Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “VITAMINS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,009 records · Page 56Linked to original sources
PubMed1987

Effects of selenium, vitamin E and vitamin C on human prostacyclin and thromboxane synthesis in vitro.

The effects of three antioxidants, selenium, vitamin E and vitamin C, on the production of anti-aggregatory prostacyclin (PGI2) by human endothelial cells and lung tissue as well as on the production of pro-aggregatory thromboxane A2 (TxA2) by human platelets and lung tissue in vitro were studied. Selenium had no effect on endothelial PGI2 synthesis but it dose-dependently inhibited the platelet production of TxA2 (84% at 10(-3) mol/l) and productions of PGI2 (64%) and TxA2 (72%) by human lung. Selenium inhibited platelet TxA2 synthesis much less in the presence of exogenous arachidonic acid (AA) (14% instead of 84%), suggesting that selenium exerts its effect predominantly on phospholipase A2. Vitamin E had no effect on endothelial PGI2, pulmonary PGI2 or TxA2 syntheses but it strongly inhibited platelet TxA2 production (50% at 10(-3) mol/l). This inhibition was only partly (from 50% to 30%) counteracted by exogenous AA suggesting that vitamin E affects both phospholipase A2 and a further step(s) in the TxA2 synthetizing cascade. Vitamin C stimulated endothelial cell PGI2 production (80% at 10(-2) mol/l) but it could not counteract the inhibition of PGI2 production (83%) exerted by 10(-2) mol/l tert-butyl hydroperoxide (TBHP), a promoter of lipid peroxidation. Vitamin C had no effect on pulmonary PGI2 production but it inhibited pulmonary TxA2 formation (38% at 10(-3) mol/l). Slight inhibition of platelet TxA2 production from endogenous AA (6%) turned to slight stimulation (8%) with exogenous AA. The in vivo significance of these results is not yet known.

Antioxidants↗
PubMed1987

Effects of vitamin E, vitamin B2 and selenite on DNA single strand breaks induced by sodium chromate (VI).

The effects of vitamin E, vitamin B2 and selenite on DNA single strand breaks induced by Na2CrO4 were examined by alkaline elution. Incubation of Chinese hamster V-79 cells with alpha-tocopherol succinate (vitamin E) for 24 h prior to exposure to Na2CrO4 resulted in a decrease of DNA breaks produced by this compound. However, similar pretreatment with riboflavin (vitamin B2) or Na2SeO3 resulted in an enhanced formation of breaks induced by Na2CrO4. Pretreatment with Na2SeO3 resulted in increased levels of glutathione in these cells while levels of glutathione remained the same with vitamin E or vitamin B2. These results suggest that Na2CrO4 induced DNA breaks appear to be mediated by the formation of free radicals and/or cellular reductive metabolism.

Animals↗
PubMed1988

The plasma binding protein for vitamin D is a site of discrimination against vitamin D-2 compounds by the chick.

The binding of 25-hydroxy-[26,27-3H]vitamin D-3 and 25-hydroxy-[26,27-3H]vitamin D-2 to the vitamin D binding protein in the plasma of both rats and chicks has been studied. In the case of rats, sucrose density gradient analysis, competitive displacement, and Scatchard analysis demonstrate that 25-hydroxyvitamin D-3 and 25-hydroxyvitamin D-2 are bound equally well to the vitamin D binding protein. In contrast, 25-hydroxyvitamin D-2 is poorly bound, while 25-hydroxyvitamin D-3 is tightly bound to the vitamin D binding protein in chick plasma. On the other hand, the chick intestinal receptor binds 1,25-dihydroxyvitamin D-2 and 1,25-dihydroxyvitamin D-3 equally well with a KD of 7.10(-11) M for both compounds. These results strongly suggest that the failure of the plasma transport protein in chicks to bind the vitamin D-2 compounds may be responsible for their relative ineffectiveness in these animals.

25-Hydroxyvitamin D 2↗
PubMed1990

Effects of growth hormone administration on vitamin D metabolism and vitamin D receptors in the pig.

