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About a fifth of the ascorbic acid is readily lost from intestinal tissue during handling procedures such as washing with saline and blotting. Further losses occur during incubation in Krebs-phosphate saline; after 10 min strips of intestine retained 80% of their original ascorbic acid content and chopped tissue only 50%. This suggests that some of the intestinal ascorbic acid is very loosely held in the tissue. The small intestine is capable of accumulating double the normal amount of ascorbic acid when animals are dosed intramuscularly and retains some ascorbic acid (0.7 to 5 µ/mg DNA) even when the animals" body stores are depleted. [ABSTRACT FROM AUTHOR]

Discusses the study on alteration in lipid metabolism produced by ethyl trichloracetate. Investigation on functions of ethyl trichloracetate in enhancing synthesis of secretion of low and very low density lipoproteins; Adverse events of ethyl trichloracetate administration; Factors affecting lipotropic action of ethyl trichloracetate.

Female rats on a diet adequate, except for pyridoxine, did not give rise to pyridoxine deficiency in their young, when extra thiamine or extra thiamine and calcium was included in the diet. A hypothesis correlating this result to the finding of Richards Is advanced. [ABSTRACT FROM AUTHOR]

In acute thiamine deficiency the increased excretion of ribofiavin occurs at the same time as loss of body weight. Animals receiving adequate amounts of thiamine, but which were losing weight through an insufficient food intake, had increased excretions of riboflavin similar to the deficient animals. In chronic thiamine deficiency there was a 25 p.c. increase in riboflavin excretion by the deficient animals when compared to litter mate controls. No significant differences could be shown in the riboflavin content of the liver from thiamine deficient animals and those receiving thiamine. [ABSTRACT FROM AUTHOR]

Cites a study conducted by researchers in Australia which examines the changes in levels of tissue nucleotides and glutathione after hyperbaric oxygen treatment. Destruction of tissue constituents by autoxidation; Factors that influenced the changes in glutathione and pyridine nucleotides; Detection of the small amounts of lipid peroxide in the erythrocytes of mice.

The results presented indicate that subcutaneous injections of ethyl trichloracetate in appropriate doses will cause a statistically significant fall in liver lipid values and statistically significant increases in liver phospholipids, of choline deficient animals. The extra phospholipids found in the liver had a similar choline content to that found in the choline deficient control livers. Assessment of the histological changes in such livers does not indicate any toxic effect of ethyl trichloracetate, nor any effect on the changes due to the amino acid imbalance of the diet used. The reduction in liver lipid found by biochemical analysis appears related to a decrease in centrolobular fat. [ABSTRACT FROM AUTHOR]

Ultrafiltration and gel chromatography on Sephadex G-75 have revealed no evidence of ascorbate-binding to protein components of the soluble fraction derived from a tissue homogenate of rat cerebellum. Furthermore, partition studies have failed to detect any binding of ascorbic acid to structural components of rat cerebellum, as the ascorbate content of cerebellar tissue exhibited linear dependence upon the concentration of free vitamin in the surrounding medium (0.1 M phosphate, pH 6.5). The accumulation of ascorbic acid in rat cerebellum is discussed, therefore, in terms of an elevated intracellular concentration maintained by active transport of the vitamin across cerebellar tissue membranes.

The level of ascorbic acid in the brain of growing rats was not influenced by efforts to accelerate neural activity. Treatments used to depress neural activity included thyroidectomy which produced a 13%-20% loss of ascorbic acid in cortical and cerebellar tissue and diazepam which produced a significant rise in the cerebellum. Ethanol and barbital were without effect.

Mice were exposed to concentrations of 20, 40 and 200 ppm ozone in air for 30 min. Ozone exposure decreased lung ascorbic acid levels and increased lung weight by up to 50% in a dose related manner. On incubation in Krebs-phosphate solution, lung slices from mice exposed to 200 ppm ozone released a smaller fraction of their content of ascorbic acid into the medium than did lung slices from control mice, suggesting that there was a preferential loss of extracellular ascorbic acid during oxone exposure. These results are consistent with the proposed function of ascorbic acid as an extracellular antioxidant in lungs.

Fifty percent of the ascorbic acid content of sliced rat lung was released from the tissue to the media within a few minutes by either washing or incubating the slices with Krebs-phosphate solution. Measurement of the lactate dehydrogenase and potassium content of the medium after incubating lung slices for 5 min showed that about 20% of the cells were damaged by slicing. Sephadex chromatography of tissue extracts prepared from washed lung slices showed that none of the ascorbic acid in these slices were bound to protein. Also, metabolic poisons were shown to deplete the ascorbic acid content of washed lung slices. Approx. 57% of the lung ascorbic acid of guinea pigs that had been supplemented with ascorbic acid and 78% of the lung ascorbic acid of ascorbic acid-deficient guinea pigs were found in the medium when lung slices from these animals were incubated with Krebs-phosphate solution. These results were taken to indicate the presence of an extracellular pool of ascorbic acid in lung which is maintained even during scurvy.

