Accumulation of ascorbate in rat cerebellum.

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.

Ascorbic acid synthesis by the mammalian fetus.

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.

Ascorbic acid in fetal rat brain.

Ascorbic acid in fetal rat brain increases from 374 mg/g on the 15th day of gestation to 710 mg/g by the 20th day and remains at that level until birth. There is an 18% drop from this plateau after birth.

Ascorbic acid changes in brain.

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.

Effects of facial cooling during exercise at high temperature.

Healthy men and women were exercised on a cycle ergometer in a hot environment (46 degrees C). Cold air (5 degrees C) was blown onto the face either as a jet from the tube directed towards the nose or being introduced under a face mask. There was a subjective feeling of increased comfort although the temperature under the mask decreased to only 28 degrees C-32 degrees C. Facial cooling did not cause any changes in either blood pressure or heart rate. It is concluded that this degree of facial cooling does not invoke the previously described peripheral vasconstriction which could inhibit further heat loss.

The binding of ascorbate to bovine serum albumin.

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.

Ascorbic acid in neural tissues.

Large amounts of ascorbic acid were readily removed from neural tissue by washing with warmed saline solutions. In areas where the original level was highest, such as cortex and cerebellum, a higher percentage was removed than from areas of lower concentration, such as pons-medulla. The residual level in both types of tissue was similar. During scurvy, the ascorbic acid retained in the guinea pig brain is more readily removed by washing than is that of the normal brain.

Tissue levels of ascorbic acid during rat gestation.

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.

Ascorbic acid in intestinal tissues.

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.

Decreased levels of ascorbic acid in lung following exposure to oxone.

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.

Maturity of fetal lungs tested by production of stable microbubbles in amniotic fluid.

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.

Factors influencing lipoprotein lipase activity in choline deficiency.

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.

The effect of ascorbic acid on infection chick-embryo ciliated tracheal organ cultures by coronavirus.

Chick embryo tracheal organ cultures showed increased resistance to infection by a coronavirus after exposure to ascorbate, while chick respiratory epithelium and allantois-on-shell preparations showed no increase in resistance to infection by an influenza virus or a paramyxovirus.

Alterations in lipid metabolism produced by ethyl trichloracetate.

Rats maintained on a choline deficient diet and treated with subcutaneous doses of ethyl trichloracetate responded by increasing plasma beta-lipoprotein and plasma triglyceride levels while excess triglyceride was being removed from the liver. There was a transient depression in plasma phospholipid at the beginning of the treatment. Continued administration of ethyl trichloracetate raised plasma triglyceride in choline depleted rats and raised hepatic phospholipid concentration in both choline deficient and supplemented rats. It is suggested that the lipotropic action of ethyl trichloracetate occurs through hepatic triglyceride being removed by the altered plasma lipids and not by inhibition of hepatic triglyceride synthesis.

Extracellular ascorbic acid in lung.

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.

Pulmonary edema and ascorbic acid loss.

Loss of ascorbic acid from lung and pulmonary edema were produced in mice by intravenous injection of either adrenaline or noradrenaline (5 mumol/kg). While adrenalectomy performed before noradrenaline administration reduced the degree of pulmonary edema, a prior dose of hexamethonium accentuated this effect. Given alone, hexamethonium caused both loss of ascorbic acid and pulmonary edema. The results show that although endogenous catecholamines can potentiate the pulmonary edema produced by either adrenaline or noradrenaline, they play no specific role in the ascorbic acid loss. The evidence suggests that lung ascorbic acid levels are decreased following the development of pulmonary edema, irrespective of how it was caused.

Transport of ascorbic acid in perfused rat lung.

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.