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PubMed1981

Abruptio placentae.

Analysis of blood samples from pregnant women has shown that the mean histamine level starts to rise when the plasma ascorbic acid level falls below 1.0 mg/100 ml; it is doubled when the ascorbate level falls to 0.5 mg/100 ml and quadrupled when it falls below 0.2 mg/100 ml. The incidence of abruptio placentae was found to be seven out of 355 (or 2.0%) in women who had plasma ascorbic acid levels above 0.4 mg/100 ml and six out of 31 (19.4%) in women with plasma ascorbate levels below 0.4 mg/100 ml. This difference is highly significant. It is suggested that ascorbic acid deficiency and histamine excess play leading roles in the etiology of abruptio placentae.

Abruptio Placentae↗
PubMed1996

Scurvy results in decreased collagen synthesis and bone density in the guinea pig animal model.

The effect of severe ascorbic acid deficiency on bone remodeling and collagen synthesis was evaluated in a 21 day experiment, using the scorbutic guinea pig model. Animals (n = 6-7/group) were assigned to one of three groups: scorbutic, pair-fed ascorbic acid-replete, or ad libitum ascorbic acid-replete groups. After 2 weeks, scorbutic animals started voluntarily decreasing food intake and losing weight. By day 19-21, at which time bone and tissue samples were collected and analyzed, scorbutic animals decreased food intake to 46% of usual and lost 9% body weight. Serum 25OHD3, 1,25(OH)2D3, calcium, and albumin were significantly lower (p < 0.05) in the scorbutic animals than in the other groups. Bone mineral density and bone mineral content of the proximal and central femur were significantly lower in the scorbutic group than in the other groups (p < 0.05). Morphometric analysis of tibia indicated significantly lower bone volume, fewer and thinner trabeculae, and a thinner growth plate in the scorbutic group, compared to the pair-fed and ad libitum groups (p < 0.05). Osteoclast surface was about 60% higher in the scorbutic group than in the pair-fed and ad libitum control groups (0.05 < p < 0.10). Mechanical strength of the femur and lumbar vertebral body tended to be lower when bone mass was altered in the same group. Collagen synthesis of articular cartilage and tendons was lower in the scorbutic group than in the pair-fed or ad libitum groups (p < 0.05). In conclusion, scurvy but not food restriction, per se, results in alterations in bone mass and tissue collagen synthesis.

Analysis of Variance↗
PubMed1990

Effect of vitamin C depletion on serum cholesterol and lipoprotein levels in ODS (od/od) rats unable to synthesize ascorbic acid.

The effect of ascorbic acid deficiency on serum and liver cholesterol, phospholipid and triglyceride levels, serum lipoprotein levels and serum lipoprotein cholesterol levels were examined in male rats with a hereditary defect in ascorbic acid synthesis (ODS rats). Male homozygotes (od/od) and male rats of their parent strain (+/+) were each divided into four treatment groups and were fed vitamin C-deficient or vitamin C-replete diets containing either 0 or 0.5% cholesterol. During the 3-wk feeding-period the ODS (od/od) rats fed the vitamin C-deficient diet gradually decreased food intake, resulting in a lower body weight than that of od/od rats given ascorbic acid. The serum cholesterol level was significantly higher in the vitamin C-deficient od/od rats fed the cholesterol diet, and it tended to be higher in those fed the control (0% cholesterol) diet, whereas the liver lipid levels remained unchanged relative to those in od/od rats fed the vitamin C-replete diet. The serum very low density lipoprotein and high density lipoprotein (HDL) cholesterol levels were lower in od/od rats fed the vitamin C-deficient diet without cholesterol, but intermediate density lipoprotein and low density lipoprotein cholesterol levels were markedly higher in the vitamin C-deficient od/od rats than in od/od rats given ascorbic acid, regardless of dietary cholesterol level. The ratio of HDL2 cholesterol to HDL3 cholesterol was also higher in the vitamin C-deficient od/od rats. The parent strain of the od/od rats (+/+) showed no change due to vitamin C deficiency. These results suggest that vitamin C deficiency delays low density lipoprotein metabolism and produces hypercholesterolemia in male od/od rats.

