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At least 343 records · Page 19Linked to original sources
PubMed1984

The effects of glucose on ascorbic acid uptake in heart endothelial cells: possible pathogenesis of diabetic angiopathies.

Glucose in concentrations of 20 mg% (or greater) significantly inhibited 14C-labelled ascorbic acid (1.25 mg%) uptake in endothelial cells in the presence of insulin (1600 microU/ml). The absence of insulin also significantly reduced ascorbic acid uptake. Furthermore, this reduction could be exacerbated by glucose (40, 160 mg%) but not equimolar concentrations of fructose. Increased ascorbic acid concentrations (two-fold) in the absence of insulin (1) significantly enhanced uptake, and (2) reversed the inhibition of glucose. These findings support earlier reports that ascorbic acid uptake into the cell may be compromised by decreased insulin and/or increased extracellular glucose levels. Since previous animal studies have correlated experimental ascorbic acid deficiencies with atherogenic processes (presumably by altering glycosaminoglycan metabolism), the postulation that the "diabetic condition" (low insulin, hyperglycemia) accelerates the cellular changes leading to atherosclerosis by impairing ascorbic acid uptake into the vascular endothelium, may now be supported.

Animals↗
PubMed2000

Ascorbic acid use in hyporesponders to Epoetin alfa.

I.v. ascorbic acid has been used in an effort to mobilize ferritin stores in hyporesponsive HD patients receiving Epoetin alfa. However, not all patients who respond to i.v. ascorbic acid therapy will have subsequent decline in feritin stores (Gastaldello et al., 1995; Tarng & Huang, 1998). Additionally, predicting those patients who will overcome their Epoetin alfa hyporesponsiveness remains unclear. Ascorbic acid's effect on hemosiderin deposits may be another possible mechanism to the increased Epoetin alfa response observed in some HD patients (Hemosiderin is a pathologic deposition of iron in tissues including the spleen, small intestine, and bone marrow). Although there are no well-controlled studies evaluating hemosiderin and i.v. ascorbic acid, it should be noted that subjects with scurvy often present with excessive iron deposits in the tissues, indicating the possible effects of ascorbic acid on hemosiderin metabolism (Bothwell et al., 1964). Ascorbic acid deficiency is often present in many HD patients due to its removal during dialysis and lack of dietary intake (Ponka & Kuhlback, 1983). It remains controversial whether oral ascorbic acid supplementation is indicated in patients receiving HD. Therefore, the Recommended Daily Allowance (RDA) of 60 mg/day should be advised (Makoff, 1999). I.v. ascorbic acid should be considered as a possible adjuvant to therapy in patients who are "iron-overloaded" and hyporesponsive to Epoetin alfa. Although the long-term effects of i.v. ascorbic acid on HD patients is unknown, the potential risk of secondary oxalosis should be considered (Costello, 1991; Pru, Eaton, & Kjellstrand, 1985). It may be necessary to monitor plasma oxalate levels if long-term therapy with i.v. ascorbic acid is used. Clinical studies have examined i.v. ascorbic acid doses from 300 mg-500 mg given up to TIW for a maximum duration of 12 weeks without any significant deleterious effects (Gastaldello et al., 1995; Tarng & Huang, 1998; Tarng et al., 1999). However, large-scale, prospective, and controlled trails are needed to determine the long-term safety and efficacy of i.v. ascorbic acid therapy in iron overloaded HD patients receiving Epoetin alfa.

Anemia↗
PubMed1975

Relation between hepatic alcohol dehydrogenase activity and the ascorbic acid in leucocytes of patients with liver disease.

1. Hepatic alcohol dehydrogenase activity and leucocyte ascorbic acid content was measured in thirty-five patients with liver disease and in ten control subjects with duodenal ulcer. The patients with liver disease were divided into three groups consisting of non-drinkers, moderate drinkers and alcoholic/heavy drinkers. 2. There was no significant difference in hepatic alcohol dehydrogenase activity between the groups with liver disease, but all patients had less than half the hepatic alcohol dehydrogenase activity of the control subjects (P less than 0-001). 3. The ascorbic acid in leucocytes was significantly lower in the alcoholic/heavy drinker group than that in the control subjects (P less than 0-02) when the Student's t-test was applied, but no significant difference was found when the Mann-Whitney U-test was used. 4. A correlation coefficient of r = 0-77 (P less than 0-001) was observed among the thirty-five patients with liver disease when hepatic alcohol dehydrogenase activity was compared with leucocyte ascorbic acid content. An insignificant correlation (r = 0-332) was found in the control subjects with no liver disease. 5. This comparison was also significant among non-drinkers with liver disease (r = 0-873; P less than 0-001), moderate drinkers (r = 0-739; P less than 0-02) and alcoholic/heavy drinkers (r = 0-702; P less than 0-005). 6. The addition of ascorbic acid in vitro (0-5-10 mmol/1) had no effect on the activity of alcohol dehydrogenase. 7. The relation between hepatic alcohol dehydrogenase activity and leucocyte ascorbic acid content is probably a consequence of liver disease, as opposed to any specific effect of ascorbic acid deficiency of alcohol consumption on alcohol dehydrogenase activity.

Alanine Transaminase↗
PubMed1989

Animal models of amyotrophic lateral sclerosis and the spinal muscular atrophies.