Twelve 36-kg pigs were given either 100 micrograms/kg porcine pituitary growth hormone (pGH) or placebo injections daily for 33 days. Serum was obtained weekly for analysis of minerals and vitamin D metabolites. On day 34, the pigs were sacrificed and renal and duodenal tissue were obtained for analysis of vitamin D receptor content (VDR). Animals treated with pGH grew faster and had a higher rate of bone accretion than did control animals. Serum concentrations of 1,25-dihydroxyvitamin D (1,25-(OH)2D) were significantly higher in pGH-treated pigs than in control pigs at all time points following initiation of treatment, with the greatest difference observed at day 28 (42.4 +/- 4.9 pg/ml in controls vs. 65.4 +/- 4.7 pg/ml in pGH-treated pigs). Serum 24,25-dihydroxy-vitamin D tended to be lower in pGH-treated pigs than in control pigs, being significantly lower on day 21 of the experiment (3.22 +/- .52 vs. 6.73 +/- 1.22 ng/ml, respectively). Serum concentrations of 25-hydroxyvitamin D and calcium were unaffected by pGH treatment. Kidneys of control pigs contained significantly more unoccupied vitamin D receptors than did kidneys from pGH-treated pigs (73.3 +/- 4.3 vs. 58.3 +/- 4.1 fmoles/mg protein). Duodenal tissue unoccupied vitamin D receptor content was similar in both pGH-treated (245 +/- 17.9 fmoles/mg protein) and control (263 +/- 21.8 fmoles/mg protein) pigs. Duodenal occupied vitamin D receptor concentration was similar in both pGH-treated (6.8 +/- .75 fmoles/mg protein) and control pigs (5.32 +/- .77 fmoles/mg protein).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Vitamin E deficiency induced neurological disease in common variable immunodeficiency: two cases and a review of the literature of vitamin E deficiency.

Vitamin E deficiency causes a neurological disorder characterised by sensory loss, ataxia and retinitis pigmentosa due to free radical mediated neuronal damage. Symptomatic vitamin E deficiency has been reported in genetic defects of the vitamin E transport protein and in malabsorption complicating cholestasis, abetalipoproteinaemia, celiac disease, cystic fibrosis and small bowel resection. There are no reports to date of vitamin E deficiency in patients with primary immunodeficiencies. We describe two CVID patients with the associated enteropathy who developed neurological disease because of vitamin E deficiency, suggesting a possible predisposition to developing this complication. We recommend that all CVID patients with evidence of an enteropathy be screened for vitamin E deficiency, as early detection and consequent treatment may prevent, halt or reverse the neurological sequelae.

Adult↗
PubMed2004

Vitamin D receptor gene polymorphisms in relation to Vitamin D related disease states.

The role in skeletal metabolism of the steroid hormone Vitamin D and its nuclear receptor (VDR) is well known. In addition, however, Vitamin D is also involved in a wide variety of other biological processes including modulation of the immune response and regulation of cell proliferation and differentiation. Variations in the Vitamin D endocrine system have thus been linked to several diseases, including osteoarthritis, diabetes, cancer, cardiovascular disease and tuberculosis. Evidence to support this pleiotropic character of Vitamin D has included epidemiological studies on circulating Vitamin D hormone levels, but also genetic epidemiological studies. Genetic studies provide excellent opportunities to link molecular insights with epidemiological data and have therefore gained much interest. DNA sequence variations which occur frequently in the population are referred to as "polymorphisms" and are usually suspected of having only modest and subtle effects. Recent studies have indicated many polymorphisms to exist in the VDR gene, but the influence of VDR gene polymorphisms on VDR protein function are largely unknown. Sofar, three adjacent restriction fragment length polymorphisms (RFLP) for BsmI, ApaI and TaqI, respectively, at the 3' end of the VDR gene have been the most frequently studied sofar. But because these polymorphisms are probably non-functional, linkage disequilibrium (LD) with one or more truly functional polymorphisms elsewhere in the VDR gene is assumed to explain the associations observed. Research is therefore focussed on documenting additional polymorphisms across the VDR gene to verify this hypothesis, and on trying to understand the functional consequences of the variations. Substantial progress has been made including the discovery of novel polymorphisms in the large promoter region of the VDR gene. Eventually, results of this research will deepen our understanding of variability in the Vitamin D endocrine system and might find applications in risk-assessment of disease and in predicting response-to-treatment.

Humans↗
PubMed2005

Selective inhibition of the C5a chemotactic cofactor function of the vitamin D binding protein by 1,25(OH)2 vitamin D3.