Animals↗
PubMed1992

Glutathione deficiency increases hepatic ascorbic acid synthesis in adult mice.

Glutathione deficiency, induced in adult mice by administering buthionine sulfoximine (an inhibitor of glutathione synthesis), led to a rapid and substantial increase in ascorbate in the liver. This effect was apparent 2-4 hr after giving the inhibitor; subsequently, the level of ascorbate decreased and that of dehydroascorbate increased markedly, supporting the conclusion that glutathione functions physiologically to keep ascorbate in its reduced form. In kidney and lung also, ascorbate levels decreased, and dehydroascorbate increased. Increased synthesis of ascorbate in glutathione-deficient adult mice seems to protect against tissue damage. In contrast, newborn rats, which (like guinea pigs and humans) apparently do not synthesize ascorbate, suffer severe damage to liver and other organs; previous studies showed that administration of ascorbate prevents such tissue damage. The findings support the view that the antioxidant actions of glutathione and ascorbate are closely linked and involve a mechanism in which decrease of the glutathione level, perhaps associated with an oxidative event, stimulates ascorbate synthesis.

Animals↗
PubMed1975

Ascorbic acid requirements and metabolism in relation to organochlorine pesticides.

Those organochlorine pesticides which possess both high lipoid solubility and high resistance to biodegradation are prone to accumulation in animal tissues and produce relatively long-term effects as toxicants. Such compounds, typified by DDT, Dieldrin, and Lindane, are profound inducers of hepatic microsomal enzymes, including parts of the glucuronic acid and ascorbic acid biosynthetic pathways. Consequently, administering such pesticides to rats in accompanied by enhanced formation and excretion of D-glucuronic acid and L-ascorbic acid, or D-glucaric acid in the case of guinea pigs. Secondarily, the efficiency in biodegrading the pesticides is reduced in ascorbic-acid-deficient guinea pigs with correspondingly greater residue accumulation in tissue. This would aggravate chronic toxic effects of the compounds. Finally, the capacity of the liver to adapt to the presence of such toxicants through enhanced microsomal enzymatic levels appears to be sensitive to its ascorbate status. Impaired enzyme induction is apparent quite early during ascorbic acid depletion in guinea pigs. The enhanced turnover of ascorbate produced by such pesticides, the poor enzymatic adaptation to them during ascorbate depletion and the dependency of the oxidase system upon adequate ascorbate, all point to the central significance of ascorbate status in the liver, and possibly other tissues, as a determinant of their chronic toxicity.

Animals↗
PubMed1979

Subcellular ascorbic acid in scorbutic guinea pig brain.

In scorbutic guinea pigs fed an ascorbic acid-deficient diet for 18 days, the ascorbic acid contents of the liver and plasma were less than 4% those of the control animals, while the content in the brain was about one-third that of the controls. In normal animals, the concentration of ascrobic acid was highest (7.55 +/- 1.46 micrograms of ascorbic acid/mg protein) in the S3 fraction and was also fairly high (5.37 +/- 0.91) in the P2p fraction (cytoplasm of nerve terminals). During ascorbic acid deficiency, the contents in the P2p and microsome fractions decreased slightly faster than those in other fractions. Even after 18 days' deficiency, no significant change was found in the acetylcholine content of the brain.

Acetylcholine↗
PubMed1986

Ascorbic acid requirement for the induction of microsomal drug-metabolizing enzymes in a rat mutant unable to synthesize ascorbic acid.

