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PubMed1982

The effect of ascorbate, hydroperoxides, and bradykinin on prostaglandin production by corneal and lens cells.

Epithelial cells from the rabbit cornea, fibroblasts from the rabbit and calf cornea, and calf lens epithelial cells were placed in individual cultures. Prostaglandin (PG) synthesis by these cell types was determined. Lens epithelial cells produced no detectable PGs under basal conditions. Corneal fibroblasts primarily produced PGE2, while epithelial cells primarily produced thromboxane A2. PG production by corneal fibroblasts was highly responsive to bradykinin, ascorbic acid, hydrogen peroxide, and t-butyl hydroperoxide, an organic peroxide. Quantitative differences in PG production between the rabbit and calf corneal fibroblasts were observed. Our results suggest that the reported therapeutic actions of ascorbic acid in the eye may, at least in part, be mediated through the PGs. Our results also support the proposed role for hydroperoxides in the control of PG synthesis.

Animals↗
PubMed1978

Drug interference in clinical chemistry: studies on ascorbic acid.

The expert group "Drug Interference in Clinical Chemistry" of the Bureau of Reference, Directorate General for Research, Science and Education of the Commission of the European Communities, consisting of one participant of each member of the European Communities, presents this first report on the final results of its activities. Within the framework of a first stage basic program, the paper describes interferences of therapeutic and elevated doses of ascorbic acid on commonly used clinical chemical methods. This is the result of a bipartite study that was jointly planned, carried out and evaluated. Local and personal influences have been eliminated, as have variations due to methodology, measurement equipment and reagents, in order to be able to present distinct causal effects of ascorbic acid. No definite influence of ascorbic acid on analytical values for urea, cholesterol, calcium, protein, bilirubin, aspartate aminotransferase and alkaline phosphatase could be detected. At therapeutic concentrations, ascorbic acid distinctly interferes with the analysis of glucose, uric acid, creatinine and inorganic phosphate. The extent and direction of interferences vary, depending on the type of reaction, kit and apparatus. In some cases the influence of ascorbic acid results in severe disturbance of the analytical methods leading to useless values.

Ascorbic Acid↗
PubMedDate not supplied

Ascorbic acid enhances hypoxic ventilatory reactivity in elderly subjects.

The reducing properties of ascorbic acid in the carotid body make it a likely modifier of hypoxia-sensing mechanisms. This open-label study aimed to determine the effect of ascorbic acid on the hypoxic ventilatory response (HVR) in a population of elderly women, in whom both hypoxic reactivity and ascorbic acid levels may be deficient. We examined the HVR to progressive eucapnic hypoxia in 18 healthy females aged 60-80 years, before and after 10 days' ascorbic acid supplementation, given as a sustained release preparation of 1 g twice daily. Respiratory variables were recorded breath by breath, and hypoxic sensitivity was assessed from the linear slopes of minute ventilation and mouth occlusion pressure plotted against oxygen saturation. We found that ascorbic acid increased the HVR by a mean of 44%, this effect being driven by a higher occlusion pressure. We conclude that augmentation of hypoxic reactivity by ascorbic acid may have therapeutic potential in pathologies associated with hypoxia, which frequently develop in old age.

Aged↗
PubMed1998

Growth suppression of malignant leukemia cell line in vitro by ascorbic acid (vitamin C) and its derivatives.

