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PubMed1990

Smoking and the antioxidant ascorbic acid: plasma, leukocyte, and cervicovaginal cell concentrations in normal healthy women.

The influence of cigarette smoking on the plasma, leukocyte, and cervicovaginal cell ascorbic acid levels in 46 healthy smokers and healthy nonsmokers was investigated. Coded peripheral venous blood and cervicovaginal lavage specimens obtained after informed consent were analyzed simultaneously for their ascorbic acid content. The findings suggest that smoking affects the levels and distribution of ascorbic acid. In smokers (n = 16), the number of exfoliated cervicovaginal epithelial cells and leukocyte ascorbic acid levels was significantly higher (p less than 0.01, p less than 0.05, respectively) compared with nonsmokers (n = 30). In addition, cervicovaginal cell ascorbic acid, plasma reduced and total ascorbic acid levels were significantly lower (p less than 0.001, p less than 0.01, p less than 0.01, respectively). The exfoliated epithelial cell ascorbic acid levels in nonsmokers was fourfold greater than that of leukocytes. The implications of these findings within the context of free radical-induced cellular pertubations in smokers are discussed.

Adult↗
PubMed1991

Investigations of the efficacy of ascorbic acid therapy in cystinuria.

We investigated ascorbic acid therapy for cystinuria in a study of seven healthy control persons and seven cystinuric patients. The study lasted 9 days. During the first period, we collected 24-h urine specimens from all subjects on 3 consecutive days. Starting on day 4, all were given 5 g ascorbic acid/day for a period of 6 days. On the last 3 days, 24-h urine specimens were again collected. Quantitative amino acid determination was performed using an HPLC method described elsewhere. During ingestion of ascorbic acid, the mean excretion of cysteine by the control group increased from 134.1 to 159 mumol/day, whereas the excretion of cystine decreased from 107.1 to 82 mumol/day. The corresponding values for the cystinuric patients increased from 352.4 to 452.1 mumol/day for cysteine and decreased from 4,131.6 to 3,663.2 mumol/day for cystine. Thus, ascorbic acid seems to have only mild reducing properties in respect to cystine.

Ascorbic Acid↗
PubMed2001

Iron loading and large doses of intravenous ascorbic acid promote lipid peroxidation in whole serum in guinea pigs.

Large doses of ascorbic acid may mobilise Fe from Fe-binding proteins in vivo which in turn could catalyse lipid peroxidation, a process associated with degenerative diseases. This hypothesis was tested in vitro in the serum of Fe-loaded animals. Eighteen male guinea pigs weighing about 500 g on arrival were allocated to two groups of nine. Fe loading was induced in one group by two intraperitoneal injections of 200 mg iron dextran given on days 1 and 5. Blood (6 ml) was drawn from all animals on day 12 by cardiac puncture. Serum and LDL were separated. Serum was tested for loosely-bound Fe (bleomycin assay) and lipid peroxidation (thiobarbituric acid reactive substances (TBARS) assay) and LDL for susceptibility to in vitro oxidation (TBARS and conjugated diene assays). On day 12, another intraperitoneal injection of 200 mg iron dextran was given to the animals in the Fe-loaded group. On day 19, all animals were given 75 mg ascorbic acid by intraperitoneal injection. Blood (6 ml) was drawn 4 h later by cardiac puncture. Serum and LDL assays were repeated. Ascorbic acid increased loosely-bound Fe and in vitro oxidation in the serum from animals of the Fe-loaded group but not in the serum from animals of the control group. Susceptibility of LDL to in vitro oxidation increased after the ascorbic acid injection in the control group but there was no further increase in the Fe-loaded group. These data suggest that large doses of ascorbic acid promote Fe mobilisation and in vitro oxidation in the serum of Fe-loaded animals.

Animals↗
PubMed1982

Ascorbic acid and cortisol metabolism in hypovitaminosis C guineapigs.

The relationship between the metabolic changes in tissue ascorbic acid (AA) and the release of 11-hydroxy corticosteroids (cortisol) into the blood of male and female guineapigs fed on vitamin C-deficient diet, has been investigated. The animals received the diet for 30 and 36 days (males and females respectively) during which tissue AA and Corticol concentrations were analysed at six-day intervals. Bodyweight and adrenal weights were also recorded. When guineapigs are deprived of vitamin C in their diet, tissue cortisol and ascorbic acid concentrations undergo concurrent metabolic changes. There is a close association between the metabolic changes in adrenal cortisol secretion and ascorbic acid release into the plasma as shown by the regression and correlation values. Adrenal ascorbic acid concentration falls as cortisol secretion into the plasma increases. These results indicate that adrenal ascorbic acid operates a modulating role over the production of adrenal steroids during stress in guineapigs.

