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Results for “ASCORBIC ACID DEFICIENCY”

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PubMedDate not supplied

[Correlation between hypercholesterolemia and vitamin C deficient diet].

The deficiency of ascorbic acid in the diet affects the activity of lecithin cholesterol acyl-transferase enzyme and transformation of cholesterol to its main catabolic product the biliary acids. Fifteen patients with normal blood levels of cholesterol and fifteen patients with hypercholesterolemia were submitted to a comparative study as to the dietary ingestion of ascorbic acid. Besides this the presence of the varicosity of the sublingual vein--indicating hypovitaminosis C--was investigated in both groups of patients. The "t" Student test and Control-Case test of the results showed that regarding the cholesterol level there was a significant difference between the patients with hypercholesterolemia (422 +/- 116.2018 mg/100 ml) and those with normal cholesterolemia (160.73 +/- 29.5356 mg/100 ml). The ingestion of ascorbic acid in he diet of the normal cholesterolemia group was found to be significantly higher than that of patients with hypercholesterolemia. The ingestion of cholesterol was high in the group of patients with hypercholesterolemia but in comparison with other groups there was no significant difference. The varicosity of the sublingual vein was observed with significantly higher frequency (p < 0.0001) in the group of patients with hypercholesterolemia and lower ingestion of ascorbic acid.

Adult↗
PubMed1991

Oxidants, antioxidants and cardiovascular disease.

Basic and clinical studies in the past decade suggest an involvement of oxygen-derived free radicals in some cardiovascular diseases including atherosclerosis and hypertension. In atherogenesis evidence indicates that low-density lipoprotein/cholesterol must be oxidized before it can be taken up by the monocytes/macrophages to form foam cells which contribute to the characteristic fatty streak. Free radicals are considered responsible for this oxidation. Population studies reveal that hypertensive patients generally have a lower intake of ascorbic acid and possibly other antioxidants. Ascorbic acid deficiency may lead to defective vasodilation and increased blood pressure due to destruction of certain endothelium-dependent relaxing factors by free radicals. Further studies in this area appear justified.

Antioxidants↗
PubMedDate not supplied

[Actual nutrition and biochemical parameters of the food status of workers exposed to chlorobenzene].

Workers of two chemical plants exposed to chlorobenzene were examined for actual nutrition and effects of the treatment and prophylactic diet on the food status. Investigation of the actual nutrition has demonstrated that the energy value of the daily diets approaches the magnitudes established for the given occupational and age group whereas the daily distribution of food with respect to the caloric value and alimentary substances does not correspond to the hygienic standards. The treatment and prophylactic diets developed for the workers were also characterized by disproportion between the dietary components. As compared to the control group, the workers exposed to chlorobenzene demonstrated a lower content of total glutathione in blood plasma. The majority of the workers manifested ascorbic acid deficiency. In accordance with the study of the coefficients of the activation of erythrocytic enzymes, it may be concluded that the workers placed on the treatment and prophylactic diet are better provided with vitamins B1, B2 and B6 than the workers of the housing and communal services. Thirty percent of the workers showed vitamin B6 deficiency. This may have an adverse action on the resistance to industrial substances conjugating with glutathione. The rate of vitamin B1 deficiency was also fairly high, whereas in the workers of one of the plants the magnitude of the TDP-effect appeared higher than normal.

Adult↗
PubMed1988

Copper nutriture, bioavailability, and the influence of dietary factors.

Copper is known to be an essential nutrient for human beings, but a Recommended Dietary Allowance has not yet been established. A safe and adequate range of intake was established in 1980 for copper and five other trace elements. The range for copper, 2 to 3 mg/day, is higher than the usual dietary copper intake of many individuals in this country. On the basis of balance studies, a requirement of 1.3 mg/day has been suggested. Recent data on copper intake and bioavailability should aid in reevaluating the dietary copper requirement. Copper deficiency symptoms have seldom been observed in human beings. When copper deficiency has been recognized, it has been under unusual conditions, such as in patients receiving parenteral nutrition. Interactions between copper and other dietary components may alter copper status, but the impact of those interactions is not yet well understood. Dietary factors that may affect the bioavailability of copper include the levels of copper, zinc, and molybdenum in the diet; iron deficiency; ascorbic acid intake; intake of carbohydrates, including fructose, glucose, and starch; and fiber and phytate intakes. Some drugs may also affect copper bioavailability.

