Presence Of Vit Research Articles

Inflammatory Response Modulation by Vitamin C in an MPTP Mouse Model of Parkinson's Disease.

Simple SummaryVitamin C (Vit C), also called ascorbic acid, is a nutrient present in many foods, particularly citrus fruits and green vegetables. Inadequate dietary Vit C intake causes hypovitaminosis resulting in the risk of developing clinical scurvy, potentially fatal if untreated. Vit C represents one of the safest and most essential nutrients, with antioxidant and anti-inflammatory properties that protect living organisms against oxidative stress; due to this propriety, it is studied for applications in the prevention and management of different pathologies, including neurodegenerative disease. Persistent neuroinflammation is detrimental for the brain and may lead to pathogenesis and progression of neurodegenerative diseases like Parkinson’s disease (PD) and Alzheimer’s disease. The role of Vit C in the central nervous system is still debated.This study, utilizing a PD mouse model, has demonstrated that Vit C reduces neuroinflammation by the modulation of microglial responses and astrocyte activation, reducing dopaminergic neuronal cell loss involved in PD insurgence.Furthermore, mouse gait and spontaneous locomotor activity were partially ameliorated. In summary, we have demonstrated that the use of Vit C has neuroprotective effects in the brain, alleviating the inflammatory cascade and reducing the progression of PD.Vitamin C (Vit C) is anutrient present in many foods, particularly citrus fruits, green vegetables, tomatoes, and potatoes. Vit C is studied for its applications in the prevention and management of different pathologies, including neurodegenerative diseases. Neuroinflammation is a defense mechanism activated by a stimulus or an insult that is aimed at the preservation of the brain by promoting tissue repair and removing cellular debris; however, persistent inflammatory responses are detrimental and may lead to the pathogenesis and progression of neurodegenerative diseases like Parkinson’s disease (PD) and Alzheimer’s disease. PD is one of the most common chronic progressive neurodegenerative disorders, and oxidative stress is one of the most important factors involved in its pathogenesis and progression.Due to this, research on antioxidant and anti-inflammatory compounds is an important target for counteracting neurodegenerative diseases, including PD. In the central nervous system, the presence of Vit C in the brain is higher than in other body districts, but why and how this occurs is still unknown. In this research, Vit C, with its anti-inflammatory and anti-oxidative properties, is studied to better understand its contribution to brain protection; in particular, we have investigated the neuroprotective effects of Vit C in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced animal model of PD and its role in the modulation of neuroinflammation. First, we observed that Vit C significantly decreased the MPTP-induced loss of tyrosine hydroxylase (TH)-positive dopaminergic neuronal cells in the substantia nigra, as well as microglial cell activation and astrogliosis. Furthermore, gait and spontaneous locomotor activity, evaluated by an automated treadmill and the Open Field test, respectively, were partially ameliorated by Vit C treatment in MPTP-intoxicated animals. In relation to neuroinflammation, results show that Vit C reduced the protein and mRNA expression of inflammatory cytokines such as IL-6, TLR4, TNF-α, iNOS, and CD40, while anti-inflammatory proteins such as IL-10, CD163, TGF-β, and IL-4 increased. Interestingly, we show for the first time that Vit C reduces neuroinflammation by modulating microglial polarization and astrocyte activation. Moreover, Vit C was able to reduce NLRP3 activation, which is linked to the pathogenesis of many inflammatory diseases, including neuroinflammatory disorders. In conclusion, our study provides evidence that Vit C may represent a new promising dietary supplement for the prevention and alleviation of the inflammatory cascade of PD, thus contributing to neuroprotection.

Effects of Vitamin C and Magnesium L-threonate Treatment on Learning and Memory in Lead-poisoned Mice.

IntroductionThe aim of this study was to investigate the effects of vitamin C (vit C) and magnesium L-threonate (MgT) on the learning ability and memory of mice intoxicated with lead acetate.Material and MethodsThe experimental male Swiss albinos were divided into five groups of 10 during a 40-day treatment period. One group were untreated controls, one received lead acetate at 90 mg/kg b.w., one additionally vit C at 40 mg/kg b.w., another additionally MgT at 100 mg/kg b.w., and the last was administered MgT without lead acetate. After a 20-day washout period, the animals were trained in the Morris water maze test for 6 days and after a 24-hour interval, were assessed for memory in the same test. At test end the mice were sacrificed and their organs sampled.ResultsThe results of total time and number of entries into the platform zone showed that significantly poorer performances were recorded for the group poisoned with lead acetate alone and significantly lower scores for learning and memory were recorded for the intoxicated and supplemented groups compared to the control group. Catalase activity was significantly reduced in the liver, pancreas and kidney but significantly potentiated in brain tissue by these two supplements compared to the control group. Lead concentration in brain tissue was significantly higher in the presence of vit C than in the control or lead acetate-only groups.ConclusionLead acetate had adverse effects on learning and memory of mice and also increased catalase activity.

