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At least 19 recordsLinked to original sources
PubMed1990

Ascorbic acid deficiency and hepatic UDP-glucuronyl transferase. Qualitative and quantitative differences.

The effect of dietary ascorbate on hepatic UDP glucuronyltransferase (UDPGT) appears to be selective in that only certain isozymes of UDPGT are jeopardized. In this study, ascorbic acid deficiency produced a 68% reduction in the specific activity of hepatic UDPGT towards p-nitrophenol. Earlier studies showed a reduction in UDPGT activity towards p-aminophenol in ascorbate-deficient guinea pigs, whereas bilirubin and acetaminophen glucuronidation were unaffected. Kinetic studies suggest that p-aminophenol and p-nitrophenol are metabolized by a single isozyme in that p-nitrophenol was found to be a competitive inhibitor of p-aminophenol glucuronidation. Both qualitative and quantitative studies on partially purified UDPGT from ascorbate-deficient and ascorbate-supplemented guinea pigs were carried out to investigate the biochemical role of the vitamin. Qualitative differences were observed in UDPGT from ascorbate-deficient animals and included an increased lability to: thermal inactivation; storage at 4 degrees; and purification with UDP-glucuronic acid agarose column chromatography. Furthermore, an analysis of the microsomal membrane showed a 14% increase in membrane fluidity in ascorbate deficiency. Ascorbic acid added in vitro could not reverse the increase in fluidity observed in ascorbate-deficient microsomal membranes; however, ascorbylpalmitate, a more lipophilic form of the vitamin, was effective. Palmitic acid had no effect on membrane fluidity in microsomes from either the ascorbate-supplemented or ascorbate-deficient animals. This increase in membrane fluidity could not be explained by differences in cholesterol, total phospholipid, or phosphatidylcholine content of hepatic microsomes. Furthermore, a quantitative reduction in UDPGT partially purified from ascorbate-deficient guinea pigs was indicated by a marked reduction in protein banding at 55,000 daltons when compared to UDPGT partially purified from ascorbate-supplemented animals.

Animals↗
PubMed1975

Changes relevant to catecholamine metabolism in liver and brain of ascorbic acid deficient guinea-pigs.

A chronic deficiency of ascorbic acid was induced in guinea pig. The level of catecholamines, copper and the activities of ceruplasmin, catecholamine oxidase, monoamineoxidase and acetylcholinesterase were checked in brain, liver and serum. Also the levels of ascorbic acid and glutathione were measured in the organs of ascorbic acid-deficient animals. The most important changes due to the ascorbic acid deficiency were observed in the brain were monoamineoxidase, catecholamineoxidase, acetylcholinesterase and the concentration of catecholamines were altered. The statement that brain is the organ most affected by the ascorbic acid deficiency is discussed.

Acetylcholinesterase↗
PubMed1977

Phagocytosis and leukocyte enzymes in ascorbic acid deficient guinea pigs.

Enzymes related to bactericidal activities of leukocytes were studied in ascorbic acid deficient guinea pig leukocytes. The activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase were not affected either under resting or phagocytizing conditions in ascorbic acid deficiency. Granule bound NADPH-oxidase activity of resting leukocytes also was not altered in ascorbic acid deficiency. However, the extent of stimulation in NADPH-oxidase activity under phagocytizing condition was found to be significantly lower in ascorbic acid deficient leukocytes than that in control leukocytes. Similary, the extent of release of acid phosphatase from lysosomes during phagocytosis was also low in ascorbic acid deficient leukocytes. Ascorbic acid deficiency did not influence the activities of glutathione reductase and myeloperoxidase of leukocytes. The significance of these enzyme changes is discussed in relation to the decreased phagocytic and bactericidal activities of leukocytes in ascorbic acid deficiency.

Acid Phosphatase↗
PubMed1991

Ascorbic acid deficiency elevates serum level of LDL-cholesterol in a rat mutant unable to synthesize ascorbic acid.