In recent years there has been a growing interest in the therapeutic application of L-ascorbic acid (AA) and its derivatives as anticancer agents. AA is a gamma-crotonolactone derivative with reactive hydroxyl groups at the 2- and 3-positions and an ethylene glycol substitution at the 4-position. Despite the various reports on AA toxicity, no work has been reported underlying the critical chemical structural features for its activity. The present study addresses this question. We tested in vivo, using malignant leukemia cell line P388D1, (i) L-AA and its isomers, (ii) substitution at the 2-position: -PO4, -SO4, O-Me, O-octadecyl, (iii) substitution at the 6-position: -PO4, -SO4, -palmitate, -stearate, (iv) substitution at the 2,6-position: dipalmitate, (v) 6-deoxy derivative: -Cl, -Br, -NH2 and (vi) dihydroxy gamma-crotonolactone with substitutions at the 4-position: -H, -CH3, -CH2-CH3 and -CH=CH2. L-AA and its isomers were very cytotoxic even at very low concentration. All 6-substituted and 6-deoxy derivatives were as toxic as AA. However, 2-substituted and 2,6-disubstituted AA derivatives were non-toxic. Interestingly, dihydroxy gamma-crotonolactone with or without substitution at the 5-position also exhibited toxicity. These results suggest that the underlying criterion for AA toxicity resides in dihydroxy gamma-crotonolactone moiety. Either substitution in the hydroxy groups or saturating the double bond render the molecule inactive.

Animals↗
PubMed1997

Effect of vitamin C on prostate cancer cells in vitro: effect on cell number, viability, and DNA synthesis.

BACKGROUND: Many studies describe the protective role of vitamin C (ascorbic acid) against cancer development and in treatment of established cancer. The present study investigated whether ascorbic acid demonstrates a therapeutic benefit for prostate cancer. METHODS: Androgen-independent (DU145) and androgen-dependent (LNCaP) human prostate cancer cell lines were both treated in vitro with vitamin C (0-10 mM). Cell counts, cell viability, and thymidine incorporation into DNA were determined. RESULTS: Treatment of DU145 and LNCaP cells with vitamin C resulted in a dose- and time-dependent decrease in cell viability and thymidine incorporation into DNA. Vitamin C induced these changes through the production of hydrogen peroxide; addition of catalase (100-300 units/ml), an enzyme that degrades hydrogen peroxide, inhibited the effects of ascorbic acid. Superoxide dismutase, an enzyme that dismutates superoxide and generates hydrogen peroxide, did not prevent decreases in cell number and DNA synthesis, suggesting further the involvement of hydrogen peroxide in vitamin C-induced changes. These results clearly indicate that reactive oxygen species (ROS) are involved in vitamin C-induced cell damage. However, that singlet oxygen scavengers such as sodium azide and hydroquinone and hydroxyl radical scavengers such as D-mannitol and DL-alpha-tocopherol did not counteract the effects of ascorbic acid on thymidine incorporation suggests that vitamin C-induced changes do not occur through the generation of these ROS. CONCLUSIONS: Vitamin C inhibits cell division and growth through production of hydrogen peroxide, which damages the cells probably through an as yet unidentified free radical(s) generation/mechanism. Our results also suggest that ascorbic acid is a potent anticancer agent for prostate cancer cells.

Androgens↗
PubMed1979

Effect of dietary supplementation of iron and ascorbic acid on lead toxicity in rats.

In our laboratory, the protective and therapeutic effects of surplus dietary iron and ascorbic acid on cadmium toxicity in rats have been studied and in this experiment, an effect of surplus iron and ascorbic acid on lead toxicity was examined. In young rats ingesting a diet containing 500 ppm of lead, growth retardation and anemia were observed. Suplementation of 400 ppm of iron and 1% of ascorbic acid to the lead containing diet prevented the growth depression and anemia and caused reductions of concentrations of lead in the kidney and tibia. Whereas, addition of 50 ppm of cadmium to the lead containing diet aggravated the growth retardation and anemia, but reduced the concentrations of lead in the kidney and tibia. Dietary supplementation of iron to the lead containing diet prevented the growth depression and anemia and reduced the accumulation of lead in the kidney, however the supplementation of ascorbic acid alone did not show any ameliolative effects. Rats were fed the lead containing diet and then transferred to the basal diet with or without iron and ascorbic acid. Recoveries from the growth retardation and anemia were not observed in rats within a week after the transfer to the non-lead diet with or without iron and ascorbic acid. These results suggest that iron prevents the growth depression and anemia in rats ingesting lead by an inhibition of lead asborption.

Animals↗
PubMedDate not supplied

[Metabolism of histamine in patients with coronary atherosclerosis].

