[Significance of intervitamin correlations. IV. Content of ascorbic and dehydroascorbic acids in organs of vitamin C-deficient and thiamine-treated guinea pigs].
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Animals↗
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Results for “ASCORBIC ACID DEFICIENCY”
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[The effect of acute deficiency and of prolonged low intake of vitamin C on the spectrum of serum lipoproteins in guinea pigs].
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Animals↗
Cholesterol: vitamin C controls its transformation to bile acids.
Cholesterol accumulates in the blood serum and in the liver of guinea pigs with chronic latent vitamin C deficiency. The reason for this is the decreased rate of transformation of cholesterol to bile acids in the liver of animals deficient in vitamin C. A significant direct correlation exists between the vitamin C concentration in the liver and the rate of cholesterol transformation to bile acids.
Animals↗
Cholesterol metabolism in inherently scorbutic rats (ODS rats).
We observed the cholesterol metabolism of a colony of Wistar rats with a hereditary defect in vitamin C synthesizing ability (the ODS (osteogenic disorder-Shionogi) rats) in six kinds of experiments. Female ODS rats aged 36 days had a low HDL (high-density lipoprotein)-cholesterol level in serum as compared with age-matched control rats in spite of the absence of scorbutic symptoms. Female ODS rats aged 63 days which revealed severe scorbutic symptoms had a very low HDL-cholesterol level (mean value; 17 mg/dl). And male ODS rats, whose lives had been prolonged by supplementing with L-ascorbic acid, also had lower serum HDL-cholesterol and had increased total cholesterol in serum and liver when the acid supplement dose was relatively insufficient. On the other hand, we examined HDL2- and HDL3-cholesterol levels in serum to determine the mechanism of low HDL-cholesterol. As a result, we observed a low HDL2-cholesterol level in ODS rats but normal HDL3-cholesterol level. But the authors observed no decrease of LCAT (lecithin: cholesterol acyltransferase) activity in serum of ODS rats. These results could be due to disturbance of lipid metabolism in a vitamin C-deficient condition, that is to say, there might be abnormalities of the cholesterol excretion pathway of bile acid from liver, and maturity of the HDL-cholesterol particle due to other factors except that of LCAT activity.
Animals↗
Scurvy in a nonalcoholic person in the United States.
Scurvy is rarely diagnosed in our society today. The authors describe the case of a 31-year-old man with weakness, gingival pain, and a rash over the lower extremities. He had a history of poor nutritional intake, no alcohol consumption, and a 13 pack-year history of cigarette smoking. Laboratory studies revealed an extremely deficient serum ascorbic acid level. Treatment was begun with oral ascorbic acid tablets and, within 3 days after discharge, all clinical symptoms of scurvy had resolved. Scurvy is an easily treated disease and should be considered when there is an appropriate history and classic clinical findings. Because vitamin C deficiency can be seen in many chronic disease states, it is important to recognize some of the early features and clinical manifestations of such nutritional deficiencies.
Adult↗
Effect of vitamin C deficiency on the metabolism of drugs and NADPH-linked electron transport system in liver microsomes.
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Aminopyrine↗
Glutathione ester delays the onset of scurvy in ascorbate-deficient guinea pigs.
Previous studies showed that administration of ascorbate to glutathione (GSH)-deficient newborn rats and guinea pigs prevented toxicity and mortality and led to increased tissue and mitochondrial GSH levels; ascorbate thus spares GSH. In the present work, we tried to answer the converse question: Does administration of GSH spare ascorbate? Because administered GSH is not well transported into most cells, we gave GSH monoethyl ester (which is readily transported and converted into GSH intracellularly) to guinea pigs fed an ascorbate-deficient diet. We found that treatment with GSH ester significantly delays appearance of the signs of scurvy and that this treatment spares ascorbate; thus, the decrease of tissue levels of ascorbate was delayed. The findings support the conclusions that (i) GSH is essential for the physiological function of ascorbate because it is required in vivo for reduction of dehydroascorbate and (ii) there is metabolic redundancy and overlap of the functions of these antioxidants. The sparing effect of GSH in scurvy may be mediated through an increase in the reduction of dehydroascorbate (which would otherwise be degraded) and to antioxidant effects of GSH that are also produced by ascorbate. Other studies indicate that GSH deficiency in adult mice stimulates ascorbate synthesis in liver. During this work we found that administration of GSH itself is highly toxic to ascorbate-deficient guinea pigs when given in divided i.p. doses totaling 3.75 mmol/kg daily.
