Potential Of Vitamin Research Articles

Role of Vitamin E in Mitigating Methomyl Induced Acute Toxicity in Blood of Male Wistar Rats

The present study was designed to evaluate the protective potential of vitamin E, if any, in attenuating the toxic effects induced by acute methomyl treatment in rats. Male Wistar rats, weighing between 230 and 250 g, received either a single oral dose of 9 mg/kg of methomyl, vitamin E alone injected intraperitoneally on alternate days (4 injections) at 50 mg/kg body for 1 week prior to methomyl treatment, or both methomyl plus vitamin E given in a similar manner. The effects of different treatments were studied on lipid peroxidation (LPO), reduced glutathione (GSH) and antioxidant enzymes, which included superoxide dismutase (SOD), glutathione-s-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GSHPx) and catalase and various hematological parameters, including total leucocytes count (TLC), differential leukocyte count (DLC), hemoglobin, platelets counts, red cell counts, and scanning electron microscopy (SEM). Acute 24-h treatment to rats resulted in a significant increase in the LPO. GSH levels and the activities of catalase, GST, and GSHPx were found to be significantly decreased following methomyl treatment. A significant elevation in the activity of SOD and in TLC was also observed after 24 h of methomyl treatment. Further, a significant increase in the neutrophils and eosinophil counts was also observed. However, lymphocytes showed a significant decrease following methomyl treatment. SEMs showed significant morphological changes following methomyl treatment. Vitamin E pretreatment to methomyl-treated rats effectively normalized the levels of LPO and GSH. Vitamin E could also significantly elevate the activity of catalase, increase platelets counts and TLC, and normalized the activities of SOD and GSHPx. Vitamin E pretreatment improved the morphology of the red blood cells. The study concludes that vitamin E affords protection in methomyl-induced toxicity in the rat.

Report on the vitamin D status of adult and pediatric patients with inflammatory bowel disease and its significance for bone health and disease

Vitamin D is a hormone responsible for calcium homeostasis and essential for bone mineralization throughout the lifespan. Recent studies revealed a high prevalence of hypovitaminosis D among healthy adults and children, especially in the northern hemisphere, and a link between this condition and suboptimal bone health. Moreover, maintenance of what are today considered optimal vitamin D stores has not been achieved throughout the year with currently recommended daily intake for vitamin D. The prevalence of hypovitaminosis D is even higher among adults with inflammatory bowel disease (IBD), a situation that may be caused by malabsorption and gastrointestinal losses through an inflamed intestine, among other factors. In children with IBD, existing reports of vitamin D status are scarce. The relationship between vitamin D status and bone health, although well-established in healthy adults and children, has been controversial among adults and children with IBD, and the reasons for this have not been investigated to date. Studies in animal models of colitis and in vitro human studies support a role of vitamin D in the regulation of the immune system of the gut and the potential of vitamin D and its derivatives as therapeutic adjuncts in the treatment of IBD. This role of vitamin D has not been investigated with translational studies to date. Currently, there are no guidelines for monitoring vitamin D status, treating hypovitaminosis D, and maintaining optimal vitamin D stores in patients with IBD. These tasks may prove particularly difficult because of malabsorption and gastrointestinal losses that are associated with IBD.

Promise of vitamin D analogues in the treatment of hyperproliferative conditions

1Alpha,25-dihydroxyvitamin D3 [1alpha,25-(OH)2D3; calcitriol] is best known as a hormone involved in calcium homeostasis but is also a potent antiproliferative agent in many cell types, particularly epithelial cells. 1Alpha,25(OH)2D3 mediates its actions through a classic steroid hormone-like transcriptional mechanism by influencing the expression of hundreds of genes. Effects of 1alpha,25(OH)2D3 have been observed on expression of cell cycle regulators, growth factors and their receptors, apoptotic machinery, metastatic potential, and angiogenesis; all of which have some effect on hyperproliferative conditions. This minireview focuses on the anticancer potential of 1alpha,25(OH)2D3 and its analogues by summarizing the promising data from animal and human trials of 1alpha,25(OH)2D3 and some of the more interesting synthetic vitamin D analogues in the treatment of a variety of different animal cancer models and in human patients with advanced cancer. Optimal administration of vitamin D analogues is only just being achieved with high-dose intermittent administration overcoming bioavailability and hypercalcemia problems and combination therapy with cytotoxic agents (taxols and cisplatins), antiresorptive agents (bisphosphonates), or cytochrome P450 inhibitors being attempted. Although the potential of vitamin D as an antiproliferative drug has been realized in the treatment of psoriasis and in parathyroid cell hyperplasia associated with secondary hyperparathyroidism, the search for an anticancer treatment incorporating a vitamin D analogue remains elusive.