Copper↗
PubMed1977

[Iron metabolism during proteoenergetic malnutrition in children].

The iron stores are normal in marasmic kwashiorkor in kivu, but they notably decrease on re-feeding. On admission, the total iron binding capacity depends not only on the severity of the protein depletion but also on the iron stores. There exists an abnormality of the iron release from the stores; this cannot be attributed to the hypotransferrinemia or to the hypoceruloplasminemia, which are too moderate, nor to an ascorbic acid deficiency, but possibly to the inflammatory state which is a feature of kwashiorkor. The iron deficiency which occurs on re-feeding is not explained by abnormalities of iron absorption or by increased iron loss, but by the raised requirement for iron. Parental iron treatment alone is required to normalise the packed cell volume and the red cell volume after re-feeding.

Child↗
PubMed1981

Leg ulcers in the eighteenth and early nineteenth centuries.

Compared to today, ulceration of the legs was much more common in the eighteenth and early nineteenth centuries and occurred in much younger people. The evidence for this, based mainly on the records of the hospitals, the dispensaries and medical records of the navy and army, is discussed. It is likely that the underlying pathology was much more varied in the past, with the possibility that ascorbic acid deficiency played a significant part in the high frequency of leg ulcers.

Adolescent↗
PubMed1977

Pyomyositis in Swaziland.

Pyomyositis was studied in 25 patients over a period of 1 year. The patients lived in a subtropical region, latitude about 27 degrees S, but the disease described is the same as that which occurs in the tropics and which goes by the name of "tropical myositis". The aetiology proposed for tropical myositis is regarded as not applicable to the same disease described here, of which the cause remains uncertain. This aspect of the problem is discussed with reference to the possible role played by a deficiency of ascorbic acid in the diet. Incision and drainage is the only method of treatment.

Adolescent↗
PubMed1993

Studies on neurolathyrism.

Neurolathyrism is a neurological condition seen among people who eat the seeds of Lathyrus sativus (LS) as a principal source of food energy for 2 months or more. It is characterized by severe muscular rigidity and paralysis of the lower limbs. beta-N-Oxalyl-L-alpha,beta-diaminopropionic acid is the principal toxin found in the seed. No experimental animal model for neurolathyrism could be produced by feeding either the seeds or the toxin, although the condition has been known for centuries. We discovered that experimental neurolathyrism could be produced in guinea pigs and primates that needed an external supply of ascorbic acid by making them subclinically deficient in ascorbic acid and feeding them the seeds of LS or extracts thereof. Autoclaving the seeds of LS with lime removes the toxin.

Animals↗
PubMed2002

Increased oxidative damage in vitamin C deficiency is accompanied by induction of ascorbic acid recycling capacity in young but not mature guinea pigs.

Ascorbic acid (AA) recycling, i.e. the intracellular regeneration of AA from its oxidized forms semidehydroascorbyl radical and dehydroascorbic acid (DHA), presumably has a key function in maintaining redox homeostasis. Like humans, guinea pigs cannot synthesize AA. In the present paper, the effects of severe AA deficiency on the AA recycling capacity in erythrocytes (RBCs) and liver homogenates were studied in young and mature guinea pigs. Twelve animals of each age category were divided into weight-matched groups of six animals and fed either an AA deficient or sufficient diet. After 5 weeks, they were sacrificed and RBC and liver ascorbate recycling was estimated along with glutathione, tocopherols, AA, SOD, and malondialdehyde (MDA). For young animals, AA recycling capacity was significantly increased in RBCs from the deficient group as compared to the controls (p < 0.001). RBC MDA was not increased by incubation with t-butylhydroperoxide (TBH) while the initial MDA level was significantly elevated (p < 0.001). In mature animals, neither RBC recycling nor MDA levels depended on AA status. Liver recycling capacity was not affected by age or diet, while liver MDA was significantly higher in young but not in mature deficient animals compared to respective controls (p < 0.01). In young animals, incubation with TBH resulted in significant MDA formation in the deficient compared to sufficient animals in both liver and RBCs (p < 0.05). RBC glutathione was not significantly changed by age or diet indicating that the observed changes in recycling capacity are enzyme dependent. The results suggest that young guinea pigs may have a more adaptable antioxidant defense system compared to mature animals while also being more susceptible to oxidative stress.