We investigated the requirement of ascorbic acid for the induction by polychlorinated biphenyls (PCB) of hepatic drug-metabolizing enzymes in ODS-od/od rat (OD rat) which is a rat mutant unable to synthesize ascorbic acid. ODS- +/+ rats (+/+ rat), which can synthesize ascorbic acid, were used as controls. In OD rats, the dietary requirement of ascorbic acid to maintain normal growth and prevent any signs of scurvy is about 300 mg of ascorbic acid per kilogram diet. In this study, dietary levels of ascorbic acid tested were 0, 50, 300, 1000 and 3000 mg ascorbic acid per kilogram diet with or without 200 mg of PCB per kilogram diet. Feeding PCB did not affect growth in rats of either genotype. When statistical analysis was done within groups fed diets without PCB, ascorbic acid deficiency caused significant decreases in body weight gain, hepatic activities of drug-metabolizing enzymes and level of hepatic cytochrome P-450. When OD rats were fed a diet without PCB, the supplementation of about 300 mg ascorbic per kilogram diet was sufficient to maintain normal activities of hepatic aminopyrine N-demethylase, aniline hydroxylase, cytochrome c reductase and reduction of cytochrome P-450 and a normal level of hepatic cytochrome P-450. However, when OD rats were fed a diet supplemented with 200 mg PCB per kilogram of diet, significantly higher activities of hepatic aminopyrine N-demethylase and aniline hydroxylase and significantly higher level of hepatic cytochrome P-450 were observed in OD rats fed a diet supplemented with 1000 mg or 3000 mg ascorbic acid per kilogram of diet than in rats fed a diet supplemented with 300 mg of ascorbic acid. It is concluded that the dietary requirement of ascorbic acid is increased severalfold by the administration of xenobiotics, such as PCB, for the maximum induction of hepatic drug metabolism.

Aminopyrine N-Demethylase↗
PubMed1975

Changes in ascorbic acid metabolism of the offspring following high maternal intake of this vitamin in the pregnant guinea pig.

Guinea pigs were fed a control (0.05%) or a high (0.5%) ascorbic acid diet during the last half of pregnancy. When the pups were tested at 5 and 10 days of life the ones from the high-ascorbic-acid group demonstrated a marked increase in 14CO2 excretion, compared with the control pups, following an intraperitoneal injection of 14C-labeled ascorbic acid. When the animals were weaned to an ascorbic-acid-deficient diet signs of scurvy appeared earlier in the pups from the high vitamin C group and their survival was shorter. When excretion of labeled CO2 in both groups was correlated with the day of onset of scurvy signs, a linear correlation was found between these two parameters, suggesting that the earlier appearance of signs of scurvy in the experimental pups is secondary to an increased rate of ascorbic acid catabolism.

Animals↗
PubMed1978

Ascorbic acid and cytochrome P-450.

Liver microsomal cytochrome P-450 is significantly reduced in ascorbic acid-deficient guinea pigs and studies are presented on the biochemical basis for this effect. The activities of the key enzymes involved in heme synthesis, delta-aminolevulinic acid (ALA) synthetase. ALA dehydratase and ferrochelatase, were not significantly reduced in livers from ascorbic acid-deficient animals. In addition, there was no significant difference in the amount of "mitochondrial heme" in normal and ascorbic acid-deficient livers. However, ascorbic acid deficiency did affect induction with diethyl-1,4-dihydro-2,4,6-trimethylpyridine-3,5-dicarboxylate; a 6-fold increase in ALA synthetase activity occurred in liver homogenates prepared from normal animals in contrast to no significant increase in homogenates prepared from ascorbic acid-deficient animals. Multiple forms of cytochrome P-450 exist in guinea-pig microsomes as has been demonstrated in microsomes from other species. Separation of 44,000 to 60,000 dalton polypeptides (molecular weight region for the various forms of cytochrome P-450) by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate revealed quantitative differences in the polypeptides from normal and ascorbic acid-deficient microsomes. Ascorbic acid-deficient microsomes consistently demonstrated reductions in three polypeptide bands (molecular weight 44,000, 52,000 and 57,000) and increases in two polypeptide bands (54,000 and 55,000) compared with normal microsomes. Evidence that these polypeptides are cytochrome P-450 was obtained from heme staining with tetramethylbenzidine and from induction studies with phenobarbital and 3-methylcholanthrene. The results indicate that ascorbic acid deficiency does not affect the availability of heme for cytochrome P-450 synthesis and the effect of ascorbic acid may be on the apoprotein moiety of cytochrome P-450.

Animals↗
PubMed1987

[Effect of ascorbic acid on 25-hydroxyvitamin D3 metabolism in the kidneys and 1,25-dihydroxyvitamin D3 reception in the small intestine mucosa of guinea pigs].

