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Li H, Li WC, Hu XR. Association between vitamin C, D, and K intake and inflammatory bowel disease risk: findings from 2009 to 2010 NHANES. BMC Gastroenterol 2025; 25:177. [PMID: 40097943 PMCID: PMC11912713 DOI: 10.1186/s12876-025-03747-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/30/2024] [Accepted: 02/28/2025] [Indexed: 03/19/2025] Open
Abstract
BACKGROUND Micronutrient deficiency is commonly observed in patients with inflammatory bowel disease (IBD), yet the role of certain dietary trace elements in the risk of IBD development remains unclear. OBJECTIVES This study aimed to investigate the relationship between vitamin C, D, and K intake and IBD risk. METHODS This study included 3,591 participants from the 2009-2010 National Health and Nutrition Examination Survey (NHANES). Multivariable logistic regression were conducted to assess associations between vitamin C, D, and K intake and IBD risk while controlling for multiple confounders. Subgroup analyses were employed to test the robustness of the associations across participants with various characteristics. Additionally, restricted cubic spline (RCS) analysis was conducted to investigate potential nonlinear relationships. RESULTS In the fully adjusted model, each 1 mcg increase in vitamin D intake was linked to an approximately 51% decrease in IBD risk (adjusted OR = 0.49, 95% CI: 0.25-0.98, p = 0.045). The benefit appeared stronger in women, individuals without hypertension, and non-smokers. No statistically significant associations were found between vitamin C or vitamin K intake and IBD risk. However, among individuals without diabetes, each 1 mcg increase in vitamin K intake was associated with an approximate 67% reduction in IBD risk (adjusted OR = 0.33, 95% CI: 0.12-0.94, p = 0.039). RCS analysis suggested a linear relationship between dietary micronutrient intake and IBD risk (vitamin D: p for nonlinearity = 0.127, p for overall = 0.015; vitamin C: p for nonlinearity = 0.984, p for overall = 0.937; vitamin K: p for nonlinearity = 0.736, p for overall = 0.434). CONCLUSION Increased vitamin D intake may reduce the risk of IBD, with more pronounced benefits in certain subgroups, highlighting the potential of vitamin D supplementation as a novel therapeutic approach for IBD prevention and management. Future well-designed studies should further test the therapeutic effects of vitamin D supplementation and investigate the associations of other dietary trace elements with IBD risk to better inform prevention and treatment approaches.
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Affiliation(s)
- Hui Li
- The Tenth Affiliated Hospital of Southern Medical University (Dongguan People's Hospital), Dongguan, 523000, China
| | - Wen-Chao Li
- The Tenth Affiliated Hospital of Southern Medical University (Dongguan People's Hospital), Dongguan, 523000, China
| | - Xia-Rong Hu
- The Tenth Affiliated Hospital of Southern Medical University (Dongguan People's Hospital), Dongguan, 523000, China.
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Assessment of the Substance Antioxidative Profile by Hyaluronan, Cu(II) and Ascorbate. Pharmaceutics 2021; 13:pharmaceutics13111815. [PMID: 34834230 PMCID: PMC8617742 DOI: 10.3390/pharmaceutics13111815] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/07/2021] [Revised: 10/21/2021] [Accepted: 10/26/2021] [Indexed: 11/30/2022] Open
Abstract
In the minireview presented here, the authors discuss the evaluation of inhibitory effect of substances in the phases of initiation and propagation of high-molar-mass hyaluronan oxidative degradation. The experimental approach should be considered as original since on using a simple experimental assay it is possible to prove both the so-called “preventive” and “chain-breaking” antioxidant activity of investigated water-soluble endo- or exogenous substances.
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Khosravi-Largani M, Pourvali-Talatappeh P, Rousta AM, Karimi-Kivi M, Noroozi E, Mahjoob A, Asaadi Y, Shahmohammadi A, Sadeghi S, Shakeri S, Ghiyasvand K, Tavakoli-Yaraki M. A review on potential roles of vitamins in incidence, progression, and improvement of multiple sclerosis. eNeurologicalSci 2018; 10:37-44. [PMID: 29736427 PMCID: PMC5934114 DOI: 10.1016/j.ensci.2018.01.007] [Citation(s) in RCA: 29] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/05/2017] [Revised: 12/08/2017] [Accepted: 01/19/2018] [Indexed: 02/06/2023] Open
Abstract
Multiple Sclerosis (MS) is an inflammatory and neurodegenerative disease, with unknown etiology. Vitamins, as important micronutrients playing different roles in body, seem to be important in MS pathogenesis. In vitro, in vivo and human studies, supports the protective role of some vitamins in MS occurrence or progression. Current study reviews recent insights and reports about the importance of vitamins in MS incidence or progression. In accordance, the importance of all water and fat-soluble vitamins in MS pathogenesis based on observational studies in human population and their role in the function of immune system as well as possible therapeutic opportunities are discussed in depth throughout this review.