Aging↗
PubMed1993

[Effects of ascorbic acid on trace element metabolism in the choroid-retina of streptozotocin-induced diabetic guinea pigs].

In order to investigate the effect of ascorbic acid on trace element metabolism in the choroid-retina, experimental diabetes mellitus was induced in Hartley guinea pigs with intraperitoneal injection of streptozotocin. After 4 weeks, ascorbic acid-deficient feed was given for 3 weeks. Trace elements of the choroid-retina were measured with inductively-coupled plasma emission spectrometry. The activity of superoxide dismutase and lipid peroxide content also were measured. The results indicated that zinc and magnesium increased in diabetes mellitus. However, with ascorbic acid deficiency in diabetes mellitus, zinc and magnesium significantly decreased. On the other hand, the activity of superoxide dismutase showed no change between either condition and lipid peroxide content decreased under ascorbic acid deficiency in diabetes mellitus. These findings suggested that ascorbic acid played an important role in chorioretinal damage of diabetes mellitus. However, it was also suggested that lipid peroxide has little influence on the choroid-retina under these conditions.

Animals↗
PubMed1965

VITAMINS B AND C.

Explore the source record for details and available documents.

Ascorbic Acid Deficiency↗
PubMed1998

The effect of aqueous humor ascorbate on ultraviolet-B-induced DNA damage in lens epithelium.

PURPOSE: High levels of ascorbic acid are known to be present in the aqueous humor of many diurnal species, whereas nocturnal animals have low concentrations of the compound. The purpose of this study was to test the hypothesis that the high concentration of aqueous ascorbate in diurnal animals protects the lens against ultraviolet (UV)-induced damage to the eye. This study compares the effect of UV-B-induced DNA strand breaks on the lens epithelia of guinea pigs and rats after depletion or elevation of aqueous humor ascorbate, respectively. METHODS: Eyes of guinea pigs and rats were exposed to UV-B radiation (0.25-0.75 J/cm2 on the cornea) for 10 minutes, and DNA strand breaks in lens epithelium were measured by single-cell gel electrophoresis. Ascorbic acid concentration in the aqueous humor, lens, and lens-capsule epithelium were assayed by spectrophotometric and electrochemical methods. For depletion of aqueous humor and lens ascorbate in guinea pigs, the animals were maintained on an ascorbate-deficient diet. Aqueous ascorbic acid was elevated in the rat by intraperitoneal injections of sodium ascorbate (1 g/kg). RESULTS: The ascorbate concentration in the aqueous humor of the normal rat was approximately 3% that of the guinea pig, whereas the concentration of the compound in the lens of the normal rat was 10% that of the guinea pig. Guinea pigs fed an ascorbate-deficient diet showed a dramatic drop of more than 80% in aqueous humor ascorbate in the first week, whereas lens ascorbate decreased by approximately 25% during this time period. After a single intraperitoneal injection of sodium ascorbate in the rat, aqueous humor ascorbic acid increased nearly 30 times that in the control, whereas lens ascorbate increased by approximately 30%. The extent of DNA damage in the lens epithelium of a normal rat exposed to UV-B was significantly greater than that occurring in lenses of normal guinea pigs after exposure to the same dose of radiation. Lenses from ascorbate-deficient guinea pigs showed 50% more DNA damage than those from normal guinea pigs after UV exposure, whereas the lenses in ascorbate-injected rats exhibited significant protection against UV-induced DNA strand breaks. CONCLUSIONS: High levels of ascorbic acid in the aqueous humor had a protective effect against UV-induced DNA damage to lens epithelium. The results were consistent with the hypothesis that high ascorbic acid in diurnal animals protects the lens against the cataractogenic effect of UV radiation in sunlight.

Animals↗