The effect of ascorbic acid deficiency on serum levels of high density lipoprotein- (HDL-), low density lipoprotein- (LDL-), very low density lipoprotein- (VLDL-) and chylomicron-cholesterol was examined in ODS-od/od rat (ODS rat), that is a rat mutant unable to synthesize ascorbic acid. Male ODS rats were fed an ascrobic acid-free diet for 20 days. In another two groups, the diet supplemented with 300 mg ascorbic acid/kg diet was fed either ad libitum (ad libitum control) or in pair-feeding (pair-fed control). Pair-fed rats received the same amount of diet as rats fed the ascorbic acid-free diet. Serum level of total cholesterol in the ad libitum control rats, ascorbic acid-deficient rats, and the pair-fed control rats were 100.1 +/- 8.4 mg/dl, 92.8 +/- 6.2 mg/dl and 72.2 +/- 4.8 mg/dl, respectively. The level of LDL-cholesterol in ascorbic acid-deficient rats was significantly higher than that in the ad libitum control or that in the pair-fed control. The level of HDL-cholesterol in ascorbic acid-deficient rats was lower than that in the ad libitum control, but was not changed as compared with that in the pair-fed control. Ascorbic acid deficiency did not affect serum level of VLDL-cholesterol or chylomicron-cholesterol as compared with those in the controls. These results demonstrate that ascorbic acid deficiency causes the elevation of serum level of LDL-cholesterol both in ad libitum feeding condition and pair feeding condition.

Animals↗
PubMed1992

Examination for lipid peroxidation in liver microsomes of guinea pigs as a causal factor in the decrease in the content of cytochrome P-450 due to ascorbic acid deficiency.

The content of cytochrome P-450 in liver microsomes from guinea pigs was decreased by ascorbic acid-deficiency. Since ascorbic acid is an antioxidant in vivo, the possible involvement of lipid peroxidation in this phenomenon was investigated. In fact, the level of lipid peroxides in liver homogenates of guinea pigs was increased by ascorbic acid deficiency. The level was significantly decreased when the animals were given tocopherol acetate (25 mg/kg/day, s.c.) with an ascorbic acid-free diet. The activities of aminopyrine N-demethylase, aniline hydroxylase, p-nitroanisole O-demethylase and 7-ethoxycoumarin O-deethylase, and the content of cytochrome P-450 spectrally determined did not restore the control level by the administration of tocopherol acetate to the ascorbic acid-deficient animals. Western blot analysis of liver microsomes with antibodies to rat P-450IA2 (P-448-H), P-450IIB1 (P-450b) and human P-450IIIA4 (P-450NF) showed that ascorbic acid-deficiency resulted in a decrease in the amount of cytochrome P-450 immunochemically related to P-450IA2, but not the amounts of the forms of cytochrome P-450 cross-reactive with antibodies to P-450IIB1 and P-450IIIA4. The reduced amounts of cytochrome P-450 cross-reactive with antibodies to rat P-450IA2 in liver microsomes of ascorbic acid-deficient animals remained unchanged even when lipid peroxidation was inhibited by tocopherol acetate, suggesting that there is a mechanism(s) other than lipid peroxidation involved in the reduction of amounts of cytochrome P-450 by ascorbic acid deficiency.

7-Alkoxycoumarin O-Dealkylase↗
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↗
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↗
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↗
PubMed1978

Effects of ascorbic acid deficiency on adrenal mitochondrial hydroxylations in guinea pigs.