1680 Evaluation of antioxidant potential of vitamin E and M rna synthesis in Cyclophosphamide treated rat brain

1680 Evaluation of antioxidant potential of vitamin E and M rna synthesis in Cyclophosphamide treated rat brain

Potential of Vitamin E and Zinc-Amino Acid Complex for the Reduction of Cellulitis in Broilers

Downs, K.M., Norton, R.A., Macklin, K.S. and Hess, J.B. 2003. Potential of vitamin E and zinc-amino acid complex for the reduction of cellulitis in broilers. J. Appl. Anim. Res., 23: 25–32. A research study was conducted to determine the effects of dietary supplementation with vitamin E and a zinc-amino acid complex (Zn-AA) on the incidence of cellulitis in broiler chickens. Vitamin E and Zn-AA supplementation did not influence body weight, but subtle feed conversion and mortality treatment differences were observed. Furthermore, a trend in cellulitis lesion reduction was indicated through combined supplementation of vitamin E and Zn-AA. The results of this study indicate an overall positive effect from higher dietary vitamin E and Zn-AA level on cellulitis incidence.

The loss of Smad3 results in a lower rate of bone formation and osteopenia through dysregulation of osteoblast differentiation and apoptosis.

Smad3 is a well-characterized intracellular effector of the transforming growth factor beta (TGF-beta) signaling pathway and was implicated recently in the potentiation of vitamin D receptor (VDR)-mediated signaling. Given that both TGF-beta and vitamin D are important regulators of bone remodeling, it is expected that Smad3 plays an integral role in normal maintenance of bone. However, the exact mechanisms by which Smad3 functions in bone remodeling are unknown. Here, we show that mice with targeted deletion of Smad3 are osteopenic with less cortical and cancellous bone compared with wild-type littermates. Decreases in bone mineral density (BMD) in Smad3 null mice reflect the inability of osteoblasts to balance osteoclast activity, although osteoclast numbers are normal and vitamin D mediated serum calcium homeostasis is maintained. The osteopenia of Smad3 null mice is attributed to a decreased rate of bone formation associated with increased osteocyte number and apoptosis. These findings are supported by studies with isolated primary osteoblasts that show TGF-beta can no longer inhibit the differentiation of osteoblasts in the absence of Smad3; yet, TGF-beta-stimulated proliferation remains intact. Together these data support a model that a loss of Smad3 increases the osteocyte fate of the osteoblast and decreases the duration of osteoblast function by shortening lifespan, ultimately resulting in osteopenia.

Potentiation of vitamin K antagonists by high-dose intravenous methylprednisolone.

Oral anticoagulants and pulse high-dose intravenous methylprednisolone are often administered concomitantly, but no data on potential interactions are available. To assess possible potentiation of oral anticoagulation by high-dose intravenous methylprednisolone. Prospective cohort study. University hospital in Paris, France. 10 consecutive patients concomitantly receiving methylprednisolone and oral anticoagulants (fluindione and acenocoumarol) and 5 consecutive controls receiving methylprednisolone alone. Serial determinations of the international normalized ratio (INR) and clotting factors during administration of pulse methylprednisolone. The total plasma fluindione concentration was determined in 3 patients. The mean INR was 2.75 (range, 2.02 to 3.81) at baseline and increased to 8.04 (range, 5.32 to 20.0) after methylprednisolone administration. Plasma fluindione concentrations and the INR increased after methylprednisolone administration. Methylprednisolone alone did not increase prothrombin time. The action of oral anticoagulants is potentiated by intravenous high-dose methylprednisolone. The INR should be monitored daily during concomitant administration of these medications.