Adrenal Glands↗
PubMed1977

Effect of ascorbic acid on plasma cholesterol in humans in a long-term experiment.

During the period of a low vitamin C intake (approximately equal to 20 mg per day) ascorbic acid in a dose of 2 x 500 mg per day was administered to 82 men and women aged 50-75 years. A correlation of plasma cholesterol levels determined before and after a three months' administration of ascorbic acid showed the effect of vitamin C to be dependent on the starting concentration of plasma cholesterol: the higher the initial cholesterolemia, the greater the hypocholesterolemic effect of ascorbic acid. On restricting the experimental group to subjects with an initial cholesterolemia above 230 mg%, the effect of the same dose of ascorbic acid on cholesterolemia was followed in three-month periods for a further 9 months. In all these time intervals, ascorbic acid was found significantly to depress cholesterolemia and its effects persisted 6 weeks after termination of the experiment. The administration of 2 x 500 mg ascorbic acid daily during one year resulted in an abrupt increase of ascorbemia and a marked accumulation of ascorbic acid in the leucocytes. Six weeks following interruption of ascorbic acid intake, vitamin C concentration in the leucocytes significantly declined but still continued to be twice higher than in the control receiving no ascorbic acid supplement.

Aged↗
PubMed1986

Stimulatory effect of ascorbic acid on norepinephrine biosynthesis in digitonin-permeabilized adrenal medullary chromaffin cells.

The regulatory role of ascorbic acid in norepinephrine biosynthesis was studied using digitonin-permeabilized chromaffin cells. When permeabilized chromaffin cells were incubated with [3H]3,4-dihydroxyphenylethylamine ([3H]dopamine) in calcium-free medium, the amounts of radioactive dopamine and norepinephrine measured in the cell fraction were increased as a function of incubation time and dopamine concentration. Both the accumulation of dopamine and the formation of norepinephrine were shown to require the presence of Mg-ATP in the medium. These results indicate that the permeabilization of chromaffin cells by digitonin treatment does not disrupt the functions of chromaffin granules, including dopamine uptake, norepinephrine formation, and storage of these amines. Using this permeabilized cell system, the effect of ascorbic acid on the rates of dopamine uptake and hydroxylation was investigated. The formation of norepinephrine was stimulated by ascorbic acid at concentrations of 0.5-2 mM in the presence of Mg-ATP. By contrast, dopamine uptake was not affected by the presence or absence of ascorbic acid in the medium. These findings provide evidence that ascorbic acid may stimulate the conversion of dopamine to norepinephrine by increasing dopamine beta monooxygenase activity rather than by increasing the substrate supply of dopamine. These observations also suggest that the rate of norepinephrine biosynthesis in adrenal medullary cells may be regulated by the concentration of ascorbic acid within the cell cytoplasm.

Adenosine Triphosphate↗
PubMed2000

Aortic wall damage in mice unable to synthesize ascorbic acid.

By inactivating the gene for L-gulono-gamma-lactone oxidase, a key enzyme in ascorbic acid synthesis, we have generated mice that, like humans, depend on dietary vitamin C. Regular chow, containing about 110 mg/kg of vitamin C, is unable to support the growth of the mutant mice, which require L-ascorbic acid supplemented in their drinking water (330 mg/liter). Upon withdrawal of supplementation, plasma and tissue ascorbic acid levels decreased to 10-15% of normal within 2 weeks, and after 5 weeks the mutants became anemic, began to lose weight, and die. Plasma total antioxidative capacities were approximately 37% normal in homozygotes after feeding the unsupplemented diet for 3-5 weeks. As plasma ascorbic acid decreased, small, but significant, increases in total cholesterol and decreases in high density lipoprotein cholesterol were observed. The most striking effects of the marginal dietary vitamin C were alterations in the wall of aorta, evidenced by the disruption of elastic laminae, smooth muscle cell proliferation, and focal endothelial desquamation of the luminal surface. Thus, marginal vitamin C deficiency affects the vascular integrity of mice unable to synthesize ascorbic acid, with potentially profound effects on the pathogenesis of vascular diseases. Breeding the vitamin C-dependent mice with mice carrying defined genetic mutations will provide numerous opportunities for systematic studies of the role of antioxidants in health and disease.

Animals↗
PubMed1984

Hydroxylation of deoxyguanosine at the C-8 position by ascorbic acid and other reducing agents.