The effect of ascorbic acid deficiency on adrenal hydroxylation of cholesterol and deoxycorticosterone in guinea pigs was studied by using mitochondria and isolated cytochrome P-450 fractions. The effects obtained were compared with the effects of long-term treatment with ACTH. Advanced scurvy as well as treatment with ACTH resulted in an increase in the weight of the adrenals, the total amount of cytochrome P-450, the cholesterol side-chain cleavage activity, the cortisol level in plasma, and the excretion of unconjugated cortisol in urine. Total 11beta- and 18-hydroxylation of deoxycorticosterone were not stimulated or were stimulated only to a small extent. It is suggested that the major effects observed in advanced scurvy are due to ACTH, the level of which was significantly increased, most probably as a consequence of the stress. In animals kept on a scorbutogenic diet for 2-4 weeks or, with a small dose of ascorbate added, for several weeks, changes were observed that could not be fully explained as effects of ACTH on normal adrenals. Although the plasma levels of ACTH and cortisol were increased only to a small extent and excretion of unconjugated cortisol in urine was unaffected, there was a significant increase in the total capacity of adrenal mitochondria to hydroxylate exogenous cholesterol. It is concluded that the level of ascorbate in the adrenals might be of some importance for the capacity to convert cholesterol into pregnenolone. The normal feed-back regulation is, however, intact in moderate ascorbate deficiency and the plasma level of cortisol is kept within normal limits.

Adrenal Glands↗
PubMed1977

The effects of ascorbic acid deficiency on collagen synthesis by mouse molar tooth germs in organ culture.

Second molar tooth germs from 2-day-old Swiss-Webster mice, grown in organ culture for 7 days in ascorbic-acid-deficient medium, synthesized about 65% as much protein (measured by incorporation of [14C]proline during a 24-h pulse) as did ascorbic-acid-supplemented controls. The newly synthesized proteins from ascorbic-acid-deficient cultures contained only about 7% of the hydroxyproline content of the controls. Collagenase digestion of the newly synthesized proteins showed that collagen comprised the same fraction of the total protein synthesized under both culture conditions. This result indicates that the ascorbate-deficient cultures made significant quantities of underhydroxylated collagen. Partial characterization of the collagen alpha chains on carboxymethyl cellulose columns showed an alpha1/alpha2 ratio of about 5, suggesting that at least two different species of collagen were synthesized. The alpha1/alpha2 ratio of the chains recovered from the ascorbate-deficient cultures was also about 5 but the chains were slightly underhydroxylated and the total amount of these chains which could be identified accounted for only a small fraction of the total collagen which was synthesized. A large fraction of the synthesized collagenous protein was found in the culture medium, mostly in the form of lower molecular weight peptides. It is concluded that most of the collagen which is synthesized by ascorbate-deficient tooth-bud cultures is not utilized by the component tissues, but is probably degraded and released into the medium.

Animals↗
PubMed1991

Muscular changes in the guinea pig caused by chronic ascorbic acid deficiency.

The present study was undertaken in order to decide whether chronic ascorbic acid (AA) deficiency only causes myopathy in the guinea pig or whether it also causes central nervous system pathology. Juvenile male animals, fed an optimally balanced, purified diet with minimal amounts of AA, developed a nutritional myopathy complicated by trauma, arthrogenic factors and defective repair. The absence of changes in the spinal pyramidal tracts, the anterior horn cells and peripheral nerve agrees with the absence of neurogenic changes in muscle specimens as target, targetoid, or small angulated fibers, group atrophy, type grouping, or changes in the distribution pattern of fibers. We conclude that chronic AA deficiency in the guinea pig cannot serve as an animal model of human amyotrophic lateral sclerosis.

Amyotrophic Lateral Sclerosis↗
PubMed1979

Ascorbic acid deficiency and hypertrophic osteodystrophy in the dog: a rebuttal.