Gastroduodenal Mucosal Vitamin-C Levels in Helicobacter pylori Infection

Background: Vitamin C is an important endogenous antioxidant, and epidemiologic evidence suggests that it may protect against the development of gastric cancer. We therefore determined mucosal vitamin-C levels in the stomach and duodenum of subjects with and without Helicobacter pylori infection. Methods: The patients were 30 subjects undergoing routine gastroscopy for investigation of dyspepsia. High-performance liquid chromatography with electrochemical detection was used to determine mucosal ascorbic acid and total vitamin-C levels. Results: In H. pylori-negative subjects with normal gastroduodenal histology the antrum contained significantly higher levels of ascorbic acid and total vitamin C than the corpus or duodenum (P < 0.05). No significant changes were seen in gastric mucosal ascorbic acid or total vitamin-C levels in the presence of H. pylori infection and related inflammation. The presence of gastric atrophy did not affect mucosal ascorbic acid or total vitamin C levels. Duodenal ascorbic acid and total vitamin-C levels did not change significantly in the presence of gastric H. pylori or duodenal inflammation. Conclusions: Although high levels of vitamin C are present in the gastroduodenal mucosa, these are not altered in the presence of H. pylori infection and inflammation. These observations suggest that the mucosal antioxidant potential of vitamin C is not impaired by H. pylori infection.

Vitamins as Radioprotectors In Vivo. I. Protection by Vitamin C against Internal Radionuclides in Mouse Testes: Implications to the Mechanism of Damage Caused by the Auger Effect

The potential of vitamin C, an antioxidant, to protect the radiosensitive spermatogonial cells in mouse testes against the effects of chronic irradiation by radionuclides incorporated into tissue was investigated. Interestingly, when injected intratesticularly, a small and nontoxic amount of vitamin C (1.5 microgram in 3 microliters saline) protected the spermatogonia against the damage associated with high-LET radiation caused by Auger electrons from similarly administered 5-(125I)-iodo-2'-deoxyuridine (125IdU). A dose modification factor (DMF) of 2.3 was obtained. In contrast, no protection was observed when 210Po, an alpha-particle emitter, was administered similarly. These findings suggest that the mechanism of action of the Auger effect is of an indirect nature, which is in contrast to the direct action generally believed to be responsible for biological damage caused by high-LET radiations.

Inhibition of human oral squamous carcinoma cell (SCC-25) proliferation by prostaglandin E2 and vitamin E succinate.

The primary objective of this investigation was to study the effect of D-alpha-tocopherol acid succinate (vitamin E succinate) and prostaglandin E2 (PGE2), individually and in combination, on the proliferation of human tongue squamous carcinoma cells (SCC-25) in vitro. Test compounds in varying concentrations were incubated with cells in serum-free Dulbecco's Modified Eagle's Medium-Ham's F-12 Medium (50:50), supplemented with 0.1% albumin for sixteen hours. Cell proliferation was measured by the incorporation of [3H] thymidine in acid-insoluble material (i.e. DNA). Prostaglandin E2 and vitamin E succinate, individually at 10(-9)-10(-6) M, caused significant dose-dependent inhibition in DNA synthesis. A combined dose of each compound at 10(-5) M resulted in significant additive inhibition which averaged 43.53% (p < 0.005). Addition of indomethacin (INDO) to cell cultures induced significant dose-dependent stimulation in DNA synthesis. Hence, we might suggest that the overall potential of vitamin E in controlling malignant cell proliferation in vivo could be due to its own effect combined with that of endogenous PGs which are normally produced in excessive amounts by malignant cells.

Potentiation of vitamin A hepatotoxicity by butylated hydroxytoluene

The interaction between the natural vitamin A ester retinyl acetate (RA) and the phenolic antioxidant butylated hydroxytoluene (BHT) in the induction of biliary hyperplasia and hepatic fibrosis in female Sprague-Dawley rats was characterized. Using a 3 × 3 matrix design, rats were fed diets supplemented with (per kilogram diet) 0, 125, or 250 mg RA and/or 0, 2500, or 5000 mg BHT. The 125-mg dose of RA induced no gross hepatotoxicity, while the 250-mg dose of RA induced a low incidence of hepatic fibrosis in rats examined after 120 and 180 days of exposure. Exposure to BHT alone induced hepatocellular hypertrophy and dose-related increases in liver weight, but no hepatocellular pathology. Simultaneous administration of RA plus BHT resulted in significant increases in the incidence of biliary hyperplasia and hepatic fibrosis compared to that induced by RA alone. BHT reduced total hepatic vitamin A content at all RA dose levels. Thus, mechanisms other than increases in liver vitamin A levels must underlie the potentiation by BHT of RA hepatotoxicity.

Characterization of vitamin E status in cholestatic children by conventional laboratory standards and a new functional assay.