The Vitamin D binding protein (DBP) is a multifunctional plasma protein that can significantly enhance the chemotactic response to complement fragment C5a. The chemotactic cofactor function of DBP requires cell surface binding in order to mediate this process. The goal of this study was to investigate the effect of ligating DBP with its two primary physiological ligands, Vitamin D and G-actin, on both binding to neutrophils and the ability to enhance chemotaxis to C5a. There was no difference in neutrophil binding between of the holo (bound) forms versus the apo (unbound) form of radioiodinated DBP, indicating that the cell binding region of DBP is likely distinct from the Vitamin D sterol and G-actin binding sites. Likewise, G-actin, 25(OH)D3, and G-actin plus 25(OH)D3 bound to DBP did not alter its capacity to enhance chemotaxis toward C5a. However, the active form of Vitamin D (1,25(OH)2D3) completely eliminated the chemotactic cofactor function of DBP. Dose-response curves demonstrated that as little as 1pM 1,25(OH)2D3 significantly inhibited chemotaxis enhancement. Moreover, at physiological concentrations 1,25(OH)2D3 needs to be bound to DBP to mediate the inhibitory effect. Neutrophil chemotaxis to optimal concentrations of C5a, formyl peptide, CXCL8 or leukotriene B4 was not altered by 1,25(OH)2D3, indicating that the active vitamin does not have a global inhibitory effect on neutrophil chemotaxis. Finally, inhibition of cell surface alkaline phosphatase (AP) with sodium orthovanadate completely reversed the inhibitory effect of 1,25(OH)2D3. These results indicate that the cell binding and co-chemotactic functions of DBP are not altered when the protein binds G-actin and/or Vitamin D. Furthermore, the co-chemotactic signal from DBP can be eliminated or counteracted by 1,25(OH)2D3.

Actins↗
PubMedDate not supplied

Skin is an autonomous organ in synthesis, two-step activation and degradation of vitamin D(3): CYP27 in epidermis completes the set of essential vitamin D(3)-hydroxylases.

The current understanding of the vitamin D(3) system shows skin as the unique site of vitamin D(3) production and liver is thought to be the main site of conversion to 25(OH)D(3). Skin is capable of activating 25(OH)D(3) via 1alpha-hydroxylation and the resulting 1alpha,25(OH)(2)D(3) plays a role in epidermal homeostasis in normal and diseased skin. It also rapidly up-regulates the major vitamin D(3) metabolizing enzyme 24-hydroxylase at the mRNA level, which is an established indicator for 1alpha,25(OH)(2)D(3)-presence. We investigated the capability of primary human keratinocytes to produce 25(OH)D(3) and subsequent metabolites from vitamin D(3). Thus, by orchestrating the entire system of production, activation and inactivation, skin could be independent of other organs in supply of hormonally active vitamin D(3). First, we demonstrated substantial conversion of (3)H-D(3) to (3)H-25(OH)D(3) in primary human keratinocytes. 25-Hydroxylation was slow, followed first order rate kinetics and was not saturable under our experimental conditions. Then we showed expression of 25-hydroxylase mRNA and compared it to levels of 1alpha-hydroxylase and 24-hydroxylase. Pre-incubation with vitamin D(3) resulted in dose and time dependent up-regulation of 24-hydroxylase mRNA, whereas neither 1alpha-hydroxylase nor 25-hydroxylase expression was affected. Since both, D(3) and 25(OH)D(3) are lacking intrinsic 24-hydroxylase-inducing capacity, up-regulation had to be the consequence of a two-step activation process via 25-hydroxylation and subsequent 1alpha-hydroxylation. 24-Hydroxylase-activities closely followed the corresponding mRNA levels. When 1alpha,25(OH)(2)D(3) itself or its precursor 25(OH)D(3) were used as inducing agents, 24-hydroxylase mRNA and enzyme activity followed a transient time course. In contrast, induction observed with physiological doses of D(3) remained high, even after a 20 h-time period. These differing characteristics may be explained by the slow but constant formation of 1alpha,25(OH)(2)D(3) from a large reservoir of D(3) in the target cell, providing constant supplies for induction.

Calcitriol↗
PubMed1999

C-6 functionalized analogs of 25-hydroxyvitamin D3 and 1alpha,25-dihydroxyvitamin D3: synthesis and binding analysis with vitamin D-binding protein and vitamin D receptor.

