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PubMed1984

Effects of ascorbic acid deficiency on methyl mercury dicyandiamide toxicosis in guinea pigs.

Methylmercury dicyandiamide (MMD) when given intraperitoneally at a dosage of 4 mg/kg of body weight at weekly intervals for 3 weeks resulted in death of guinea pigs fed an ascorbic acid deficient diet. Controls fed an ascorbic acid deficient diet survived during this period as did guinea pigs given MMD and fed an ascorbic acid adequate diet. In a second experiment, guinea pigs fed an ascorbic acid deficient diet containing 22 ppm of MMD died within 26 days and had severe hemorrhagic and ulcerative gastroenteritis and coagulative necrosis of the liver. Ascorbic acid deficient controls died at 34 days. The MMD-containing ascorbic acid adequate diet killed guinea pigs in 150 days. Guinea pigs fed an ascorbic acid deficient diet with 44 ppm of MMD died within 20 days with acute neurologic signs. Pathologic changes were mostly in the gray matter. Guinea pigs fed MMD and a diet with adequate ascorbic acid survived for 38 days whereas the ascorbic acid deficient controls survived for 47 days. Results indicate that ascorbic acid deficiency can be a factor in the location and severity of clinical signs and lesions of MMD.

Animals↗
PubMed1975

The effects of ascorbic acid deficiency on calcium and collagen metabolism in cultured fetal rat bones.

The effects of ascorbic acid deficiency on growth and calcification of bone were studied in whole 18-day fetal rat radii and ulnae cultured in a chemically defined medium. Ascorbic acid deficiency decreased the formation of labeled hydroxyporline from labeled proline in both bone shafts and cartilage ends while incorporation of tryptophan was maintained. Dry weights and collagen content of bone and cartilage were decreased, but calcification was not affected. The optimun initial concentration of ascorbic acid for collagen synthesis was 200 mug/ml. The effect of ascorbic acid was not antagonized by glucoascorbic acid or replaced by dithiothreitol. Decreased collagen synthesis in ascorbic acid deficiency could not be ascribed to loss of available peptidyl proline hydorxylase. Formation of underhydroxylated collagen and its release into the medium accounted for much of the decrease in hydroxylated collagen in ascorbic acid deficient bones. Nevertheless, the total newly synthesized collagen, as measured by collagenase digestion, was still decreased. Similar effects were exerted by alpha, alpha'-dipyridyl which also inhibited general protein synthesis. Ascorbic acid did not stimulate proline incorporation into collagen in the presence of alpha, alpha'-dipyridyl.

Animals↗
PubMed1996

Ascorbic acid deficiency reduces hepatic apolipoprotein A-I mRNA in scurvy-prone ODS rats.

Using the ODS rat (genotype od/od) as a model, we investigated the effect of ascorbic acid deficiency on the expression of the apolipoprotein A-I gene. Male ODS rats (7 wk old, body weight approximately 140 g) were fed a basal diet containing ascorbic acid (300 mg/kg) or a diet without ascorbic acid for 14 d. Ascorbic acid deficiency lowered the serum apolipoprotein A-I concentration. The apolipoprotein A-I mRNA level in the liver of ascorbic acid-deficient rats was lowered to about 40% (P < 0.05) of that of control rats fed sufficient ascorbic acid. The mRNA level in jejunum was not affected by ascorbic acid deficiency. Ascorbic acid deficiency did not change the transcriptional rate of the hepatic apolipoprotein A-I gene, suggesting that post-transcriptional regulation was involved in lowering the mRNA level. The low level of hepatic apolipoprotein A-I mRNA was restored to the control level within 3 d after the administration of sufficient ascorbic acid. These data indicate that ascorbic acid deficiency lowers serum apolipoprotein A-I concentration through lowering its mRNA level and subsequent depression of its synthesis in liver.

Animals↗
PubMed1976

Ascorbic acid deficiency in liver disease.