Maternal rat lung, liver, kidney and portions of small intestine lost up to 40% of their ascorbic acid between early pregnancy and the 15th day of gestation. From then to the end of pregnancy, the ascorbic acid content of the tissues increased by 30 to 60%. Ascorbic acid in fetal lung doubled in concentration on the 18th day of fetal life before a pre and post natal value of 200 micrograms/g tissue was established. Fetal liver had a minor rise in ascorbic acid concentration on the 18th day. Just prior to birth, the ascorbic acid content in fetal lung was 30% and fetal liver 50% higher than maternal.

About a fifth of the ascorbic acid is readily lost from intestinal tissue during handling procedures such as washing with saline and blotting. Further losses occur during incubation in Krebs-phosphate saline; after 10 min strips of intestine retained 80% of their original ascorbic acid content and chopped tissue only 50%. This suggests that some of the intestinal ascorbic acid is very loosely held in the tissue. The small intestine is capable to accumulating double the normal amount of ascorbic acid when animals are dosed intramuscularly and retains some ascorbic acid (0.7 to 5 microgram/mg DNA) even when the animals' body stores are depleted.

Ultrafiltration has been used to investigate the interaction of ascorbate with bovine serum albumin in 0.1 M sodium phosphate buffer, pH 6.5. The results are interpreted in terms of the binding of ascorbate to four equivalent and independent protein sites, governed by an intrinsic association constant of 2 600 +/- 700 M-1 at 20 degrees C, thereby providing evidence for specificity of the interaction over a range of vitamin concentration (0.08-1.5 mM) pertinent to the physiological situation.

Lung surfactant in amniotic fluid, and hence the maturity of the fetal lungs, can be assessed by observation of stable microbubbles (less than 15 micron diameter). Bubbles are formed by agitation with a Pasteur pipette and examined in hanging drops under the 10 x power of a microscope. Either after a count of bubbles, or after a general survey of hanging drops, the fluid is given a stable microbubble rating. A 'strong' rating indicates that the idiopathic respiratory distress syndrome will not occur after delivery, and that the lecithin/sphingomyelin ratio will indicate maturity. Complete absence of stable microbubbles suggests a high risk of respiratory trouble for the newborn infant, as does a weak or lower rating in the 30 to 37 week gestational age group. The test takes 5 to 10 minutes to perform, is cheap and easy, is not affected by blood, but may be affected by meconium. If a 'strong' rating is found, measurement of the L/S ratio can safely be omitted.

Subcutaneous injections of the lipotropic agent, ethyl trichloracetate, to rats with established choline deficiency raised their plasma triglycerides by 60% and completely removed the hyperglyceridaemic response of Triton WR 1339. The plasma triglyceride levels of choline-supplemented rats were depressed slightly by ethyl trichloracetate administration, which was effective in abolishing response to Triton WR 1339. Lipoprotein lipase activity of epididymal fat pad was stimulated 60% while plasma lipoprotein was not stimulated by ethyl trichloracetate. The increased peripheral removal of low-density lipoprotein-triglyceride complex, allowing greater use to be made of existing apo-proteins, may explain the lipotropic character of the ester.

Rat lungs were perfused by recycling Krebs-bicarbonate solution in an apparatus which allowed negative pressure ventilation of the lungs. After addition of either reduced or oxidized ascorbic acid to the perfusion fluid serial samples were taken over 60 min and assayed for ascorbic acid. At the end of perfusion, lungs were assayed for ascorbic acid. The results show that reduced ascorbic acid was taken up by the lung and concentrated in the tissue. No appreciable transport of oxidized ascorbic acid was measured.

Fetal rat liver can synthesize ascorbic acid after 16 days of gestation. Fetal kidney was inactive and neither fetal guinea pig liver nor kidney possessed ascorbic acid synthetic ability.

Young rats were fed choline-deficient diets and maintained at different environmental temperatures. The hepatic lipid level remained normal in rats at 2 degrees when 25 mg of choline per 100 g of food was fed; 50 mg of choline per 100 g food was required at 21 degrees and 100 mg of choline per 100 g food at 33 degrees to prevent excessive lipid accumulation. These values were equivalent to a mean daily intake per rat of 3 mg of choline at 2 degrees, 5.5 mg at 21 degrees, and 7 mg at 33 degrees respectively. When the growth rate was slower owing to a slight inadequacy of histidine in the basal choline-deficient diet, normal hepatic lipid was maintained by supplements of 50 mg of choline per 100 g food at 21 degrees and 33 degrees. Increasing the methionine content of the diet two- or three-fold from a basal value of 340 mg per 100 g food was as effective as 200 mg of choline per 100 g of food in lowering hepatic lipids at 2 degrees, 21 degrees, and 33 degrees.