Acta vitaminologica et enzymologica最新文献

There is evidence that oxygen-derived free radicals may play a role in myocardial ischaemic and reperfusion injury. Major sources of O2 free radicals formation during ischaemia and reperfusion are: the enzyme xanthine oxidase, activated neutrophils and the myocardial mitochondria. However, in the heart there are defense mechanisms against the toxic oxygen metabolites. They include the enzyme superoxide dismutase, catalase and glutathione peroxidase plus endogenous antioxidants like vitamin E, ascorbic acid and cysteine. We have investigated in the isolated rabbit hearts the effects of ischaemia and reperfusion on these defence mechanisms. 90 min of ischaemia and/or hypoxia induced a significant reduction of mitochondrial superoxide dismutase, and of reduced glutathione/oxidized glutathione ratio which was further declined after reperfusion indicating that an oxidative stress has occurred. These alterations are associated with massive tissue and mitochondrial calcium accumulation, loss of mitochondrial function and severe membrane damage. The effects of vitamin E on these parameters have been investigated. Administration of 1.1 mg of dl-alpha-tocopherol acetate showed a protective effect on mitochondrial function but it failed to improve the recovery of mechanical function during reperfusion.

Dysplasia is an alteration of organ and tissues cellular composition. It means quantitative and qualitative variations (differentiation) of the cells. More recently many Authors have investigated about epithelial neoplasia (breast, cervix, lung, respiratory tract, bladder, colon) and dysplastic epithelial processes and about their medical treatment and prevention of potentially transformative lesions. The view that certain vitamins such as vitamin A (in the form of retinol or its precursor beta-carotene) and vitamin E may protect against the risk of cancer has recently attracted much scientific attention. The potential use of retinoids (and alpha tocopherol) for chemoprevention has been demonstrated by numerous recent experiences. In gynaecology there are no evidence of therapeutical investigations about endometrial and ovarian dysplastic lesions, and then about protective role for consequent neoplasia development. Regarding cervical cancer there are only epidemiological retrospective data about dietary intake of vitamin A. The clinical trial is insufficient, perhaps for technical difficulties of administration, but we hope to obtain satisfactory results in the future. Benign breast disease, instead, so present in woman's life (in particular in fertile phase) is the most common clinical syndrome encompassing several distinct histopathological varieties. BBD is associated with an increase in breast cancer risk, particularly related to the presence of epithelial hyperplasia. In our study (collaborative study; University of L'Aquila--University of Rome) we have treated a group of women (double-blind trial) affected by breast dysplasia, with vitamin A and E association to evaluate the effectiveness of retinoids and alpha-tocopherol in reducing or resolving clinical palpable breast findings (with pain, tension, nodularity and instrumental patterns).(ABSTRACT TRUNCATED AT 250 WORDS)

The epithelio-protective activity of a combination of retinol and tocopherol has been studied. The two vitamins have been administered orally to a group of patients suffering from different corneal diseases. A control group was treated with a placebo associated to the usual topical therapies. With some reserve, the evaluation of the vitamin therapy is positive as the epithelial repairing was more rapid in the vitamin treated group, but the poor homogeneity of the corneal diseases permits a qualitative analysis only.

It is known that the bioflavonoids as the Ca++ have an enhancing effect on the transmitter release in different cholinergic nerve-endings. For this reason, it is seemed interesting to study the influence of the separately tested 4-methylesculetin or associated with the ascorbic acid and comparatively the Ca++ concentration increase on the isolated rat stomach response by electrical transmural stimulation achieved in presence or absence of hexamethonium. Both the 4-methylesculetin and the ascorbic acid have always increased the response of the preparation submitted to electrical transmural stimulation. The 4-methylesculetin effect resulted particularly strong if the substance was employed with the ascorbic acid. The enhancing effect of the 4-methylesculetin, obtained with or without the ascorbic acid, is resulted comparatively lesser in presence of hexamethonium. On the basis of the evident analogy between the 4-methylesculetin effects and the ones determined by the increased Ca++ concentration, it can be supposed that the bioflavonoid facilitates the transmitter release in the pre- and postganglionic nerve-endings. The results here reported, confirm other previous observations accomplished on different cholinergic nerve-endings and could substain the hypothesis according to which the 4-methylesculetin increase the Ca++ transport through the biological membranes.

The effect of some reductones such as ascorbic acid (AsA), triose reductone (TR), epinephrine (Ep) and their derivatives on cyclic 3', 5'-adenosine monophosphate phosphodiesterase (cAMP PDE) was studied in the presence or absence of Cu2+. AsA, TR, Ep and the reductones related to them inhibited cAMP PDE activity. Among the reductones, TR showed the highest inhibition. AsA, 5-methyl-3,4-dihydroxytetrone, pyrocatechol, p-hydroxyquinone and resorcinol had a relatively high inhibiting activity. The type of inhibition of AsA, TR and Ep was uncompetitive, competitive and noncompetitive, respectively. Cu2+ enhanced the inhibitory action of the reductones markedly and altered the type of inhibition of the reductones.

