.
Poultry susceptibility to avitaminosis K-induced granulomatous endocardial lesions was studied in broiler and layer chicks. They were fed either a practical corn-soybean meal diet with and without added vitamin K (vit K), or a 61% raw sugar-isolated soybean protein diet (RS-IS) with no added vit K for 10 weeks. Heart lesions were not found in birds fed any of the experimental diets. Mortality, body weight gain, and prothrombin time did not differ significantly between birds fed the practical diet regardless of vit K supplementation. In contrast, the RS-IS diet significantly increased mortality, prothrombin time, and markedly decreased growth. Furthermore, more than a third of the birds fed the high sugar diet had subcutaneous edema, which resembled exudative diathesis. Compared with swine, poultry are apparently less susceptible to granulomatous endocardial lesions induced by a vit K deficiency.
Animals↗
[Lipid peroxidation and disturbance in Ca2+ transport through sarcoplasmic reticulum membranes during E-avitaminosis].
The antioxidant effect of alpha-tocopherol in biolgoical membranes in vivo is described. Experimental E-avitaminosis is accompanied by accumulation of products of free-radical oxidation of phospholipids and by a loss of Ca2+-transporting ability of the muscle cells microsomal fraction. The role of alpha-tocopherol in stabilization and as a "radical trap" in biological membranes is discussed.
Antioxidants↗
[Changes in the activity of alkaline phosphatase and the level of thiamine diphosphatase in simulations of B1 avitaminosis].
Alimentary B1 avitaminosis was attended by a declining activity of alkaline phosphatase in the brain and spleen of rats. A single administration of oxythiamine to rats in a dose of 400 mg/kg produced during the first hours an increased activity of alkaline phosphatase in the liver, brain and, to a lesser extent, in a number of other organs and reduced the thiamine-diphosphate content in the liver, brain and other tissues. The thiamin-diphosphate level in the brain returned back to normal in 12 hours, and in other tissues-towards the 3--5th day. In 24 hours after introduction of oxythiamine the activity of alkaline phosphatase was up in the liver alone, while in the brain the activity of the enzyme decreased. Thiamine, used in a dose of 400 mg/kg, exerted on the activity of alkaline phosphatase in a number of tissues an action similar to that of oxythiamine. It is suggested that the activation of alkaline phosphatase 3--12 hours following adminstration of a large dose of thiamine or oxythiamine is of a non-specific nature. Subcutaneous introduction of a commercial alkaline phosphatase preparation to rats brought down the thiamine-diphosphate level in all of the tissues under investigation. The presumed mechanisms accounting for the fall of thiamine-diphosphate and the possible part played in this process by alkaline phosphatase are discussed.
4-Nitrophenylphosphatase↗
[Differences in potential and content of the mucus in the stomach of the rat with avitaminosis A].
Vitamin A (vit. A) acts in the synthesis of glycoproteins and in cell surface phenomena of epithelia. Since the glycoproteins of gastric mucus and the integrity of gastric cell membranes are components of gastric barrier (GB), vit. A could play a role in GB. Five groups of rats were used: I) rats fed on vit. A deficient diet; II) rats pair-fed plus a daily oral dose of 45 micrograms vit. A; III) normal rats; IV) rats recovered from avitaminosis A (avit. A) after 20 days of daily oral dose of 300 micrograms vit. A; V) rats pair-fed plus a daily oral dose of 45 micrograms vit. A. We measured: 1) transparietal gastric potential difference (PD) in vivo (by means of agar-KCl electrodes); 2) mucus (by binding of Alcian blue): in gastric mucosa; adherent to gastric mucosa; in gastric lumen; 3) dry weight of the stomach. Avit. A induced: i) a decrease of PD and mucus in mucosa and lumen; ii) an increase of mucus adherent to mucosa; iii) an increase of the percentage of dry weight on wet weight. All parameters were normal after recovery from avit. A. Results suggest that avit. A could reduce either mucus synthesis or its erosion. Moreover avit. A might modify mucus structure and sterical configuration of mucosal cells. The alteration of mucosal cell membranes could decrease PD. In conclusion the modifications of some components of rat GB seem specifically caused by avit. A and suggest a protective role of vit. A.
Animals↗
[Limited-time feeding ("meal-feeding") and avitaminosis A : respiratory exchange and metabolic adaptation in rats].
Weanling male rats were fed ad libitum for 6 weeks with a normal or vitamin-A-deficient diet and then meal-fed 1 1/2 hours per 24 hours a 65 p. 100 glucose diet for not less than 3 weeks. The stomach of meal-fed rats develop and food intake is sufficient to ensure a normal rate of growth until deficients reached a plateau of weight. After the single daily meal the respiratory quotients are remaining high (QR greater than 1) all throught the day and decreases during the night (0,8) with all the animals. Fasting glycemia, insulinemia and liver glycogen of meal-feds are higher than ad libitum rats ones, but lower in deficients than in controls. Activities of NADPH2-linked enzymes (G6PDH, 6PGDH and NADP malate DH) are increased in meal-feeding, but avitaminosis A reduces by half this increase.
Adaptation, Physiological↗
[Quantitative and qualitative analysis of cell lesions from the pancreas after 4 weeks of B1-avitaminosis (author's transl)].
Light- and electronmicroscopical observations are made on the pancreas of 18 rats after 4 weeks of B1-avitaminosis. The B1-avitaminotic animals show a definite decrease in bodyweight and in the weight of their pancreas. The mitochondria of the acinar cells are swollen and invaded by numerous vacuoles. Single cells die by eosinoplilic necrosis. The islets of Langerhans demonstrate a definite hyperplasia (polynesis) and hypertrophy (macronesis). The mitochondria are swollen and also transformed into vacuoles. There is a lysosomial granulolysis. Only occasional lesions are observed in the A1 and A2 cells of the islets.
Animals↗
[Effect of avitaminosis A on retinal photoreceptor ultrastructure in adult hens].
A-avitaminosis has been shown to provoke important ultrastructural changes in the external segments of the rods whose membrane disks disorient and disappear. No changes in the external segments of the cones were observed. The ellipsoid and paraboloid of visual cells, both rods and cones, undergo changes. The increase in the number and length of mitochondrial cristae and also the increase in the number of mitochondria themselves is noted in the ellipsoid. In the paraboloid, on the membranes of elements of endoplasmic reticulum, the number of ribosomes increase, and the number of polyribosome complexes increases in the cytoplasm. By means of the colorimetrical method, a decrease in the quantity of vitamin A is shown in the liver and retina of the sick hens. Their feedings on vitamin A provokes a restoration of the ultrastructure of membrane disks of the external segments of the rods.
Animals↗
[Degradation of thiamine diphosphate in subcellular fractions of mouse liver in the dynamics of the development of alimentary B1-avitaminosis].
Alterations in activity of specific and unspecific phosphatases, hydrolyzing thiamin diphosphate, were studied in microsomes, mitochondria and cytosol of mice liver cells in dynamics of alimentary B1-avitaminosis (4-21 days). Activity of the enzymes studied was increased as thiamin deficiency developed. Administration of thiamin into the avitaminous animals normalized the enzymatic activity, indicating the specific dependence of these alterations on the thiamin level in animal tissue.
Animals↗