In patients with coronary atherosclerosis in I and III stages content of histamine in blood, excretion of free histamine with urine, activities of serum histidine decarboxylase and diaminooxidase, histaminopexy of blood serum and content of antihistamine factor were studied. In patients with the disease of the I stage during the attacks of stenocardia content of histamine in blood, the activity of diaminooxidase and content of degranulated basophils were increased, but the histidine decarboxylase activity, histaminopexy, content of antihistamine factor and excretion of free histamine with urine were normal. During the stenocardia attacks in patients with coronary atherosclerosis of the III stage content of degranulated basophils, the histidine decarboxylase activity were increased, histaminopexy and titres of antihistamine factor were decreased. Between the content of histamine in blood and the diaminooxidase activity no correlation was observed. This lack of correlation could cause development of hyperhistaminaemia and increased excretion of free histamine with urine. Antihistamine and desensitizing preparations (pipolphen, heparin, amidopyrine and ascorbic acid) increased the therapeutic efficiency of vasodilating drugs, decreased stenocardia attacks, accelerated both clinical improvement and normalization of histamine metabolism.

Coronary Disease↗
PubMedDate not supplied

Results of a phase II protocol for evaluation of new chemotherapeutic regimens in patients with inoperable non-small cell lung carcinoma (EST-2575, generation I).

Two hundred and eighty-four patients with inoperable non-small cell lung carcinoma were randomized by the Eastern Cooperative Oncology Group to receive one of seven primary chemotherapy regimens: cyclophosphamide and methotrexate; Baker's antifol; vincristine, bleomycin, and methotrexate; melphalan; cyclophosphamide and CCNU (control arm); 5-FU procarbazine; and hexamethylmelamine, doxorubicin, and methotrexate (HAM). Patients with disease progression were eligible for treatment with VM-26 or ascorbic acid. HAM resulted in higher response rates than cyclophosphamide and CCNU in patients with adenocarcinoma (32%) and large cell carcinoma (23%). It was not tested in patients with squamous cell carcinoma. In terms of survival, HAM was significantly better than cyclophosphamide and CCNU in patients with limited disease. Its toxicity was predominantly hematologic and gastrointestinal. This regimen is being further evaluated by the Eastern Cooperative Oncology Group in patients with inoperable non-small cell lung carcinoma. Crossover therapy with VM-26 or ascorbic acid had no therapeutic benefit.

Adenocarcinoma↗
PubMedDate not supplied

Reversible effects of sodium fluoride ingestion on spermatozoa of the rat.

The effects of ingestion of sodium fluoride (NaF), 10 mg/kg body weight for 50 days, on the structure and metabolism of sperm of albino rats (Rattus norvegicus), were investigated. In different groups of rats, the reversible effects upon withdrawal of NaF treatment and by administering some therapeutic agents, viz., ascorbic acid and calcium alone and in combination with NaF (50 and 70 days), on sperm structure and metabolism were also studied. The results revealed that the sperm acrosomal hyaluronidase and acrosin were reduced after 50 days of NaF treatment. Sperm stained with acidic alcoholic silver nitrate revealed acrosomal damage and deflagellation, which might be causative factors for the reduced activity of the enzymes. These alterations also resulted in a decline in sperm motility. The cauda epididymal sperm count was decreased, perhaps because of spermatogenic arrest. Thus, the low sperm motility and count ultimately contributed toward reduction in fertility by NaF treatment. However, withdrawal of NaF treatment for 70 days produced incomplete recovery, while administration of ascorbic acid and calcium, individually and in combination, brought about significant recovery of fluoride-induced effects. Thus, the effects of fluoride on sperm structure and metabolism of rats are transient and reversible.

Acrosin↗
PubMed1996

[Angiodysplasia of the right colon and aortic stenosis. A case report].