Leucocyte ascorbic acid (LAA) levels were measured in 138 patients with liver disease. Significantly reduced levels were found in 37 patients with alcoholic liver disease (P less than 0-01) and 25 patients with primary biliary cirrhosis (P less than 0-05). In the primary biliary cirrhosis patients, cholestyramine therapy was associated with significantly lower levels of the vitamin (P less than 0-05). Liver ascorbic acid measured in Menghini needle biopsies in 20 patients was significantly correlated with LAA (r=0-807, P less than 0-001). No significant correlation was found between LAA and haematological indices, conventional liver function tests, or cholesterol levels in any group of patients. Patients with LAA levels below 100 nM/10(8) WBC had significantly higher antipyrine half-lives (mean=28-3 h) than patients with LAA levels above this level (mean=18-6 h) (P less than 0-05). Delayed drug metabolism related to low LAA should be considered when drugs metabolised by the liver are prescribed for patients with alcoholic liver disease or primary biliary cirrhosis.

Alcoholism↗
PubMed1970

Ascorbic acid deficiency and pituitary adrenocortical activity in the guinea-pig.

1. Guinea-pigs kept on a diet deficient in ascorbic acid lost weight and became moribund in about 24 days.2. The adrenal ascorbic acid concentration fell rapidly during the first 2 weeks, and the plasma corticosteroid concentration and 17-oxogenic steroid excretion rose sharply in the third week of ascorbic acid deficiency.3. Both histamine and corticotrophin increased the plasma corticosteroid concentration when injected during the second week but failed to change the pre-existing high concentration of the steroid in the third week of ascorbic acid deficiency.4. The observations confirm that ascorbic acid is not involved in corticoidogenesis and that scurvy is a severe stress which increases adrenocortical activity to such an extent that the rate of synthesis of corticosteroids is incapable of matching the rate of their release.

Adrenal Cortex Hormones↗
PubMed1977

Glycolytic, hexose monophosphate shunt and bactericidal activities of leukocytes in ascorbic acid deficient guinea pigs.

It is well known that glycolytic and hexose monophosphate shunt activities of leukocytes increase during phagocytosis. The relevance of these metabolic changes to particle uptake and particle destruction is also well established. In the present study, these metabolic activities were studied to assess the phagocytic function of leukocytes isolated from ascorbic acid deficient guinea pigs. Glycolytic activity which provides the necessary energy for particle uptake was found to be decreased in both resting and phagocytizing leukocytes for ascorbic acid deficient guinea pigs. The direct oxidation of glucose through the hexose monophosphate shunt (HMS) was stimulated to a significantly lesser extent during phagocytosis in ascorbic acid deficient leukocytes. There was a progressive decline in phagocytosis induced shunt activity of leukocytes as the deficiency of ascorbic acid progressed. These findings show that particle uptake (as indicated by glycolytic activity) as well as particle destruction (as indicated by HMS activity) by leukocytes are impaired in ascorbic acid deficiency. Bactericidal capacity of leukocytes against Escherichia coli was also found to be low in ascorbic acid deficient guinea pigs as compared to those in the pair-fed control group.

Adrenal Glands↗
PubMed1975

Cerebral monoamine metabolism in guinea-pigs with ascorbic acid deficiency.

Guinea-pigs kept on a diet deficient in vitamin C showed, after 3 weeks, a marked decrease of ascorbic acid in brain and blood leucocytes as well as of the activity of alkaline phosphatase in blood plasma. Pair-fed animals did not exhibit these changes. The alpha-methyl-p-tyrosine (alpha MpT)-induced diminution of noradrenaline in the hypothalamus and the rest of the brain was attenuated in pair-fed animals, but restored in guinea-pigs deficient in ascorbic acid. The cerebral noradrenaline content (without administration of alpha MpT) showed a decrease in both pair-fed and ascorbic acid deficient animals. The noradrenaline of the heart exhibited a similar tendency. The alpha MpT-induced dopamine decrease in the striatum of ascorbic acid deficient animals was attenuated and the dopamine content (without alpha MpT administration) decreased. Pair-fed animals showed a similar tendency. The striatal concentration of homovanillic acid (HVA) was diminished in both pair-fed and ascorbic acid deficient guinea-pigs. The cerebral content of 5-hydroxyindoleacetic acid showed a decrease in pair-fed as well as in ascorbic acid deficient animals. It is concluded that ascorbic acid deficiency enhances the turnover of brain noradrenaline, whereas under-nutrition without ascorbic acid deficiency (pair-feeding) diminishes the turnover of cerebral noradrenaline, 5-hydroxytryptamine and striatal dopamine.

