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Results for “ASCORBIC ACID DEFICIENCY”

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At least 73 records · Page 4Linked to original sources
PubMed1985

Carrageenan colitis in the guinea pig: pathological changes and the importance of ascorbic acid deficiency in disease induction.

In guinea pigs deprived of ascorbic acid, the oral administration of degraded E. spinosum carrageenan induced mild to moderate colitis, while E. cottonii consistently induced severe colitis. A variable degree of colitis was observed in scorbutic animals not receiving carrageenan. By contrast, in animals given large daily supplements of ascorbic acid, neither type of carrageenan consistently induced colitis and severe disease was rarely observed. The severe colitis induced by E. cottonii in scorbutic animals markedly affected the mid and distal colon and showed histological changes similar to human ulcerative colitis.

Animals↗
PubMed1982

Activity of alkaline phosphatase in the serum of normal and ascorbic-acid-deficient guinea pigs.

Guinea pigs well supplied with vitamin C show a linear relation between serum alkaline phosphatase activity and body weight. Investigations in guinea pigs induced to low ascorbic-acid levels by two different procedures (complete and partial deprivation of vitamin C) demonstrated that the activity of the alkaline phosphatase is not generally decreased in the serum of ascorbic-acid-deficient guinea pigs. Decreases of the serum enzyme levels reported in guinea pigs completely deprived of vitamin C, i.e. in acute deficiency, may be due to stress factors.

Aging↗
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↗
PubMed1990

Ascorbic acid deficiency affects the metabolism of cytosolic ferritin but not lipid-associated ferritin in livers of guinea pigs.

Two physicochemically and metabolically separate pools of ferritin, namely cytosolic ferritin and lipid-associated ferritin, are present in the livers of guinea pigs. In this paper we establish that the iron content of cytosolic ferritin is dependent on and linearly related to ascorbic acid concentration, whereas changes in concentration of this vitamin do not affect the iron content of lipid-associated ferritin. In livers of ascorbic acid-deficient guinea pigs both synthesis and degradation of cytosolic ferritin are diminished equally. Consequently cytosolic ferritin is metabolized more slowly without changes in its pool size. In contrast with cytosolic ferritin, the metabolism of lipid-associated ferritin is unaffected by ascorbic acid deficiency. The differential effects of ascorbic acid deficiency on the physicochemical characteristics as well as on the metabolism of cytosolic ferritin and lipid-associated ferritin suggest that the two forms of ferritin have different functional roles.

Animals↗
PubMed1983

Combined effect of ascorbic acid deficiency and underfeeding on the hepatic carnitine level in guinea-pigs.

Liver carnitine level decreased from 249 +/- 16.1 nmoles/g (mean +/- SEM) control value to 148 +/- 9.8 nmoles/g (59.4%) in ascorbic acid deficient guinea-pigs, while in the underfed ('pair-fed') group it decreased to 181 +/- 14.1 nmoles/g (72.6%). Underfeeding also resulted in lower ascorbic acid levels; the depression of carnitine in the underfed animals could be prevented by an overdose (200 mg daily) of ascorbic acid.

Animals↗
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↗
PubMed2002

Morphological influence of ascorbic acid deficiency on endochondral ossification in osteogenic disorder Shionogi rat.

The influences of chronic deficiency of L-ascorbic acid (AsA) on the differentiation of osteo-chondrogenic cells and the process of endochondral ossification were examined in the mandibular condyle and the tibial epiphysis and metaphysis by using Osteogenic Disorder Shionogi (ODS) rats that bear an inborn deficiency of L-gulonolactone oxidase. Weanling male rats were kept on an AsA-free diet for up to 4 weeks, until the symptoms of scurvy became evident. The tibiae and condylar processes of scorbutic rats displayed undersized and distorted profiles with thin cortical and scanty cancellous bones. In these scorbutic bones, the osteoblasts showed characteristic expanded round profiles of rough endoplasmic reticulum, and lay on the bone surface where the osteoid layer was missing. Trabeculae formation was deadlocked, although calcification of the cartilage matrix proceeded in both types of bone. Scorbutic condylar cartilage showed severe disorganization of cell zones, such as unusual thickening of the calcification zone, whereas the tibial cartilage showed no particular alterations (except for a moderately decreased population of chondrocytes). In condylar cartilage, hypertrophic chondrocytes were encased in a thickened calcification zone, and groups of nonhypertrophic chondrocytes occasionally formed cell nests surrounded by a metachromatic matrix in the hypertrophic cell zone. These results indicate that during endochondral ossification, chronic AsA deficiency depresses osteoblast function and disturbs the differentiation pathway of chondrocytes. The influence of scurvy on mandibular condyle cartilage is different from that on articular and epiphyseal cartilage of the tibia, suggesting that AsA plays different roles in endochondral ossification in the mandibular condyle and long bones.

Animals↗
PubMed1982

Effect of ascorbic acid deficiency on serum ferritin concentration in patients with beta-thalassaemia major and iron overload.

The incidence of ascorbic acid (AA) deficiency and its effect on serum ferritin concentration relative to body iron stores was studied in 61 unchelated patients with beta-thalassaemia major. Thirty-nine (64%) of patients had subnormal leucocyte ascorbate concentrations without clinical evidence of scurvy. The lowest leucocyte ascorbate concentrations tended to occur in the most transfused patients. No correlation was found between the units transfused and serum ferritin concentration in the AA-deficient patients but a close correlation (r = +0.82; p less than 0.005) existed for the AA-replete group. Similarly a close correlation (r = +0.77; p less than 0.005) was obtained between liver iron concentration and serum ferritin in AA-replete patients but only a weak correlation (r = +0.385; p less than 0.025) existed for the AA-deficient group. When AA-deficient patients were treated with ascorbic acid, serum iron and percentage saturation of iron binding capacity rose significantly; serum ferritin rose in 13 of 21 patients despite the simultaneous commencement of desferrioxamine therapy. In contrast all three measurements tended to fall in AA-replete patients with ascorbic acid and desferrioxamine therapy. Thus, AA deficiency is commonly present in beta-thalassaemia patients with iron overload and may give rise to inappropriate serum ferritin concentrations in relation to body iron stores.

Adolescent↗
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↗