In the present study, the clinical application of a new functional test for vitamin E deficiency was evaluated. Erythrocytes from cholestatic children at risk for vitamin E deficiency and appropriate controls were incubated in vitro with hydrogen peroxide and the malondialdehyde generated and released into the supernatant quantitated. The results of these incubations were compared with fasting plasma vitamin E levels, the ratio of plasma vitamin E to plasma lipid levels, and, in some instances, hydrogen peroxide hemolysis tests. Malondialdehyde formation was less than 6% in controls and vitamin E-sufficient cholestatic children. However, cholestatic vitamin E-deficient children had a mean malondialdehyde formation of 41%. The results also suggest that for children less than 4 months of age, a ratio of plasma vitamin E to total plasma lipids less than 0.6 mg/g may be sufficient to provide protection from in vitro peroxidation. The authors suggest that this functional assay of vitamin E status be included in the evaluation of individuals with the potential for vitamin E deficiency.

Characterization of Vitamin E Status in Cholestatic Children by Conventional Laboratory Standards and a New Functional Assay

SummaryIn the present study, the clinical application of a new functional test for vitamin E deficiency was evaluated. Erythrocytes from cholestatic children at risk for vitamin E deficiency and appropriate controls were incubated in vitro with hydrogen peroxide and the malondialdehyde generated and released into the supernatant quantitated. The results of these incubations were compared with fasting plasma vitamin E levels, the ratio of plasma vitamin E to plasma lipid levels, and, in some instances, hydrogen peroxide hemolysis tests. Malondialdehyde formation was less than 6% in controls and vitamin E‐sufficient cholestatic children. However, cholestatic vitamin E‐deficient children had a mean malondialdehyde formation of 41%. The results also suggest that for children less than 4 months of age, a ratio of plasma vitamin E to total plasma lipids less than 0.6 mg/g may be sufficient to provide protection from in vitro peroxidation. The authors suggest that this functional assay of vitamin E status be included in the evaluation of individuals with the potential for vitamin E deficiency.

Protective effect of vitamin E on genotoxicity of methylmercury.

The cytogenetic effects of methylmercury (MeHg) producing chromosomal breakages, C-mitosis, and sister chromatid exchange are well documented. The present investigation was to determine whether vitamin E, which has been shown to exert a certain protective measure on the nervous system of animals exposed to methylmercury, also will diminish the genotoxicity of MeHg. Adult hamsters were given a daily injection (ip) of methylmercury chloride at a dosage of 2.0 mg/kg body weight (kg b.w.) and/or with 2.0 mg/kg b.w. vitamin E for 3 wk. All animals were sacrificed 5 d after the last day of MeHg exposure. Fibroblast cultures were established with cells obtained from skins of these animals. Chromosome preparations were made from these cultures and evaluated, using a double-blind system, for incidences of chromosomal breakage. It was found that all the fibroblast cultures grew well except from those animals treated with MeHg. Furthermore, while the saline control and vitamin E alone cultures showed no significant number of chromosomal breakages, cells from animals treated with only MeHg showed a high incidence of chromosomal damage (50% with 1 break and 15% with 2 or more breaks). Such chromosomal damage, however, was totally eliminated by vitamin E treatment (no chromosomal breakage was observed in cultures from MeHg/vitamin E animals). Our present study represents the first report on in vitro chromosomal damages as a result of in vivo MeHg exposure. Furthermore, our investigation also demonstrated the protective potential of vitamin E against genotoxicity of methylmercury.

Histamine degradative potential of ascorbic acid: considerations and evaluations.

The above points clearly bring out the histamine degradative potential of ascorbic acid and its beneficial effect in stress. However, it should not be assumed that this indicates an almost universal therapeutic action of this vitamin. Obviously, as plain reasoning suggests, such a small molecule cannot be the curative factor for handling a number of unrelated maladies. It is probably the removal of excess histamine, elevated under stress situations, which leads to the suppression of the side effects which otherwise would have been triggered by histamine. Hence there is a better resistance and apparent relief. Other effects, like influencing the cyclic AMP levels etc., have also been suggested to account for the medical potential of vitamin C.

Platinum Potential of Vitamin C Solutions in Contact with Molecular Oxygen

THE platinum potential of solutions containing biological oxidation-reduction agents can be measured when exposed to air by means of a relatively simple technique1.