We report the case of a female patient who came to our observation for a severe enterorrhage. Following colonoscopic examination and color-Doppler M-B Mode echocardiography we made the following diagnosis: "angiodysplasia of the right colon in females with aortic stenosis". It was possible to ascertain whether there were similar lesions in other parts of the gastro-intestinal tract because the patient opposed firmly. In agreement with other authors, we believe that colonoscopic examination is the appropriate method to diagnose gastro-intestinal angiodysplasia. The advanced age and the clinical conditions of the patient did not allow surgical treatment, so we treated her with antihaemorrhagic drugs and elevated doses of ascorbic acid (4 g/die). The disappearance of enterorrhagies, the rapid clinical recovery and the normalization of red blood cell (RBC) count allowed us to discontinue antihaemorrhagic treatment and to continue the administration of elevated doses of ascorbic acid. Eight days later, the patient was discharged in good clinical condition and ascorbic acid was prescribed to be continued at home. A good clinical and haemodynamic balance was observed at the six-month follow-up. In conclusion we think that the clinical case we observed, characterized by the association angiodysplasia of the right colon-aortic stenosis, may be included in the diction Heyde's syndrome. In aging patients with severe concomitant diseases, ineligible for surgical interventions, the enterorrhage caused by a non complicated angiodysplastic lesion of the gastro-intestinal tract may benefit from the acute administration of ascorbic acid as the therapeutic agent of first choice capable to loose and/or stop the haemorragic complication and, in chronic administration, to reduce the number of relapses.

Aged↗
PubMed1997

Quercetin protects cutaneous tissue-associated cell types including sensory neurons from oxidative stress induced by glutathione depletion: cooperative effects of ascorbic acid.

Oxidation reactions are essential biological reactions necessary for the formation of high-energy compounds used to fuel metabolic processes, but can be injurious to cells when produced in excess. Cutaneous tissue is especially susceptible to damage mediated by reactive oxygen species and low-density lipoprotein oxidation, triggered by dysmetabolic diseases, inflammation, environmental factors, or aging. Here we have examined the ability of the flavonoid quercetin to protect cutaneous tissue-associated cell types from injury induced by oxidative stress, and possible cooperative effects of ascorbic acid. Human skin fibroblasts, keratinocytes, and endothelial cells were cultured in the presence of buthionine sulfoximine (BSO), an irreversible inhibitor of glutathione (GSH) synthesis. Depletion of intracellular levels of GSH leads to an accumulation of cellular peroxides and eventual cell death. Quercetin concentration-dependently (EC50: 30-40 microM) reduced oxidative injury of BSO to all cell types, and was also effective when first added after BSO washout. BSO caused marked decreases in the intracellular level of GSH, which remained depressed in quercetin-protected cells. Ascorbic acid, while by itself not cytoprotective synergized with quercetin, lowered the quercetin EC50 and prolonged the window for cytoprotection. The related flavonoids rutin and dihydroquercetin also decreased BSO-induced injury to dermal fibroblasts, albeit less efficaciously so than quercetin. The cytoprotective effect of rutin, but not that of dihydroquercetin, was enhanced in the presence of ascorbic acid. Further, quercetin rescued sensory ganglion neurons from death provoked by GSH depletion. Direct oxidative injury to this last cell type has not been previously demonstrated. The results show that flavonoids are broadly protective for cutaneous tissue-type cell populations subjected to a chronic intracellular form of oxidative stress. Quercetin in particular, paired with ascorbic acid, may be of therapeutic benefit in protecting neurovasculature structures in skin from oxidative damage.

3T3 Cells↗
PubMed1989

In vivo antimutagenic effect of ascorbic acid against mutagenicity of the common antiamebic drug diiodohydroxyquinoline.

We have previously shown that the common antiamebic drug diiodohydroxyquinoline (DIHQ) exhibits mutagenic activity in the in vivo micronucleus test in Swiss albino mice. Results of experiments undertaken to study the influence of ascorbic acid (vitamin C) on the mutagenicity of DIHQ in this model system showed that ascorbic acid acts as an antimutagen against DIHQ. The effective antimutagenic doses of ascorbic acid themselves do not show any genotoxic effects in this in vivo system. It will be necessary, however, to elucidate the mechanism of action of ascorbic acid as well as its effects on the therapeutic properties of DIHQ before a practical use of ascorbic acid is contemplated for this purpose.

Administration, Oral↗