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Affiliation(s)
| | | | | | | | - Elahe Noroozi
- School of Medicine, Iran University of Medical Sciences, Tehran, Iran
| | - Ali Mahjoob
- School of Medicine, Iran University of Medical Sciences, Tehran, Iran
| | - Yasaman Asaadi
- Department of Biotechnology, College of Science, University of Tehran, Tehran, Iran
| | | | - Sarina Sadeghi
- School of Medicine, Iran University of Medical Sciences, Tehran, Iran
| | - Shiva Shakeri
- School of Medicine, Iran University of Medical Sciences, Tehran, Iran
| | - Kimiya Ghiyasvand
- School of Medicine, Iran University of Medical Sciences, Tehran, Iran
| | - Masoumeh Tavakoli-Yaraki
- Department of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
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Bivona JJ, Patel S, Vajdy M. Induction of cellular and molecular Immunomodulatory pathways by vitamin E and vitamin C. Expert Opin Biol Ther 2017; 17:1539-1551. [PMID: 28905653 DOI: 10.1080/14712598.2017.1375096] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
INTRODUCTION Vitamins E and C are well known small molecules that have been used to maintain health for decades. Recent studies of the cellular and molecular pathways leading to immunomodulation by these molecules have been of interest, as have their anti-oxidant properties and signal transduction pathways for curing or improving infectious diseases and cancer. Areas covered: Herein, the authors provide a definition and the structural classification of vitamins E and C and how these molecules influence cellular function. The studies include in vitro, ex vivo and in vivo studies in animal models as well as clinical trials. The authors give particular focus to the scientifically factual and putative roles of these molecules in innate and adaptive immunomodulation and prevention or cure of diseases. Expert opinion: The antioxidant properties of vitamins E and C are well studied. However, whether there is a link between their antioxidant and immunomodulation properties is unclear. In addition, there is a strong, albeit putative, prevailing notion that vitamin C can prevent or cure infectious diseases or cancer. Presently, while there is proven evidence that vitamin E possesses immunomodulatory properties that may play a positive role in disease outcomes, this evidence is less available for vitamin C.
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Affiliation(s)
- Joseph J Bivona
- a EpitoGenesis, Inc , Vernon , CT , USA.,b Department of Medicine , University of Vermont , Burlington , VT , USA
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Marim RG, de Gusmão AS, Castanho REP, Deminice R, Therezo ALS, Jordão Júnior AA, de Assis MR, Taipeiro EDF, Martins LPA. EFFECTS OF VITAMIN C SUPPLEMENTATION ON THE CHRONIC PHASE OF CHAGAS DISEASE. Rev Inst Med Trop Sao Paulo 2016. [PMID: 26200966 PMCID: PMC4544250 DOI: 10.1590/s0036-46652015000300011] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/28/2022] Open
Abstract
Introduction: In order to examine the effectiveness of vitamin C (ascorbic acid) in combating
the oxidative insult caused by Trypanosoma cruzi during the
development of the chronic phase of Chagas disease, Swiss mice were infected
intraperitoneally with 5.0 × 104 trypomastigotes of T.
cruzi QM1strain. Methods: Mice were given supplements of two different doses of vitamin C for 180 days.
Levels of lipid oxidation (as indicated by thiobarbituric acid reactive
substances-TBARS), total peroxide, vitamin C, and reduced glutathione were
measured in the plasma, TBARS, total peroxide and vitamin C were measured in the
myocardium and histopathologic analysis was undertaken in heart, colon and
skeletal muscle. Results: Animals that received a dose equivalent to 500 mg of vitamin C daily showed
increased production of ROS in plasma and myocardium and a greater degree of
inflammation and necrosis in skeletal muscles than those that received a lower
dose or no vitamin C whatsoever. Conclusion: Although some research has shown the antioxidant effect of vitamin C, the results
showed that animals subject to a 500 mg dose of vitamin C showed greater tissue
damage in the chronic phase of Chagas disease, probably due to the paradoxical
actions of the substance, which in this pathology, will have acted as a
pro-oxidant or pro-inflammatory.