Vitamin E inhibits cyclosporin A-induced CTGF and TIMP-1 expression by repressing ROS-mediated activation of TGF-β/Smad signaling pathway in rat liver

Cyclosporin A (CsA) is the most common immunosuppressive drug used in organ transplantation. However, the clinical use of CsA is often limited by several side effects including hepatotoxicity. In the present study, it was found that administration of CsA causes a rapid activation of TGF-β/Smad signaling cascade and subsequent expression of the profibrotic genes connective tissue growth factor (CTGF) and tissue inhibitors of matrix metallproteinases-1 (TIMP-1) in rat liver. In addition, Smad phosphorylation and subsequent CTGF and TIMP-1 expression were markedly reduced in the presence of neutralizing monoclonal TGFβ1–3 antibody. Furthermore, CsA administration significantly increased the serum levels of the liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST) as well as lipid peroxidation in hepatic tissues. Moreover, significant reduction in the hepatic content of reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) was observed in CsA-alone-treated animals. Histopathological changes were also observed in CsA-alone-treated rats. Pretreatment of animals with Vitamin E (Vit E) before CsA administration significantly reduced TGF-β level as well as Smad phosphorylation and subsequent CTGF and TIMP-1 expression. Furthermore, administration of PEG-SOD clearly attenuated TGF-β/Smad signaling induced by CsA. Moreover, concomitant administration of Vit E along with CsA significantly ameliorated the histopathological changes and improved liver function as well as the antioxidant capacity. Finally, this study shows that the immunosuppressive efficiency of CsA was not altered in the presence of Vit E. These data may support the concept of using antioxidant therapy as a valuable approach for the prevention of CsA-induced tissue fibrosis.

Antioxidant ameliorating effects against H2O2-induced cytotoxicity in primary endometrial cells

Oxidative stress and a disrupted antioxidant system are involved in a variety of pregnancy complications. In the present study, the role of vitamin E (Vit E) and folate as radical scavengers on the GSH homeostasis in stress oxidative induced in rat endometrial cells was investigated. Primary endometrial stromal cell cultures treated with 50 and 200 µM of H2O2 and evaluated the cytoprotective effects of Vit E (5 µM) and folate (0.01 µM) in H2O2-treated cells for 24 h. Following the exposure of endometrial cells to H2O2 alone and in the presence of Vit E and/or folate, cell survival, glutathione peroxidase (GPx) and glutathione reductase activities and the level of reduced glutathione (GSH) were measured. Cell adhesions comprise of cell attachment and spreading on collagen were determined. Flow cytometric analysis using annexin V was used to measure apoptosis. H2O2 treatment showed a marked decrease in cell viability, GPx and GR activities and the level of GSH. Although Vit E or folate had some protective effect, combination therapy with Vit E and folate attenuated all the changes due to H2O2 toxicity. An increasing number of alive cells was showed in the cells exposed to H2O2 (50 µM) accompanied by co-treatment with Vit E and folic acid. The present findings indicate that co-administration of Vit E and folate before and during pregnancy may maintain a viable pregnancy and contribute to its clinical efficacy for the treatment of some idiopathic infertility.

Vitamin D3 treatment fails to restore glucocorticoid-induced down-regulation of interleukin-10 receptor expression on CD4+ T cells

Glucocorticoids (GC) exert some of their anti-inflammatory actions via enhancement of interleukin-10 (IL-10) production by immune cells. Interestingly, however, we previously demonstrated that oral administration of GC to asthmatic patients resulted in down-regulation of interleukin-10 receptor (IL-10R) expression on peripheral blood leukocytes. Here we wished to investigate whether addition of vitamin D3 (vit. D3) could abrogate these down-regulating actions of GC. We performed a comparative analysis of the effects of in vitro stimulation with GC and/or vit. D3 on surface expression of IL-10R on the CD4+ T cell pool. As expected, GC stimulation led to significant reduction of IL-10R. In contrast, culture in the presence of vit. D3 did not result in any significant changes of IL-10R expression. Moreover, addition of vit. D3 to GC culture did not alter GC-induced down-regulation of IL-10R expression. Thus, we conclude that anti-inflammatory actions of vit. D3 are not dependent on modification of IL-10R expression.