Forty-two female college students, age 18-29 yr. and consuming nutritionally balanced meals in the college cafeteria participated. Subjects discontinued all vitamin-mineral supplements (VMS) for 17 days and were randomly assigned to one of two treatments, either a placebo, or VMS supplying the United States Recommended Daily Allowance (USRDA) of all vitamins, zinc, iron, iodine, copper, and 60% of the USRDA of calcium, 50% of magnesium and 45% of phosphorus. Treatments were consumed for 77 days. Fasting pre-and post-treatment blood chemistries were compared. VMS yielded significant increases (p less than 0.05) in serum vitamin B-12 (+25.05 pg/ml), vitamin C (+0.35 mg/dl) and folate (+7.40 ng/ml). No significant changes (p greater than 0.05) in hematological or other blood chemistries were observed. Significant decreases in the number of below-normal serum indicators of vitamin status (p less than 0.05) and iron status (p less than 0.005) were seen with VMS. No significant changes were seen with placebo (p greater than 0.05).

Early administration of vitamin E to low birth weight (less than 1500 g) infants results in alleviation of the symptoms of retinopathy of prematurity and a lowered incidence of intraventricular hemorrhage. If vitamin E is given to children with cholestatic liver disease (orally or parenterally) before 3 years of age, neurological symptoms such as areflexia, ataxia, and sensory neuropathy are prevented or reversed. Restitution of neurological function is more limited in children ages 5-17 years even after prolonged therapy. Vitamin E is also useful in prevention of neuropathy and retinopathy associated with abetalipoproteinemia and cystic fibrosis. Blood levels of tocopherol are often low in subjects with hemolytic anemias. Administration of vitamin E to G-6-P-D-deficient subjects increased hemoglobin levels, and decreased the number of irreversibly sickled cells in sickle-cell anemia subjects. Most trials have indicated that administration of vitamin E for 6 months or more to subjects with intermittent claudication results in longer walking distance and improved blood flow. Vitamin E reduces platelet aggregation, platelet adhesion to collagen, and platelet thromboxane production. Prostacyclin production is generally enhanced. The significance of these effects to thrombotic diseases. Epidemiological studies have indicated that subjects with higher blood levels of vitamin E have lower risk of death from ischemic heart disease and cancer, a lower risk of breast cancer, and a lower incidence of infections.

The mechanism of the phenylhydrazine induced oxidative hemolysis was studied on the point of role of the free radical scavengers in rats. Phenylhydrazine resulted in the degradation of hemoglobin and the lipid peroxidation of the erythrocyte membrane. Otherwise, the elevation of coenzyme Q9, endogenous CoQ in rats, levels in plasma was observed against the phenylhydrazine induced oxidative stress. Supplementation of coenzyme Q10, exogenous CoQ in rats, inhibited the phenylhydrazine induced hemolysis according to the suppression of both the degradation of hemoglobin and the lipid peroxidation of the erythrocyte membrane. These results suggest that free radical scavengers such as coenzyme Q9 and coenzyme Q10 have important roles on the phenylhydrazine induced hemolysis in rats.

In beta-thalassemic homozygotes, low plasma levels of tocopherols may induce a red blood cell (RBC) lipid peroxidation and consequent hemolysis. This is an indication to treat these patients with vitamin E. In this study 26 beta-thalassemic homozygotes aged 2-14 years, were given vitamin E, 10 orally and 16 parenterally, 300 mg per day for 15 days. Prior to administration and blood transfusion, as compared to normal subjects of the same age, plasma and RBC tocopherols were significantly lower, whereas RBC malonyldialdehyde (MDA) was significantly increased. In both groups, after tocopherol administration, an increase in plasma and RBC tocopherols and a decrease in RBC MDA were found. The significance of these variations was greater in the parenterally treated group than in orally treated group. The treatment with vitamin E, appears to be effective to reduce the RBC oxidative damage in homozygous beta-thalassemia, principally when administered parenterally perhaps because of its poor intestinal absorption in these subjects.

Etretinate (RO 10-9359) is a synthetic retinoid used instead of Vitamin A--toxic in large dose--during treatment of some skin diseases. In this work biological properties of Etretinate were studied by administration of this drug (2 mg/kg/day) in rats in a vitamin A-deficient state. Body growth, some seric parameters and some tissue enzymatic activities were studied. Results of this restitution experiment show that Etretinate corrects all parameters affected by vitamin A-deficiency testicular growth excepted. So Etretinate exhibits properties similar to that of retinoic acid.