The C-8 position of deoxyguanosine (dGuo) was hydroxylated by ascorbic acid in the presence of oxygen (O2) in 0.1 M phosphate buffer (pH 6.8) at 37 degrees C. Addition of hydrogen peroxide (H2O2) remarkably enhanced this hydroxylation. The Udenfriend system [ascorbic acid, FeII, ethylenediaminetetraacetic acid (EDTA) and O2] was also effective for hydroxylation of dGuo in high yield. Guanine residues in DNA were also hydroxylated by ascorbic acid. Other reducing agents, such as hydroxylamine, hydrazine, dihydroxymaleic acid, sodium bisulfite and acetol, were also effective for the hydroxylation reaction, as were metal-EDTA complexes (FeII-, SnII-, TiIII-, CuI-EDTA). An OH radical seemed to be involved in this hydroxylation reaction in most of the above hydroxylating systems, but another reaction mechanism may also be involved, particularly when dGuo is hydroxylated by ascorbic acid alone or ascorbic acid plus H2O2. The possible biological significance of the hydroxylation of guanine residues in DNA in relation to mutagenesis and carcinogenesis is discussed.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2001

Biochemical and hemodynamic effects of ascorbic acid and alpha-tocopherol in coronary artery surgery.

This study was undertaken to evaluate the effects of alpha-tocopherol and ascorbic acid on markers of myocardial reperfusion injury and myocardial contractile function after coronary artery surgery. Forty-eight patients were divided into 4 groups; 300 mg/day alpha-tocopherol was given orally to the patients in group I for 14 days. In groups II and III, 4g of ascorbic acid was administered intravenously prior to induction and in the cardioplegic solution, respectively. Group IV was the control group. Blood samples were taken to determine the concentrations of creatine phosphokinase MB isoenzyme, malondialdehyde, uric acid, ascorbic acid and alpha-tocopherol in the perioperative period. Left ventricular functions were determined by means of MUGA scans and echocardiography preoperatively and on the 3rd and 7th days, postoperatively. The changes in serum creatine phosphokinase MB and malondialdehyde were significantly lower in study groups. when compared with the control group. We observed no significant changes in ventricular function, requirement for (+) inotropic agents and the incidence of ventricular arrhythmias among the groups, postoperatively. Biochemical findings are consistent with the free radical hypothesis. But we could not confirm these data with hemodynamic findings. This is probably due to the population of low-risk elective coronary surgery patients in this study.

Aged↗
PubMed1994

Ascorbic acid (vitamin C) modulates the mutagenic effects produced by an alkylating agent in vivo.

Recent reports suggest that ascorbic acid (vitamin C) inhibits tumorigenesis as well as exerts a protective effect against mutagenesis in vitro; however, there is no information on its ability to affect gene mutations induced in vivo. In this study, we have investigated the antimutagenic effects of ascorbic acid on the frequency of 6-thioguanine-resistant (6-TGr) T-lymphocytes produced in Fischer 344 rats dosed with the direct-acting alkylating agent, N-ethyl-N-nitrosourea (ENU). The frequency of 6-TGr T-lymphocytes from the spleen measured five weeks after ENU treatment indicated that ENU produced a substantial mutagenic response. Pretreatment and/or post-treatment of rats with ascorbic acid administered in the drinking water appeared to inhibit the response, but the inhibition was statistically significant only when data from the various dosing schedules were pooled. In addition, there was no clear dose-dependency to the inhibitory effect of ascorbic acid. To further evaluate the time effects of the vitamin supplement on ENU mutagenicity, rats were exposed to the mutagen together with ascorbic acid, which was given continuously for the entire duration of the experiment. At specific times after ENU treatment, the frequency of 6-TGr T-cells was determined in lymphocytes isolated from the spleen and the thymus. Time-dependent increases in the frequency of 6-TGr T-cells were observed with ENU treatment; ascorbic acid significantly reduced the ENU-mediated mutagenic responses, most dramatically in the spleen at weeks 6 and 8 (P < 0.0001), and to a lesser extent in the thymus (P < 0.01 at week 6 and P < 0.006 at week 8). Our data suggest that ascorbic acid intake affects the in vivo mutagenicity of ENU, a direct-acting mutagen/carcinogen, and that the reported inhibitory effects of the antioxidant on carcinogenesis may be partially mediated by its effects on mutagenesis. Although it is difficult to extrapolate from rodent studies to humans, the results presented suggest an explanation for epidemiological data that link vitamin C ingestion with decreased cancer risk.

Administration, Oral↗