In this article, we describe the development of a general synthetic strategy to functionalize the C-6 position of vitamin D3 and its biologically important metabolites, i.e. 25-hydroxyvitamin D3 (25-OH-D3) and 1alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3]. We employed Mazur's cyclovitamin D method to synthesize vitamin D3 analogs with several functionalities at the C-6 position. In addition, we synthesized 6-(3-hydroxypropyl) and 6-[(2-bromoacetoxy)propyl] derivatives of 25-OH-D3 15 and 16, respectively, and 6-(3-hydroxypropyl) derivative of 1,25(OH)2D3 17. Competitive binding assays of 15-17 with human serum vitamin D-binding protein showed that all these analogs specifically bound to this protein, although with significantly lower affinity than the 25-OH-D3, the strongest natural binder, but with comparable affinity with 1,25(OH)2D3, the hormone. On the other hand, 6-[3-hydroxypropyl], 1alpha,25-dihydroxyvitamin D3 17 did not show any specific binding for recombinant nuclear vitamin D receptor. These results indicated that the region containing the C-6 position of the parent seco-steroid [1,25(OH)2D3] may be an important recognition marker towards vitamin D receptor binding. Information, delineated in this article, will be important for evaluating structure-activity relationship in synthetic analogs of vitamin D and its metabolites.

Binding Sites↗
PubMed1998

Inhibition of NF-kappaB-dependent transcription of human immunodeficiency virus 1 promoter by a phosphodiester compound of vitamin C and vitamin E, EPC-K1.

We investigated the effect of EPC-K1, which is a phosphodiester compound of vitamin E and vitamin C, on NF-kappaB activity in human cultured astrocytoma cells T98G. In TNFalpha-stimulated T98G cells, treatment with EPC-K1 inhibited both DNA binding activity and transactivation of NF-kappaB in a dose-dependent manner, and the suppressive effect of EPC-K1 was stronger than either that of vitamin E or vitamin C. Moreover, we showed that in TNFalpha-stimulated T98G cells treatment with EPC-K1 repressed NF-kappaB-dependent activation of the human immunodeficiency virus 1 promoter. In contrast, TNFalpha-induced activation of the human immunodeficiency virus 1 promoter was not completely inhibited by either treatment with vitamin E or vitamin C. We, thus, suggest that EPC-K1 is considered to be one of the inhibitory agents of NF-kappaB.

Antioxidants↗
PubMed1998

Protective effect against sunburn of combined systemic ascorbic acid (vitamin C) and d-alpha-tocopherol (vitamin E).

BACKGROUND: UV radiation causes acute adverse effects like sunburn, photosensitivity reactions, or immunologic suppression, as well as long-term sequelae like photoaging or malignant skin tumors. UV radiation induces tissues to produce reactive oxygen species, eicosanoids and cytokines. Inhibition of these mediators might reduce skin damage. Antioxidants such as ascorbic acid and d-alpha-tocopherol have been found to be photoprotective in some in vitro studies and animal experiments. OBJECTIVE: Our purpose was to assess the protective effect of systemic vitamins C and E against sunburn in human beings. METHODS: In a double-blind placebo-controlled study, each of 10 subjects took daily either 2 gm of ascorbic acid (vitamin C) combined with 1000 IU of d-alpha-tocopherol (vitamin E) or placebo. The sunburn reaction before and after 8 days of treatment was assessed by determination of the threshold UV dose for eliciting sunburn (minimal erythema dose [MED]) and by measuring the cutaneous blood flow of skin irradiated with incremental UV doses against that of nonirradiated skin. RESULTS: The median MED of those taking vitamins increased from 80 to 96.5 mJ/cm2 (p < 0.01), whereas it declined from 80 to 68.5 mJ/cm2 in the placebo group. Cutaneous blood flow changed significantly (p < 0.05) for most irradiation doses with decreases in those given vitamins and increases in the placebo group. CONCLUSION: Combined vitamins C and E reduce the sunburn reaction, which might indicate a consequent reduced risk for later sequelae of UV-induced skin damage. The increase of sunburn reactivity in the placebo group could be related to "priming" by the previous UV exposure.

Administration, Oral↗
PubMed1998

Inhibition of oxidative DNA damage, 8-OHdG, and carbonyl contents in smokers treated with antioxidants (vitamin E, vitamin C, beta-carotene and red ginseng).