Ascorbic acid deficiency in vitamin D-supplied guinea pigs caused a moderate decrease of Ca in the blood and osseous tissue, a 1.5-fold decrease of 2.5-hydroxyvitamin D (25-OH D) in blood serum, a 2-fold decrease of the 25-OH D 1-hydroxylase activity in kidneys and a 1.6-fold increase of the 24-hydroxylase activity. The concentration of 1.25-dihydroxyvitamin D3 (1.25-(OH)2D3) nuclear receptors in small intestinal mucosa diminished by 20-30%; in this case the percentage of occupied hormone receptors reduced from 11.8 to 8.6%. The affinity of receptors for 1.25-(OH)2D3 did not change thereby (Kd = 0.25-0.26 nM; Kd2 = 0.06-0.10 nM). At the same time the value of cooperativity coefficient showed a decrease-from 1.7 to 1.4, which was accompanied by a reduction of the maximum capacity of receptors (1.2-1.5-fold). Vitamin C depletion augmented the manifestation of vitamin D deficiency in guinea pigs and impeded their correction after administration of cholecalciferol. This markedly retarded the restoration of the 25-OH D level in the blood as well as the number of occupied and unoccupied nuclear receptors for 1.25-(OH)2D3. The experimental results illustrate the effects of ascorbic acid on the vitamin D hormonal system function, which is manifested both at the level of 1.25-(OH)2D3 synthesis in the kidneys and of its receptor binding in target tissues.

Animals↗
PubMed1979

Scurvy and vitamin C deficiency in Crohn's disease.

A case of scurvy presenting in a patient with Crohn's disease is reported. A normal response to replacement therapy is seen. Vitamin C (ascorbic acid) deficiency was found in 7 out of 10 patients with clinically quiescent Crohn's disease, 4 of whom had an adequate oral intake of vitamin C. There was no significant difference in oral intake between patients with Crohn's disease and matched controls but there was a significant difference (P less than 0.001) in leucocyte ascorbic acid levels. It is recommended that patients with Crohn's disease be screened for vitamin C deficiency and receive prophylactic vitamin C supplements daily.

Adult↗
PubMed1984

Wide variations of plasma triglyceride concentrations in guinea pigs.

Guinea pigs have varying plasma triglyceride concentrations ranging from 28 to 1392 mg/dl, with relatively uniform plasma cholesterol and phospholipid levels. To understand why the animals exhibit such wide variations of plasma triglyceride concentrations, we have explored the triglyceride hydrolyzing system by measuring tissue lipoprotein lipase activities and plasma activator for the enzyme. Lipoprotein lipase activities of epididymal adipose tissue of these animals were 759 +/- 117 (mean +/- SE) n moles FFA X min-1 X g wet tissue-1, markedly low compared with those of rats. There were no relationships between plasma triglyceride concentrations and tissue lipase activities. Plasma activator for lipoprotein lipase was lacking in this animal. Guinea pigs with ascorbic acid deficiency for 2 weeks also showed marked variations of plasma triglyceride concentrations, without any changes in tissue lipoprotein lipase activities. Low adipose tissue lipoprotein lipase activities with deficient plasma activator for the enzyme suggest that the lipoprotein lipase-mediated triglyceride degradation could be impaired in this animal, and this may account for the marked variation of plasma triglyceride concentrations.

Adipose Tissue↗
PubMed1975

Ascorbic acid in cholesterol and bile acid metabolism.

Latent chronic ascorbic acid deficiency provokes in guinea pigs a metabolic disorder in the liver, causing an impaired cholesterol transformation to its principal catabolic product, bile acids. This metabolic disorder induces hypercholesterolemia and accumulation of cholesterol in the liver and slows the release of cholesterol from the circulation. Ascorbic acid probably intervenes into the biosynthesis of bile acids at the stage of 7 alpha-hydroxylation of the cholesterol nucleus. High doses of ascorbic acid significantly stimulate cholesterol transformation to bile acids in guinea pigs and decrease plasma cholesterol concentration in humans.

Aged↗
PubMed1979

Effect of chronic hypo and hypervitaminosis C on the brush border enzymes and the intestinal uptake of glucose and alanine.