Alkaline Phosphatase↗
PubMed1998

Ascorbic acid deficiency changes hepatic gene expression of acute phase proteins in scurvy-prone ODS rats.

The ODS rat (genotype od/od), which has a hereditary defect in ascorbic acid biosynthesis, was used to investigate the effects of ascorbic acid deficiency on the hepatic gene expression of both the positive acute phase proteins, haptoglobin and alpha1-acid glycoprotein, and the negative acute phase proteins, apolipoprotein A-I and albumin. Male ODS rats (6 wk old, body weight approximately 140 g) were fed a basal diet containing ascorbic acid (300 mg/kg diet) or a diet without ascorbic acid for 14 d. Ascorbic acid deficiency significantly elevated the serum concentration of haptoglobin and significantly lowered those of apolipoprotein A-I and albumin. The hepatic mRNA levels of haptoglobin and alpha1-acid glycoprotein in the ascorbic acid-deficient rats were significantly elevated on d 12, and reached 260 (P < 0.05) and 360% (P < 0.01) of respective values in the control rats on d 14. On the contrary, the hepatic mRNA levels of apolipoprotein A-I and albumin in the ascorbic acid-deficient rats were lowered to 68 (P < 0.01) and 71% (P < 0.05) of respective values in the control rats on d 14. Although ascorbic acid deficiency significantly elevated the serum corticosterone concentration on d 14, the changes in mRNA levels of haptoglobin, alpha1-acid glycoprotein, apolipoprotein A-I and albumin due to ascorbic acid deficiency were not affected by adrenalectomy, as assessed in a separate experiment. The serum concentration of interleukin-6, an inflammatory cytokine that stimulates gene expression of some acute phase proteins, was significantly higher in the ascorbic acid-deficient rats on d 14 than in the control rats. These results suggest that ascorbic acid deficiency causes physiologic changes similar to those that occur in the acute phase response.

Acute-Phase Proteins↗
PubMedDate not supplied

Short-term ascorbic acid deficiency induced oxidative stress in the retinas of young Guinea pigs.

We examined whether short-term ascorbic acid deficiency induces oxidative stress in the retinas of young guinea pigs. Four-week-old guinea pigs were given a scorbutic diet (20 g/animal/day) with and without adequate ascorbic acid (400 mg/animal/day) in drinking water for 3 weeks. The serum concentrations of the reduced form of ascorbic acid and the oxidized form of ascorbic acid in the deficient group were 14.1 and 4.1%, respectively, of those in the adequate group. The retinal contents of the reduced form of ascorbic acid and the oxidized form of ascorbic acid in the deficient group were 6.4 and 27.3%, respectively, of those in the adequate group. The retinal content of thiobarbituric acid-reactive substances, an index of lipid peroxidation, was 1.9-fold higher in the deficient group than in the adequate group. Retinal reduced glutathione and vitamin E contents in the deficient group were 70.1 and 69.4%, respectively, of those in the adequate group. This ascorbic acid deficiency did not affect serum thiobarbituric acid-reactive substances and reduced glutathione concentrations but increased serum vitamin E concentration. These results indicate that short-term ascorbic acid deficiency induces oxidative stress in the retinas of young guinea pigs without disrupting systemic antioxidant status.

Animals↗
PubMedDate not supplied

Dental chairside test for the diagnosis of ascorbic acid deficiency.