The chemopreventive effects of antioxidants (vitamin E, beta-carotene, vitamin C and red ginseng) on oxidative DNA and protein (globin) damages were comparatively investigated in the peripheral blood of smokers (> or = 20 cigarettes/day). Smokers showed a lower baseline level of plasma micronutrients (vitamin C and beta-carotene) (P < 0.01) and higher baseline level of oxidative DNA or protein damage than non-smokers (N = 5; P < 0.05). During daily supplementation of antioxidants (200 IU vitamin of E, 9 mg of beta-carotene, 500 mg of vitamin C, or 1.8 g of red ginseng) for 4 weeks, smokers plasma antioxidant concentrations increased linearly, while their mean levels of 8-hydroxydeoxyguanosine (8-OHdG) and carbonyl contents decreased compared with those in smokers supplemented with a placebo (P < 0.05). Levels of urinary and plasma cotinine remained steady in smokers regardless of supplementation with antioxidants. 8-OHdG and carbonyl content decreased in a time-dependent manner (as the total intake dose increased) after supplementation with vitamin E (8-OHdG, 33.8%; carbonyl content, 43.6%) or red ginseng (8-OHdG, 31.7%; carbonyl content, 21.3%). These preliminary data suggest that supplementation with antioxidants might protect smokers from oxidative damages and could reduce cancer risk or other diseases caused by free radicals associated with smoking.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1983

19-nor-10-ketovitamin D derivatives: unique metabolites of vitamin D3, vitamin D2, and 25-hydroxyvitamin D3.

Three metabolites were isolated after incubation of vitamin D3, vitamin D2, or 25-hydroxyvitamin D3 with bovine rumen microbes. They are identified as 5(E)-19-nor-10-ketovitamin D3, 5(E)-19-nor-10-ketovitamin D2, and 5(E)-19-nor-10-keto-25-hydroxyvitamin D3, respectively. The identifications were based on ultraviolet absorbance, mass spectroscopy, and chemical reactivity. All 5(E)-19-nor-10-ketovitamin D derivatives examined had an absorbance maximum at 312 nm and a characteristic fragment in their mass spectra corresponding to loss of 43 amu from their molecular ions. The vitamin D3 metabolite was identical in all essential spectral and chromatographic aspects with authentic synthetic 5(E)-19-nor-10-ketovitamin D3. These metabolites represent a unique pathway of vitamin D metabolism and the first characterized products of microbial vitamin D metabolism. The conversion of vitamin D and its metabolites to their 19-nor-10-keto forms likely represents a detoxification mechanism.

Animals↗
PubMed1992

Intake of vegetables, fruits, beta-carotene, vitamin C and vitamin supplements and cancer incidence among the elderly: a prospective study.

A cohort of 11,580 residents of a retirement community initially free from cancer were followed from 1981 to 1989. A total of 1,335 incident cancer cases were diagnosed during the period. Relative risks of cancer were calculated for baseline consumption of vegetables, fruits, beta-carotene, dietary vitamin C, and vitamin supplements. After adjustment for age and smoking, no evidence of a protective effect was found for any of the dietary variables in men. However, an inverse association was observed between vitamin C supplement use and bladder cancer risk. In women, reduced cancer risks of all sites combined and of the colon were noted for combined intake of all vegetables and fruits, fruit intake alone, and dietary vitamin C. Supplemental use of vitamins A and C showed a protective effect on colon cancer risk in women. There was some suggestion that beta-carotene intake and supplemental use of vitamin A, C, and E were associated with reduced risk of lung cancer in women, but none of these results were statistically significant. These inverse associations observed in women seem to warrant further investigation, although there was inconsistency in results between the sexes.

Aged↗
PubMed1997

Determinants of the nutritional status of vitamin E in a non-smoking Mediterranean population. Analysis of the effect of vitamin E intake, alcohol consumption and body mass index on the serum alpha-tocopherol concentration.

OBJECTIVE: Study was conducted in order to investigate the association of vitamin E intake and other factors with plasma alpha-tocopherol concentration in a non-smoking Mediterranean population. DESIGN: A cross-sectional study was conducted in a subsample of a representative sample of the Catalan population. SUBJECTS: Sample size was 143 men and women, aged between 18 and 75 y, and final response rate reached 61.9% of the initial sample. INTERVENTIONS: Serum alpha-tocopherol concentration standardized by serum total lipids was used as a proxy of the nutritional status of vitamin E. Vitamin E intake and alcohol consumption were estimated by a replicated 24 h recall method. Dietary data were collected in two different periods, winter and summer, in order to account for seasonal variation in nutrient intake, and were corrected for random within-person variability in order to account for day-to-day variation in nutrient intake. Multivariate linear regression models were fitted in order to estimate the determinants of serum alpha-tocopherol concentration. RESULTS: In this population study, for each one mg increase in vitamin E intake, serum alpha-tocopherol concentration increased, on average, 0.66 micromol/L, after adjusting for age, gender, Body Mass Index (BMI), alcohol consumption and energy intake. BMI also influenced significantly serum alpha-tocopherol concentration, whereas alcohol intake, age and gender did not show significant associations with serum alpha-tocopherol. CONCLUSIONS: The study showed that vitamin E nutritional status was associated to vitamin E intake and BMI in non-smokers.

