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Riboflavin content, deficiency

Terroine (1957) also found that 2 % ascorbic acid stimulated the growth of rats fed a riboflavin-deficient diet. As might have been expected, she found also that the food consumption was proportionate to the rate of growth. There was a slight increase in the riboflavin content of the tissues. The ascorbic acid caused a reduction, or complete abolition, of the raised excretion of anthranilic and xanthurenic acids cluiracteristic of riboflavin deficiency (Charconnet-Harding and Terroine, 19.5fi). [Pg.48]

With FA necessary for purine synthesis, and riboflavin in turn having a purine precursor, Clapper and Meade (1958) reasoned that folic deficiency should induce riboflavin deficiency. The riboflavin content of a S. faecalis strain (derived from a sulfathiazole-resistant folic-requiring Streptococcus mitis) increased as more PGA was supplied, from a low of 3.0 to 50.6 mj[Pg.26]

The daily requirement is given in Table 6.3. Deficiency symptoms are rarely observed with a normal diet and, since the riboflavin pool in the body is very stable, even in a deficient diet it is not depleted by more than 30-50%. The riboflavin content of urine is an indicator of riboflavin supply levels. Values above 80pg riboflavin/g creatinine are normal 27-79 pg/g are low and less than 27 pg/g strongly suggests a vitamin-deficient diet. Glutathione reductase activity assay can provide similar information. [Pg.413]

Although the active transport of riboflavin across the gut wall and across other cell membrane barriers within the animal is a saturable process, if large pharmacological amounts are present then the slower and less efficient but nonsaturable process of passive absorption predominates and contributes significantly to the total mass transfer. The active transport process is increased in riboflavin deficiency and decreased if the riboflavin content of the tissues is high. The transport pathway involves calcium and calmodulin but not sodium. Specific riboflavin receptors have recently been identified, as has a role for microtubules in transport. [Pg.313]

Skin wound healing was investigated in a riboflavin-deficient rat model epithelialization was prolonged, wound contraction slowed and total collagen content reduced by 25%.114... [Pg.382]

Apparently the content of the active metabolite pyridoxamine S -phosphalc is lower in human than in mouse or hamster skin.120 When inflammatory response was assessed in a pyridoxine or riboflavin deficient rat model, data suggested enhanced inflammation in pyridoxine but not riboflavin... [Pg.383]

Deane and Shaw have shown that in riboflavin deficiency there is a mild stimulation of the adrenal in the early stages which later disappears. Normal lipoid with a normal content of ketosteroid appeared to persist through most of the deficiency. Birefringent lipoid was increased in the outer fasciculata (in which the cells are reduced in size), but the mitochondria were normal. Livers in riboflavin-deficient animals showed a fatty infiltration in the early stages of deficiency, but as the deficiency increased this fat disappeared. Glycogen was present in cells near the central veins of the lobule, and the mitochondria of the liver cells were normal. [Pg.69]

The synthesis of ascorbic acid in animals has also been linked with thiamine and riboflavin (Kennaway and Daff, 1946 Roy et al., 1946). With both these deficiencies the ascorbic acid content of the tissue of rats and mice has been shown to be low. The stimulation of synthesis shown by a normal animal after chloretone treatment was not observed in animals deficient in either thiamine or riboflavin. The claim was made... [Pg.95]

The presence of substantial amounts of flavins in retina has been known for some time. The detailed function of the light-sensitive flavins in the eye as well as pathophysiological consequences of riboflavin deficiency or overload conditions are not known to date. Batey and coworkers have analyzed the flavin content in retinal tissue from rats and rabbits in some detail (76-78). Retinas from two to three rats were isolated and homogenized. Flavins were extracted by a hot water treatment and analyzed by reversed-phase HPLC (Table 5). The... [Pg.428]


See other pages where Riboflavin content, deficiency is mentioned: [Pg.1108]    [Pg.83]    [Pg.321]    [Pg.7]    [Pg.57]    [Pg.73]    [Pg.111]    [Pg.192]    [Pg.160]    [Pg.543]    [Pg.584]    [Pg.14]    [Pg.277]    [Pg.8]    [Pg.32]   
See also in sourсe #XX -- [ Pg.117 ]




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