There is a strong correlation between gingival inflammation and clinical and sub-clinical ascorbic acid deficiency. This has created a demand for a handy diagnostic test to detect the ascorbic acid deficiency. The aim of this work was to find out the efficacy of one such test, i.e. the modified Lingual Ascorbic Acid Test (LAAT). To find out the significance of ths LAAT, it was compared with plasma ascorbic acid levels and then confirmed statistically. Our findings suggest that with this simple, reliable and inexpensive method, the dental practitioners can conveniently assess the ascorbic acid status of their patients.

2,6-Dichloroindophenol↗
PubMed1980

Effects of chronic ascorbic acid deficiency on guinea pig lysosomal hydrolase activities.

Previously we have observed increased specific activities of several lysosomal hydrolases in scorbutic guinea pigs and thus the specificity of this effect was examined in guinea pigs marginally deficient in ascorbic acid (AA). Guinea pigs were fed an AA-deficient diet for 2 weeks to deplete body AA pools and then fed a stock diet containing 0.5 mg AA/g diet or the deficient diet plus oral administration of 10 mg AA/day, 1 mg AA/100 g body weight or 0.5 mg AA/100 g body weight each day. Animal were periodically killed during the 12-week experiment and lysosomes isolated from individual livers and analyzed. Serum and brain AA declined when AA was withheld, returned to normal when the stock diet or 10 mg AA were fed but remained at low levels on administation of 1.0 mg or 0.5 mg AA/100 g body weight. Brain norepinephrine followed a similar pattern to brain AA and was opposite to the pattern observed for dopamine. In guinea pigs receiving 1 mg AA/100 g body weight, amine concentrations slowly returned to normal after 8 weeks. Serum hexosaminidase and lysosomal cathepsins A and B were unchanged during the experiment, whereas lysosomal hexosaminidase and acid phosphatase were significantly higher when the experiment was terminated.

Acid Phosphatase↗
PubMedDate not supplied

Hyperlipidemia in guinea-pigs induced by ascorbic acid deficiency. The effects of cholesterol, DL-ethionine and aflatoxin.

A study was made of hyperlipidemia caused by ascorbic acid deficiency and of the effects of cholesterol, DL-ethionine and aflatoxin on plasma lipoprotein fractions of normal and scorbutic guinea pigs. The plasma lipoprotein fractions of scorbutic animals showed a significantly higher level of pre-beta-lipoprotein and a lower level of alpha-lipoprotein. By adding DL-ethionine to the control group, the pre-beta-lipoprotein fraction was remarkably elevated and by adding cholesterol, the alpha-lipoprotein level was greatly reduced and the beta-lipoprotein level was increased. Addition of aflatoxin to the control diet resulted in a rather high concentration of alpha-lipoprotein and a low pre-beta-lipoprotein level. High concentrations of triglyceride and phospholipid were seen in the plasma of scorbutic guinea pigs. The probable cause of hyperlipidemia induced by ascorbic acid deficiency is partly retarded degradation of cholesterol resulting from impaired 7 alpha-hydroxylation, and partly that ascorbic acid deficiency may affect other enzyme systems that control triglyceride of phospholipid metabolism, such as lipoprotein lipase activity, or synthesis or breakdown of these enzymes.

Aflatoxins↗
PubMedDate not supplied

Ascorbic acid deficiency and hepatic UDP-glucuronyltransferase.