Adolescent↗
PubMedDate not supplied

The comparison of vitamin C and vitamin E on the protein oxidation of diabetic rats.

1 We measured the plasma glucose and the glycosylated haemoglobin at the time of sacrifice in streptozotocin-induced diabetic mellitus (DM) rats. 2 In diabetic rats, plasma glucose and glycosylated haemoglobin was increased as compared with normal rats, and vitamin E inhibited the increase of glycosylated haemoglobin level but vitamin C had no effect. 3 The peroxidized proteins and lipids from the diabetic organs such as liver or kidney were measured to assess the oxidative damage. The 2,4-dinitrophenyl-hydrazine (DNPH) incorporation method was used to measure the peroxidized protein. In diabetic rats, DNPH incorporation was increased as compared with normal rats and vitamin E also inhibited the increase of DNPH incorporation but vitamin C had no effect. It suggests that the protein oxidation occurred on the liver in diabetic rats and the oxidative stress is general in the diabetic condition. 4 We measured the systolic arterial pressure and mean arterial pressure in normal rats, nephrectomy (NEPH)-rats, diabetic rats (DM), and NEPH-diabetic rats (NEPH-DM). Blood pressure was significantly increased in DM and NEPH-DM as compared with normal rats. 5 In conclusion, plasma glucose, glycosylated haemoglobin, and the oxidation of proteins or lipid were increased in diabetic rats. Vitamin E decreased the plasma glucose, glycosylated haemoglobin and the oxidation of proteins and lipid, but vitamin C had no effects.

Animals↗
PubMed2000

Vitamin D and autoimmunity: is vitamin D status an environmental factor affecting autoimmune disease prevalence?

The environment in which the encounter of antigen with the immune system occurs determines whether tolerance, infectious immunity, or autoimmunity results. Geographical areas with low supplies of vitamin D (for example Scandinavia) correlate with regions with high incidences of multiple sclerosis, arthritis, and diabetes. The active form of vitamin D has been shown to suppress the development of autoimmunity in experimental animal models. Furthermore, vitamin D deficiency increases the severity of at least experimental autoimmune encephalomyelitis (mouse multiple sclerosis). Targets for vitamin D in the immune system have been identified, and the mechanisms of vitamin D-mediated immunoregulation are beginning to be understood. This review discusses the possibility that vitamin D status is an environmental factor, which by shaping the immune system affects the prevalence rate for autoimmune diseases such as multiple sclerosis, arthritis, and juvenile diabetes.

Animals↗
PubMed2003

Antioxidant capacity in Fasciola hepatica patients before and after treatment with triclabendazole alone or in combination with ascorbic acid (vitamin C) and tocofersolan (vitamin E).

The aim of the present study was to investigate the effect of triclabendazole (CAS 68786-66-3) therapy alone or in combination with ascorbic acid (vitamin C, CAS 50-81-7) and tocofersolan (vitamin E, CAS 30999-06-5), in Fasciola hepatica patients, on Lipo-peroxidation (LPO) and blood antioxidant capacity. 32 Fasciola hepatica patients were divided into two groups (16 acute and 16 chronic). Each group was divided into two subgroups of 8 patients each. One subgroup was given two consecutive oral doses each of 10 mg/kg body weight of triclabendazole suspension and the other received vitamin C (1000 mg/day) and vitamin E (600 mg/day) for two months, together with the same dose of triclabendazole given to the first subgroup. Ten healthy subjects served as controls. The results revealed a significant increase in serum and erythrocyte lipid peroxide levels and a significant decrease in glutathione levels as well as in glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities in all study groups compared to their corresponding control values. After triclabendazole treatment, pronounced improvements in all studied parameters were observed which could be attributed to the fasciolicidal effect of the drug. The significant improvement of SOD and GPX activities and in lipid peroxide levels after vitamins supplementation as compared to their corresponding values after treatment with triclabendazole alone could be explained on the basis of the potent action of these vitamins in protection against oxidative damage.

Acute Disease↗