Brush border sucrase and alkaline phosphatase activities are considerably enhanced in the intestine of ascorbic acid deficient guinea-pigs. Similar increase in the uptake of D-glucose and L-alanine also occurs in chronic vitamin C deficiency. However the permeability of D-glucose and L-alanine in the intestine of animals fed with large doses of vitamin C is severely depressed, with a reduction in the levels of sucrase and alkaline phosphatase activities.

Alanine↗
PubMed1990

Ascorbic acid effects on vitamin D hormone metabolism and binding in guinea pigs.

Ascorbic acid deficiency in guinea pigs fed a vitamin D-replete diet caused a moderate reduction of Ca level in serum and bone; 25-hydroxy-cholecalciferol or 25-hydroxyergocalciferol (25-OHD) serum concentration tended to decline; renal 25-hydroxycholecalciferol-1-hydroxylase (1-OHase) activity decreased 50%; and 25-hydroxycholecalciferol-24-hydroxylase activity increased 1.6-fold. Chromatin 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] receptor concentration in the intestinal mucosa decreased 20-30%, and the percentage of occupied receptors decreased from 12-15% to 6-8%. Receptor affinity for 1,25-(OH)2D3 did not change (Kd = 0.24-0.26 nmol/L, Kd2 = 0.06-0.10 nmol/L), but the cooperativity coefficient decreased from 1.7 to 1.4. Vitamin C deficiency potentiated effects of vitamin D deprivation and impaired a restorative action of vitamin D. It was accompanied by a marked delay in the elevation of 25-OHD concentration in serum as well as decreased 1-OHase activity in kidneys and a lower concentration of occupied 1,25-(OH)2D3 receptors in the intestinal mucosa. The data demonstrate a critical role for ascorbic acid in vitamin D metabolism and binding.

25-Hydroxyvitamin D 2↗
PubMed2001

Postischemic myocardial recovery and oxidative stress status of vitamin C deficient rat hearts.

OBJECTIVE: To investigate the role of vitamin C tissue content as a protective agent during myocardial ischemia-reperfusion injury, we have evaluated the postischemic functional recovery and free radical release of osteogenic disorder Shionogi (ODS) inherently scorbutic rat hearts and compared them to healthy Wistar rat hearts. METHODS: Isolated perfused hearts of ODS or Wistar rats underwent 30 min of a global total normothermic ischemia followed by 30 min of reperfusion. The lipid-soluble spin trap alpha-phenyl N-tert-butylnitrone (3 mM) was perfused upstream of the coronary bed. Functional parameters were recorded and samples of coronary effluents were analysed using electron spin resonance spectroscopy to characterise and quantify the amount of radical species released. RESULTS: From the onset of reperfusion, a large and long-lasting release of alkyl/alkoxyl radicals was detected, with a peak value of 29.0+/-3.2 nM obtained after 13 min, which was associated with a persistent contractile dysfunction. However, ODS rat hearts showed a higher myocardial recovery with lower left ventricular end diastolic pressure (44.34+/-1.74 vs. 55.03+/-1.57 mmHg for Wistar), higher recovery of rate pressure product (12.3+/-1.4 vs. 1.9+/-1.7x10(3) mmHg beats/min for Wistar) and shorter duration of contractile abnormalities during reperfusion (3.7+/-1.0 vs. 20.8+/-5.3 min for Wistar). Moreover, free radical release was identical in ODS rat hearts as compared to control Wistar rats. Ascorbic acid tissue content was significantly altered in ODS rats (31.9+/-3.3 vs. 591.0+/-54.9 mmol/g of tissue for Wistar) but superoxide dismutases, glutathion peroxidases and inducible heat shock protein 70 genes were up-regulated. CONCLUSIONS: This study shows that ascorbic-acid-deficient ODS rat hearts are more resistant to an ischemic insult than control Wistar rats, probably through the development of alternative protective defences, like the induction of heat shock proteins. These paradoxical results raise the question of the relative importance of each endogenous antioxidant in the cardiac resistance to ischemia-reperfusion injury.

Analysis of Variance↗