Plasma ascorbic acid (PAA) in normal Labrador Retriever dogs less than one year of age averaged 1.22 +/- 0.05 mg/dl (x +/- sem) and was significantly higher than the value of 0.89 +/- 0.03, for Labrador Retrievers two years of age and older. No significant diurnal variation in PAA was observed. Oral or intravenous administration of 0.5 or 1.0 g of ascorbic acid (AA) elevated PAA for less than 8 hours. Injection of ACTH caused a significant decline in PAA for the initial 2 days, with variable results thereafter. Labrador Retriever puppies fed a ration high in protein, energy and calcium developed the typical skeletal diseases of overnutrition, including hypertrophic osteodystrophy (HOD). The addition or oral AA (0.5 g twice daily) had no ameliorating effect on the skeletal lesions. Instead AA supplementation resulted in relatively higher serum calcium values which, presumably by enhanced hypercalcitoninism, decreased bone resorption. Thus, AA treatment of dogs with HOD is contraindicated, as it can only aggravate the osseous lesions of HOD. The decreased PAA reported in dogs with HOD is interpreted to be the result of stress from pain.

Adrenocorticotropic Hormone↗
PubMed1977

Ultrastrutural studies of vascular and muscular changes in ascorbic acid deficient guinea-pigs.

Disorganization of muscle structures such as fragmentation of myofilaments with a loss of contrast in the Z bands, swelling of mitochondria and glycogenic infiltration, was seen in ascorbic acid deficient guinea-pigs. Vacuolar degeneration of external and internal endothelial cell membranes with accompanying dystrophic changes of the surrounding muscle and lack of collagen formation were consistent findings. Chondroblasts showed a marked dissolution of the matrix vesicle and a lack of hyaline droplets.

Animals↗
PubMed1991

Ascorbic acid deficiency decreases specific forms of cytochrome P-450 in liver microsomes of guinea pigs.

Ascorbic acid (VC) deficiency resulted in a decrease in the activities of aminopyrine N-demethylase, aniline hydroxylase, and p-nitroanisole O-demethylase and in the content of cytochrome P-450, as spectrally determined, whereas it caused an increase in the activities of 6 beta-hydroxylases for testosterone and progesterone in liver microsomes of guinea pigs. Western blot analysis of liver microsomes with antibodies to rat P-448-H (P-4501A2), P-450j (P-450IIE), P-450 PB-1 (P-450IIIA), and P-450b (P-450IIB1) showed that VC deficiency decreased the amount of cytochrome P-450 immunochemically related to P-450IA2 and P-450IIE but did not change the amount of the form that was cross-reactive with antibodies to P-450IIB1 and tended to slightly increase (not statistically significantly) the amount of the form of the cytochrome immunochemically related to P-450IIIA. The larger decrease by VC deficiency in the amount of cytochrome P-450 that was cross-reactive to the rat P-450IA2 resulted in a lower capacity of liver microsomes to activate promutagens, such as 2-amino-3-methyl-imidazo(4,5-f)quinoline and aflatoxin B1. These results indicate that VC deficiency in guinea pigs differentially affects the content of individual forms of cytochrome P-450.

Aflatoxin B1↗
PubMed1992

Skeletal lesions and anemia associated with ascorbic acid deficiency in juvenile rhesus macaques.

Young rhesus macaques housed in outdoor corn cribs and fed a commercially prepared primate diet became weak, depressed, were reluctant to move, and expressed locomotor abnormalities. Thirteen severely affected animals were hospitalized for evaluation. Physical examination disclosed swellings and instabilities involving the ends of long bones. Radiography confirmed physeal fractures in 11 of 13 animals. Affected bones included the distal femur, proximal humerus, distal tibia/fibula, and distal radius/ulna. Other, less obvious changes were noted on radiographs. Anemia was a consistent finding. Ascorbic acid deficiency was suspected and therapy was initiated that consisted of vitamin supplements, diet change, cage rest, and support bandages. Feed samples were submitted to a laboratory for analysis and were confirmed deficient in vitamin C. Follow-up radiographs showed large calcifying subperiosteal hematomas in epiphyseometaphyseal regions, consistent with a diagnosis of scurvy. Twelve of 13 animals recovered clinically. Subsequent radiographs documented improvement of initially severe angular deformities associated with displaced fractures.

Anemia↗