Vitamin D Enhances ALA-Induced Protoporphyrin IX Production and Photodynamic Cell Death in 3-D Organotypic Cultures of Keratinocytes

Photodynamic therapy (PDT) with 5-aminolevulinic acid (ALA) is based upon the intracellular synthesis of protoporphyrin IX (PpIX), which absorbs light and targets metabolically active cells. We tested the hypothesis that levels of PpIX within keratinocytes might be increased by vitamin D (Vit D), a differentiation-promoting hormone. Vit D promoted terminal differentiation in monolayer cultures of rat epidermal keratinocytes (REKs), but high PpIX signals were found only in stratifying islands. To simulate a normal epidermis, REKs were grown in organotypic cultures. The presence of Vit D (10(-10) M for 4 days) led to heightened expression of terminal differentiation markers (stratum corneum, K10, and loricrin). PpIX levels, at 4 hours after addition of ALA (1 mM), were significantly increased in the Vit D-preconditioned cultures by confocal fluorescence microscopy and semiquantitative image analysis. Maximal PpIX induction was seen at (Vit D) 10(-12)-10(-10) M. Phototoxic cell killing after exposure to 635 nm light was significantly higher in Vit D-preconditioned cultures. No differences in apoptotic markers between Vit D and control cultures were seen, suggesting that Vit D augments photodynamic cell death via alternative pathways (e.g., necrosis). In summary, Vit D may be useful as a biological enhancer of ALA-based PDT.

Effect of vitamins C and E on oxidative processes in human erythrocytes

The oxidative action of 1 mmol l(-1) phenylhydrazine hydrochloride (PH) was studied on human erythrocytes treated with the antioxidants vitamin C (vit. C) and vitamin E (vit. E). The erythrocytes were resuspended in PBS to obtain 35% cell packed volume, and then submitted to the oxidative action of PH for 20 min, with or without previous incubation for 60 min with vit. C or vit. E. Heinz bodies and methemoglobin formation by PH were inhibited in the presence of vit. C. At the concentration of 90 mmol l(-1), vit. C, not only seemed to lose its antioxidant effect, but it also promoted an increase in methemoglobin formation. Vit. C (0.5-80 mmol l(-1)) did not protect against GSH depletion by PH. Vit. C alone produced insignificant hemolysis, but, in the presence of PH, the hemolysis indices were more accentuated. Heinz body formation by PH was inhibited in the presence of vit. E. Formation of methemoglobin induced by PH was decreased by vit. E (0.1-2 mmol l(-1)), although vit. E (3-80 mmol l(-1)) did not lower the concentration of methemoglobin and did not lead to the recovery of the GSH depleted by PH. The results obtained suggest that vit. C and vit. E contribute to the decrease in oxidative stress caused by PH.

Effect of vitamin B1 and mixtures of B1 with other vitamins on cytostatic efficiency of sanazole under irradiation. A study in vitro

Experiments in vitro, using bacteria Escherichia coli (AB 1157) as a biological model, showed that the cytostatic efficiency of sanazole (AK-2123, a nitrotriazole-type radiosensitizer) in radiation treatment can be strongly influenced by the presence of various vitamins. In airfree media the sanazole action is increased by a factor of 2.5 in the presence of vitamin (vit.) B1, vit. C E-acetate and β-carotene, whereas vit. B1 used individually possesses a 2.7-times higher cytostatic activity than sanazole itself. In media containing air the highest increase of sanazole action is observed in the presence of vit. B1 and C, whereas the individual use of vit. B1 shows a radiation protection effect. In media saturated with N 2O the addition of the vit. B1 and C causes a 1.8-times larger sanazole activity, but the application of vit. B1 alone brings about a very high radiation protection. From studies of vit. B1-radiolysis it can be concluded that OH radicals are the major primary transients leading to substrate degradation. The results are of interest for the radiation therapy of cancer.