Animals↗
[Vitamin C deficiency and its effect upon the 17-ketosteroids and dehydroepiandrosterone secretion in monkeys].
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17-Ketosteroids↗
Comparison of absorption of erythorbic acid and ascorbic acid in guinea pig small intestine.
Both the ascorbic acid (AsA) and erythorbic acid (ErA) absorption in the small intestine of guinea pigs were determined by the perfusion of the small intestine using isotonic phosphate buffer recycled in situ. The absorption rate of AsA in the small intestine of guinea pigs was higher than that of ErA; however, Km of AsA absorption was lower than that of ErA in normal guinea pigs. In AsA-deficient guinea pigs, the absorption rates of both AsA and ErA were higher than those in normal ones. The absorption of AsA and ErA in the small intestine of guinea pigs was inhibited by ouabain. Furthermore, AsA and ErA inhibited each other's absorption. Based on the results, the net amount of the absorbed ErA in the small intestine may be lower than that of AsA, and ErA absorption mechanism seemed to be similar to that of AsA. The absorption rate of both AsA and ErA in the small intestine of guinea pig might be dependent on the AsA level in the tissues.
Animals↗
Effect of NO2 inhalation and vitamin C deficiency on protein and lipid accumulation in the lung.
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Animals↗
Elevated activity of low molecular weight insulin-like growth factor-binding proteins in sera of vitamin C-deficient and fasted guinea pigs.
We have previously reported that scorbutic and fasted guinea pig sera contain an insulin-like growth factor-I (IGF-I)-reversible inhibitor of collagen, proteoglycan, and DNA synthesis in cultured cells. Here we report that IGF-binding protein (IGFBP) activity is increased in serum containing the inhibitor [125I]IGF-I or -II bound to these sera was eluted in the 30- to 50-kDa region of an S200 gel column. [125I]IGF-I affinity cross-linking analysis revealed that a 38-kDa cross-linked species increased markedly in fasted and scorbutic sera, with a lesser increase in a 34-kDa species, while scorbutic sera also yielded a 44-kDa species. Gel filtration of unlabeled sera showed a 10-fold increase in the activity of two proteins in the 30- to 50-kDa region from the experimental sera. Their activity correlated with their ability to inhibit binding of [125I]IGF-I to its cellular receptor, suggesting that they have the potential to inhibit IGF-I-dependent functions. Ligand blotting showed that 29 and 35-kDa IGFBPs were almost undetectable in normal serum, but were dramatically induced by scurvy and fasting, so that they accounted for close to 40% of the total circulating BPs. Total IGFBP-3 in the experimental sera was increased about 30%, while there was little effect of scurvy or fasting on the level of BP-3 activity isolated by acid extraction of the high mol wt region of the S200 column. An IGF-I analog with normal affinity for the 30- to 50-kDa BPs from fasted and scorbutic sera, but with reduced affinity for the cell receptor, was equivalent to IGF-I in reversing the inhibition of collagen synthesis by scorbutic guinea pig serum in human fibroblasts. Thus, reversal of inhibition appears to require initial saturation of IGFBPs. The overall results suggest that two circulating IGFBPs with unoccupied binding sites are induced in vitamin C-deficient or fasted guinea pigs and may be responsible for inhibition of IGF-I-dependent functions by sera from these animals.
Animals↗
The bone marrow in nutritional deficiencies.