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Affiliation(s)
| | | | | | - Rafael Deminice
- Department of Medical Clinic, Division of Nutrition and Metabolism, Ribeirão Preto Medical School, Ribeirão Preto, São Paulo, Brazil
| | | | - Alceu Afonso Jordão Júnior
- Department of Medical Clinic, Division of Nutrition and Metabolism, Ribeirão Preto Medical School, Ribeirão Preto, São Paulo, Brazil
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Boatright WL. Oxygen dependency of one-electron reactions generating ascorbate radicals and hydrogen peroxide from ascorbic acid. Food Chem 2015; 196:1361-7. [PMID: 26593628 DOI: 10.1016/j.foodchem.2015.07.141] [Citation(s) in RCA: 33] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/07/2015] [Revised: 07/24/2015] [Accepted: 07/30/2015] [Indexed: 11/17/2022]
Abstract
The effect of oxygen on the two separate one-electron reactions involved in the oxidation of ascorbic acid was investigated. The rate of ascorbate radical (Asc(-)) formation (and stability) was strongly dependent on the presence of oxygen. A product of ascorbic acid oxidation was measurable levels of hydrogen peroxide, as high as 32.5 μM from 100 μM ascorbic acid. Evidence for a feedback mechanism where hydrogen peroxide generated during the oxidation of ascorbic acid accelerates further oxidation of ascorbic acid is also presented. The second one-electron oxidation reaction of ascorbic acid leading to the disappearance of Asc(-) was also strongly inhibited in samples flushed with argon. In the range of 0.05-1.2 mM ascorbic acid, maximum levels of measurable hydrogen peroxide were achieved with an initial concentration of 0.2 mM ascorbic acid. Hydrogen peroxide generation was greatly diminished at ascorbic acid levels of 0.8 mM or above.
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Affiliation(s)
- William L Boatright
- Department of Animal and Food Sciences, University of Kentucky, 412 W.P. Garrigus Building, Lexington, KY 40546-0215, United States.
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7
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Nakagawa Y, Inomata A, Ogata A, Nakae D. Comparative effects of sulfhydryl compounds on target organellae, nuclei and mitochondria, of hydroxylated fullerene-induced cytotoxicity in isolated rat hepatocytes. J Appl Toxicol 2015; 35:1465-72. [PMID: 25809591 DOI: 10.1002/jat.3137] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/07/2015] [Revised: 01/29/2015] [Accepted: 02/01/2015] [Indexed: 11/06/2022]
Abstract
DNA damage and cytotoxicity induced by a hydroxylated fullerene [C60 (OH)24 ], which is a spherical nanomaterial and/or a water-soluble fullerene derivative, and their protection by sulfhydryl compounds were studied in freshly isolated rat hepatocytes. The exposure of hepatocytes to C60 (OH)24 at a concentration of 50 μM caused time (0 to 3 h)-dependent cell death accompanied by the formation of cell surface blebs, the loss of cellular levels of ATP and reduced glutathione, accumulation of glutathione disulfide, and induction of DNA fragmentation assayed using alkali single-cell agarose-gel electrophoresis. C60 (OH)24 -induced cytotoxicity was effectively prevented by pretreatment with sulfhydryl compounds. N-acetyl-L-cysteine (NAC), L-cysteine and L-methionine, at a concentration of 2.5 mM, ameliorated cell death, accompanied by a decrease in cellular ATP levels, formation of cell surface blebs, induction of reactive oxygen species (ROS) and loss of mitochondrial membrane potential caused by C60 (OH)24 . In addition, DNA fragmentation caused by C60 (OH)24 was also inhibited by NAC, whereas an antioxidant ascorbic acid did not affect C60 (OH)24 -induced cell death and DNA damage in rat hepatocytes. Taken collectively, these results indicate that incubation of rat hepatocytes with C60 (OH)24 elicits DNA damage, suggesting that nuclei as well as mitochondria are target sites of the hydroxylated fullerene; and induction of DNA damage and oxidative stress is ameliorated by an increase in cellular GSH levels, suggesting that the onset of toxic effects may be partially attributable to a thiol redox-state imbalance caused by C60 (OH)24 .