Oxidative stress response of a recombinant Aspergillus niger to exogenous menadione and H 2O 2 addition

A recombinant strain of Aspergillus niger (B1-D), engineered to produce the marker protein hen egg white lysozyme (HEWL), was investigated with regard to its susceptibility to oxidative stress. The culture response to oxidative stress, produced either by menadione (MD) or by H 2O 2, was characterised in terms of the intracellular activities of two key defensive enzymes, catalase (CAT) and superoxide dismutase (SOD), in the presence or absence of a range of vitamin supplements. Addition of either ascorbate (Vit C) or α-tocopherol (Vit E) resulted in different responses of A. niger cultures to exogenous H 2O 2 (1 mM). In the presence of Vit C the activity of SOD was increased by 50% compared to control cultures, whereas incorporation of Vit E appeared to have a “protective” effect against reactive oxygen species (ROS). Continuous addition of menadione (1.2 mmole l −1 h −1) to submerged cultures of A. niger in the bioreactor resulted in an increase of CAT and SOD activities during the exponential phase of growth, whereas enzyme levels remained almost constant during that phase in control cultures. Comparison of these results with the response to oxidative stress caused by addition of exogenous H 2O 2 and elevated dissolved oxygen tension (DOT) [1] shows that these three stressors are quite distinct.

In vitro evaluation of the biofunctionality of osteoblasts cultured on DegraPol-foam

The biofunctionality of osteoblasts cultured on DegraPol-foam, a biodegradable, elastic, and highly porous polyesterurethane-foam, was determined here to examine the possible use of this structure as bone repair material. Osteoblasts from rat tibia and from the cell line (MC3T3-E1) exhibited relatively high attachment and low doubling time that result in a confluent cell multilayer on the surface of the foam. They produced high concentrations of collagen type I and osteocalcin, and expressed increasing alkaline phosphatase activity. Exposure to 1,25-dihydroxy vitamin D (Vit. D) increased dose-and time-dependent alkaline phosphatase activity and osteocalcin concentration, and decreased the level of collagen type I and cell density. Maximal effects of Vit. D on alkaline phosphatase activity (2.2 fold), osteocalcin (1.5 fold), collagen type I (50% reduction), and on cell density (35% reduction) were found at 100 ng Vit. D ml-1. Osteoblasts cultured on DegraPolfoam in the presence of Vit. D exhibited more spreading and less spindle-like morphology than cells cultured in the absence of Vit. D. Cell ingrowth into the pores of the foam was not affected by Vit. D treatment. Taken collectively, the osteoblasts, capability of responding to Vit. D confirms the osteoblast compatibility of DegraPol-foam and the possible use of this scaffold in the bone healing process.

Inhibition of Tryptophan Oxidation in the Presence of Iron–Vitamin C by Bovine Lactoferrin

An increasing number of foods are fortified with iron and vitamin C (vit C) before processing, but in the presence of vit C, the iron can catalyze the production of free radical species which can oxidize tryptophan (Trp). We confirmed the higher catalytic effect of copper compared to iron but demonstrated a stronger effect of temperature on iron-catalyzed reactions. The results indicate that lactoferrin, added at a concentration which allows total chelation of the iron present in the medium, partially inhibits iron-induced vit C oxidation and almost totally that of Trp. This inhibitory effect decreases when some iron remain free, even though a significant effect is still notable with only 1/5 iron chelated by lactoferrin. Heat treatments above 90°C induce lactoferrin denaturation and negate the chelation activity of the protein. The significance of the effect of lactoferrin is therefore substantially diminished by the heat sensitivity and the cost of the protein.

Choline requirement of rats as influenced by age, strain, vitamin B12 and folacin.

Summary(1) Weanling rats of the Sprague-Dawley (SD) strain have a lower choline requirement for protection against renal hemorrhage and a higher requirement for maintenance of normal liver fat than was observed in rats of the Alabama Experiment Station (AES) strain. (2) Forty-two-day-old rats of either strain grew rapidly and failed to develop hemorrhagic kidneys when they were fed the choline-dencient basal diet supplemented with only vit. B12 and folacin. However, liver fat of the SD strain rats was 33% (dry basis) as compared to 62% for the AES strain rats. (3) The addition of vit. B12 and folacin to the basal diet supplemented with suboptimal choline chloride markedly suppressed the accumulation of fat in the liver, reduced the incidence of renal damage and increased the choline content of the livers of the SD strain of rats. Liver fat values averaging 12.8% (dry basis) were obtained with a 0.20% choline chloride supplement in the presence of vit. B12 and folacin as compared to a requirement of 0.40% ...

Effect of vitamins E, B12 and folacin on CCL4 toxicity and protein utilization in rats.

Vit. E and vit. B12 can replace each other in promoting protein utilization and in protecting against acute carbon tetrachloride toxicity in young rats reared on 10% protein diets deficient in these factors. The vit. B12 requirement for protection against CCl4 is considerably higher than for growth. Folacin supplements, alone, had no effect, but, in the presence of vit. B12 or vit. E, this factor markedly improved protein utilization and growth. L-Cystine protected against the acute toxicity but a synergism between cystine and vit. E was not noted.