The overwhelming majority of nutritional deficiencies that affect the bone marrow and blood are due to the lack of vitamin B12, folic acid, or iron or combinations thereof. The two vitamins are closely related in DNA synthesis, whereas iron is the most abundant heavy metal in the body and is chiefly utilized for hemoglobin synthesis. Concomitant conditions of vitamin B12 and/or folate deficiency along with iron deficiency are not infrequent, and one type of anemia may mask the other. It is important to establish the correct diagnoses, as therapy directed at the wrong deficiency may hide the real deficiency with disastrous results. Specific diagnostic tests are now available to determine definitive diagnoses, and specific therapy is readily available to restore and maintain a normal nutrient status.
Anemia, Hypochromic↗
The effect of vitamin C deficiency on complement systems and complement components.
The changes in the complement systems and complement hemolytic activities through classical and alternative pathways, and the individual components, C1, C4, C2 and C3 were demonstrated in the course of vitamin C deficiency in guinea pigs. During the course of vitamin C deficiency during the first week after the start of the experiment, all components except C1 slightly decreased, gradually increasing in the following weeks. This indicates that this period is important in the formation of an immune defence system in the host. At the time the symptoms of vitamin C deficiency appeared, C1, C2 and CH50 started to decrease. C3 increased when vitamin C deficiency became severe and showed a completely different pattern from those of the other components. The lowered C1 will be due to a collagen-like region in the characteristic of Clq subcomponent, since insufficient vitamin C state produces impaired collagen formation. The activity of the alternative pathway did not produce any change in this course, even in the severe stage. This indicates that the increase in C3 will contribute to maintaining the level of the alternative pathway and maintaining the body defence system in the vitamin D-deficient state, and that the complement system will be supported through the alternative pathway.
Animals↗
Nutrition of elderly men living alone. Part 2, Vitamin C and thiamine status.
A dietary survey using the five day record method was carried out on 35 elderly men living alone in the Christchurch area. The mean calculated intake of vitamin C for these men was 31 mg/day. These dietary intakes of vitamin C were significantly correlated with both plasma vitamin C levels and with leucocyte vitamin C levels. Twelve men (34 percent) with lowered dietary intakes of vitamin C were in the range for asymptomatic scurvy. The mean calculated intake of thiamine was 1.05 mg/day. The mean TPP effect was 12.9 percent (n = 27). Dietary intakes of thiamine showed a significant inverse relationship with TPP effect. Eight subjects (23 percent) who too, less than the Australian dietary allowance had an elevated TPP effect. By both dietary and biochemical methods there was evidence of subclinical vitamin C and thiamine deficiencies in more than a quarter of these men.
Aged↗
[Metabolism of the pesticide trichlorometaphos-3 and its effect on the monooxygenase system depending upon the supply of lysine, methionine, threonine and vitamins A, B and C].
Metabolism of organophosphate pesticide trichlorometaphos-3 and its effect on liver monooxygenase system were studied in male rats of WAG strain, maintained on a diet deficient in lysine, methionine, threonine and vitamins A, C, E. Long-term deficiency of these essential nutrients led to inhibition of monooxygenase induction in acute intoxication with pesticide (150 mg/kg) and to restriction of the induction in chronic intoxication (3 mg/kg) within 3 and 6 months. As a result of the intoxication highly toxic intermediate 2,4,5-trichlorophenol was accumulated in liver tissue of the animals kept on the disbalanced diet. The data obtained suggest that the increased accumulation of 2,4,5-trichlorophenol in liver tissue, as a result of intoxication with trichlorometaphos-3, potentiated the effect of essential nutrients deficiency on stimulation of the monooxygenase system.
Amino Acids, Essential↗
Vitamin C deficiency and risk of myocardial infarction: prospective population study of men from eastern Finland.