The causes of human amyotrophic lateral sclerosis (ALS) and the spinal muscular atrophies (SMA) are, almost without exception, unknown. This ignorance has stimulated the search for animal models to obtain insight into the etiology, pathogenesis and biochemical mechanisms underlying the human disorders. None of the 38 animal models, described in this review, provides an exact animal copy of a specific human motor neuron disease. Most of the models reproduce certain structural or physiological aspects of their human counterparts. The various experimental models can be classified according to the pathogenetic mechanism involved and according to the structural changes observed. Models based on experimentally induced disease, include heavy metals and trace elements (lead intoxication in guinea pigs, rabbits, rats, cats and primates; mercury intoxication in rats; aluminium intoxication in rabbits; swayback in goat kids; calcium and magnesium deficient rabbits and primates and calcium deficient cynomolgus monkeys), toxins (IDPN, vincristine, vinblastine, podophyllotoxin, colchicine, maytansine, maytanprine, L-BMAA, lectins, adriamycin), nutritional factors (ascorbic acid deficient guinea pigs), virus infection (spongiform polioencephalomyelitis, attenuated poliovirus, lactate dehydrogenase-elevating virus), and immunological factors (immunization with motor neurons). Hereditary models comprise hereditary canine spinal muscular atrophy, hereditary neurogenic amyotrophy in the pointer dog, Stockard paralysis, Swedish Lapland dog paralysis, "wobbler" mouse, "shaker" calf, and hereditary spinal muscular atrophy in zebra foals, crossbred rabbits,

Amyotrophic Lateral Sclerosis↗
PubMed1997

Studies on the essential role of ascorbic acid in the energy dependent release of insulin from pancreatic islets.

Pancreatic islets from young normal and scorbutic male guinea pigs were examined for their ability to release insulin when stimulated with depolarizing levels of KCl (45 mM) and by 20 mM D-glyceraldehyde. Islets from normal guinea pigs released insulin in a K+ and D-glyceraldehyde dependent manner showing a rapid initial secretion phase followed by secondary waves of insulin release during a 120 min period. Islets from scorbutic guinea pigs were able to respond to elevated K+ in a manner identical to that of the control islets. In contrast, insulin release from ascorbic acid deficient islets in response to the secretagogue, D-glyceraldehyde, was significantly delayed and decreased responses were observed during the 120 min period after D-glyceraldehyde stimulation. The results are consistent with the site of action of ascorbic acid on energy-dependent insulin release lying between the triose-phosphate level of glycolysis and the generation of ATP by oxidative phosphorylation.

Animals↗
PubMed1986

Ascorbic acid and cholesterol levels in patients with diabetes mellitus and coronary artery disease.

Indian and black patients admitted to King Edward VIII and R. K. Khan Hospitals with a diagnosis of cardiac infarction and diabetes mellitus were studied. The mean serum cholesterol levels were higher in the indian group. This preliminary study suggests a negative correlation between leucocyte ascorbic acid and serum cholesterol levels in Indians, especially in patients with infarction. This, however, does not preclude an effect of latent ascorbic acid deficiency on the vessel wall. The possible relevance of the findings to the development of atherosclerosis is discussed.

Adult↗
PubMed1990

Nutritional needs assessment of rural agricultural migrants of southern Brazil: designing, implementing and evaluating a nutrition education program.

A nutritional needs assessment was conducted among rural agricultural migrant women (target group) and children (less than 5 years). The study was conducted in Vila Diogo, a slum located on the periphery of Nuporanga, a village in Sao Paulo state, Brazil. A nutrition education program was designed on the basis of evidence obtained from demographic/socioeconomic information of the study population and a nutritional needs assessment of women (target group) and children less than 5 years of age. The nutritional needs assessment consisted of anthropometry, dietary assessment, and nutrition knowledge, attitudes, and beliefs questionnaires. Formative and summative evaluation of the nutrition education program, using appropriately selected criteria and comparisons of nutrition knowledge scores before and after the program, were used to determine program effectiveness. Major findings of the study were: Diets of Vila Diogo residents were generally simplistic, consisting primarily of rice, beans, and coffee with sugar. Vila Diogo women appeared to be at a relatively high risk for vitamin A, iron, calcium, ascorbic, and riboflavin deficiencies, based on comparisons of 24-hour dietary intake data with FAO recommendations. Children (2-5 years) appeared at high risk for vitamin A, iron, and ascorbic acid deficiencies, based on comparisons of 24-hour dietary intake data with FAO recommendations. All children less than 5 years of age had been breast-fed at birth, but more than one half of children had been weaned by the third month. Infant feeding practices during fever and diarrhea were nutritionally detrimental. Women generally recognized a relationship between dietary intake during pregnancy and fetal nourishment. Using weight-for-height index, a significant number of women were probably undernourished; a small percentage of women, however, were overweight or obese. Although children less than 5 years of age did not generally appear malnourished, a relatively large number were stunted in growth. Although Vila Diogo women reported many food taboos during various physiological states (menstruation, pregnancy, immediately post partum, lactation), relatively few food taboos had potentially negative nutritional consequences. For women who participated in the nutrition education program, nutrition knowledge scores after the program showed improvement which was statistically significant at alpha = 0.05, using Wilcoxon signed rank test.

Brazil↗