The effect of dietary ascorbic acid on hepatic microsomal UDP-glucuronyltransferase (UDPGT) activity towards p-aminophenol, bilirubin, and acetaminophen was investigated. Ascorbate deficiency produced a 33% reduction in the specific activity of UDPGT towards p-aminophenol, whereas there was no difference between microsomes from ascorbate-deficient and supplemented guinea pigs in the activity towards bilirubin and acetaminophen. This suggests that the effect of the vitamin is on a specific isozyme. This reduction was correlated with the reduced quantity of hepatic microsomal cytochrome P-450, which has been previously reported for ascorbate-deficient guinea pigs. No difference was found in the apparent affinity for the substrate, p-aminophenol, or the cofactor, UDP-glucuronic acid. Differences in microsomal UDPGT activity towards p-aminophenol occurred between the two groups with membrane-perturbing processes such as sonication and Triton X-100. Sonication and magnesium chloride were found to increase activity 329% in ascorbate-supplemented animals and 138% in the ascorbate-deficient group. The addition of ascorbate acid in vitro, or its analog d-isoascorbic acid, could protect against the detrimental effects of excess substrate by maintaining a linear enzymatic rate over a 30-min time period; there was no significant effect on the initial rate of hepatic microsomal UDPGT activity in the ascorbate-supplemented animals whereas there was a significant increase in the ascorbate-deficient group. Glutathione was as effective as ascorbic acid in protecting against the detrimental effects of excess substrate whereas cysteine and dimethyltetrapteridine were only partially effective. Ascorbyl-2-sulfate and alpha-tocopherol had no significant effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗
PubMed1988

The effect of ascorbic acid deficiency on leukocyte phagocytosis and killing of actinomyces viscosus.

The ascorbic acid content of guinea pig leukocytes is reduced by a factor of 16:1 between normal and scorbutic guinea pigs. Ascorbic acid deficiencies do not appear to affect phagocytic activity but do change leukocyte morphology. A deficiency of this vitamin appears to significantly interfere with the in vitro bactericidal effectiveness of circulating leukocytes against ingested, cell-associated, and extracellular bacterial cells of the oral pathogen, Actinomyces viscosus. Leukocytes from scorbutic guinea pigs killed 13% of ingested and cell-associated Actinomyces viscosus compared to 83% killed by normal leukocytes by both acridine orange staining and viable count. Degranulation resulted in extracellular killing in normal but not scorbutic leukocytes. This decreased bactericidal activity can be reversed by adding supplements of the vitamin to the diet of scorbutic animals. Chemotactic responses were much lower in vivo and absent in vitro in scorbutic leukocytes. The acridine orange staining technique is an excellent indicator of leukocyte health. This study supports the important role for ascorbic acid in leukocyte function and also discusses its probable protective and bactericidal activities related to oral pathogens.

Actinomyces↗
PubMed1986

Ascorbic acid deficiency and the flavin-containing monooxygenase.

Activity of the flavin-containing monooxygenase (FMO) was reduced significantly in ascorbic acid deficient guinea pigs. Reduction in oxidation of dimethylaniline (DMA) and of thiobenzamide was associated with a decrease in the activity of the FMO. In both ascorbate supplemented and deficient guinea pig hepatic 12,000 g supernatant fractions, SKF-525A and n-octylamine did not inhibit DMA N-oxidation. Phenobarbital pretreatment did not increase the rate of N-oxidation of DMA. In addition, hepatic supernatant fractions thermally treated at 50 degree were unable to N-oxidize DMA, but 80% of the cytochrome P-450 activity was retained. Also, N-oxidation of DMA was reduced by 53% at pH 7.0, while oxidation of cytochrome P-450 specific substrates was inhibited by only 19%. Kinetic studies of DMA N-oxidation indicate no significant change in the apparent Km in ascorbate supplemented or deficient animals. The in vitro addition of ascorbic acid had no effect on the activity of the FMO. The toxicological implications of the reduction in FMO activity in ascorbic acid deficiency are discussed.

Aminopyrine N-Demethylase↗
PubMed1986

A comparative study on the effects of ascorbic acid deficiency and supplementation on endurance and mitochondrial oxidative capacities in various tissues of the guinea pig.

The aim of this study was to ascertain the effects of ascorbic acid deficiency and supplementation on endurance and mitochondrial oxidative capacities in various tissues of guinea pigs. Endurance capacity was significantly reduced by ascorbic acid deficiency and supplementation. Oxidative capacities were reduced in heart, liver and brown adipose tissue but it seems as if skeletal muscle is protected against ascorbic acid deficiency and supplementation-induced oxidative damage. Skeletal muscle and liver but not heart appear to be susceptible to exercise-induced oxidative damage. To a certain extent oxidative capacities could be related to the glutathione status in the various tissues.

Animals↗