OBJECTIVE: To examine the association between plasma vitamin C concentrations and the risk of acute myocardial infarction. DESIGN: Prospective population study. SETTING: Eastern Finland. SUBJECTS: 1605 randomly selected men aged 42, 48, 54, or 60 who did not have either symptomatic coronary heart disease or ischaemia on exercise testing at entry to the Kuopio ischaemic heart disease risk factor study in between 1984 and 1989. MAIN OUTCOME MEASURES: Number of acute myocardial infarctions; fasting plasma vitamin C concentrations at baseline. RESULTS: 70 of the men had a fatal or non-fatal myocardial infarction between March 1984 and December 1992.91 men had vitamin C deficiency (plasma ascorbate < 11.4 mumol/l, or 2.0 mg/l), of whom 12 (13.2%) had a myocardial infarction; 1514 men were not deficient in vitamin C, of whom 58 (3.8%) had a myocardial infarction. In a Cox proportional hazards model adjusted for age, year of examination, and season of the year examined (August to October v rest of the year) men who had vitamin C deficiency had a relative risk of acute myocardial infarction of 3.5 (95% confidence interval 1.8 to 6.7, P = 0.0002) compared with those who were not deficient. In another model adjusted additionally for the strongest risk factors for myocardial infarction and for dietary intakes of tea fibre, carotene, and saturated fats men with a plasma ascorbate concentration < 11.4 mumol/l had a relative risk of 2.5 (1.3 to 5.2, P = 0.0095) compared with men with higher plasma vitamin C concentrations. CONCLUSIONS: Vitamin C deficiency, as assessed by low plasma ascorbate concentration, is a risk factor for coronary heart disease.
Adult↗
Treatment of anemia with microencapsulated ferrous fumarate plus ascorbic acid supplied as sprinkles to complementary (weaning) foods.
BACKGROUND: Standard therapy for anemia in infants is ferrous sulfate drops administered 3 times/d. Adherence to treatment, however, is often poor. One likely reason for poor adherence is the unpleasant side effects associated with drops. OBJECTIVE: The objective was to evaluate the use of a new form of iron and a delivery system to treat anemia in infants that is likely to produce better adherence to treatment. DESIGN: Using a prospective, randomized, controlled design, we studied 557 anemic children aged 6-18 mo (hemoglobin: 70-99 g/L) in rural Ghana. One group received a daily sachet of microencapsulated ferrous fumarate (80 mg elemental Fe) in powder form plus ascorbic acid to be sprinkled onto any complementary food eaten (sprinkles group); a control group received ferrous sulfate drops 3 times/d for 2 mo (total dose: 40 mg elemental Fe). Hemoglobin and serum ferritin concentrations were measured at baseline and at the end of treatment. RESULTS: Successful treatment of anemia (hemoglobin > 100 g/L) occurred in 58% of the sprinkles group and in 56% of the drops group, with minimal side effects in both groups. Geometric mean ferritin concentrations increased significantly in each group from baseline to the end of treatment (P < 0.001). CONCLUSION: Use of ferrous sulfate drops or a single daily dose of microencapsulated ferrous fumarate sprinkles plus ascorbic acid resulted in a similar rate of successful treatment of anemia without side effects. To our knowledge, this is the first demonstration of the use of microencapsulated iron sprinkles to treat anemia. Improved ease of use may favor the use of sprinkles to deliver iron.
Anemia, Iron-Deficiency↗
Vitamin nutrition in older adults.
Proper vitamin nutrition is essential for all people but especially for elderly persons, because they are at higher risk for deficiency than younger adults. A review of the clinical effects of vitamin deficiency shows how easily deficiency can masquerade as other morbidities, such as skin, neurologic, and gait abnormalities. Given the numerous readily available forms and sources of supplementation, their low cost, and their rather limited potential for harm, the goal of good vitamin nutrition for the elderly is easily attainable. To be successful in this goal, physicians must look for patients at risk and for those with features of frank vitamin deficiency. Laboratory testing is most helpful with respect to vitamin B12 and folate deficiency. Given the great value of clinical assessment, the low cost of vitamins, and the higher cost of laboratory testing, the authors do not recommend testing before instituting multivitamin use or extra supplementation with individual vitamins unless the diagnosis of deficiency is in question or the use of supplementation would put the patient at risk. The authors' general recommendations are * one multivitamin daily * extra vitamin E for patients with cardiovascular risk factors or Alzheimer's dementia * extra vitamin D for patients with known osteoporosis, osteoporosis risk factors, or strong risk factors for vitamin D deficiency * extra folate for patients with cardiovascular risk factors (especially smokers) and alcoholics * extra thiamine for alcoholics.
Aged↗