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Affiliation(s)
- Yoshio Nakagawa
- Division of Toxicology, Tokyo Metropolitan Institute of Public Health, 3-24-1, Hyakunin-cho, Shinjuku-ku, Tokyo, 169-0073, Japan
| | - Akiko Inomata
- Division of Toxicology, Tokyo Metropolitan Institute of Public Health, 3-24-1, Hyakunin-cho, Shinjuku-ku, Tokyo, 169-0073, Japan
| | - Akio Ogata
- Division of Toxicology, Tokyo Metropolitan Institute of Public Health, 3-24-1, Hyakunin-cho, Shinjuku-ku, Tokyo, 169-0073, Japan
| | - Dai Nakae
- Division of Toxicology, Tokyo Metropolitan Institute of Public Health, 3-24-1, Hyakunin-cho, Shinjuku-ku, Tokyo, 169-0073, Japan
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Fiorani M, Azzolini C, Cerioni L, Guidarelli A, Cantoni O. Superoxide dictates the mode of U937 cell ascorbic acid uptake and prevents the enhancing effects of the vitamin to otherwise nontoxic levels of reactive oxygen/nitrogen species. J Nutr Biochem 2013; 24:467-74. [DOI: 10.1016/j.jnutbio.2012.01.009] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/17/2011] [Revised: 11/09/2011] [Accepted: 01/17/2012] [Indexed: 01/08/2023]
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Valachová K, Hrabárová E, Priesolová E, Nagy M, Baňasová M, Juránek I, Soltés L. Free-radical degradation of high-molecular-weight hyaluronan induced by ascorbate plus cupric ions. Testing of bucillamine and its SA981-metabolite as antioxidants. J Pharm Biomed Anal 2011; 56:664-70. [PMID: 21782370 DOI: 10.1016/j.jpba.2011.06.015] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/02/2011] [Revised: 06/17/2011] [Accepted: 06/21/2011] [Indexed: 11/25/2022]
Abstract
High-molecular-weight hyaluronan (HA) samples were exposed to free-radical chain-degradation reactions induced by ascorbate in the presence of Cu(II) ions - the so-called Weissberger's oxidative system. The concentrations of both reactants [ascorbate, Cu(II)] were comparable to those that may occur during an early stage of the acute phase of joint inflammation. The time-dependent changes of the viscosity of the HA solution in the absence of the substance tested were monitored by rotational viscometry. However, when the anti- or pro-oxidative effects of the antioxidants/drugs were investigated, their dose-dependency was also examined. Additionally, the anti-oxidative activities of these substances were screened by the well-established ABTS and DPPH decolorization assays. The actions of the disease-modifying anti-rheumatic drugs, namely bucillamine and D-penicillamine, were compared to those of L-cysteine and of SA981, the oxidized metabolite of bucillamine. The results indicated that bucillamine was the most efficient scavenger of hydroxyl- and/or peroxyl-type radicals, even at the lowest drug concentration. In contrast, SA981 demonstrated no scavenging activity against the aforementioned free radicals. D-Penicillamine and L-cysteine showed a dual effect, i.e. a pronounced anti-oxidative effect was, after a given time period, followed by a significant pro-oxidative effect.
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Affiliation(s)
- Katarína Valachová
- Institute of Experimental Pharmacology and Toxicology, Slovak Academy of Sciences, SK-84104 Bratislava, Slovakia.
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10
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Protective effects of manganese(II) chloride on hyaluronan degradation by oxidative system ascorbate plus cupric chloride. Interdiscip Toxicol 2010; 3:26-34. [PMID: 21217868 PMCID: PMC2984120 DOI: 10.2478/v10102-010-0001-7] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/12/2009] [Revised: 01/18/2010] [Accepted: 01/21/2010] [Indexed: 11/20/2022] Open
Abstract
The degradation of several high-molar-mass hyaluronan samples was investigated in the presence of ascorbic acid itself and further by an oxidative system composed of ascorbic acid plus transition metal ions, i.e. Fe(II) or Cu(II) ions. The latter oxidative system imitates conditions in a joint synovial fluid during early phase of acute joint inflammation and can be used as a model for monitoring oxidative degradation of hyaluronan under pathophysiological conditions. The system Cu(II) plus ascorbate (the Weissberger oxidative system) resulted in a more significant decrease of hyaluronan molar mass compared to the oxidative system Fe(II) plus ascorbate. Addition of manganese(II) chloride was found to decrease the rate of the oxidative damage of hyaluronan initiated by ascorbate itself and by the Weissberger system.
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11
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Šoltés L, Kogan G. Catabolism of hyaluronan: involvement of transition metals. Interdiscip Toxicol 2009; 2:229-38. [PMID: 21217859 PMCID: PMC2984116 DOI: 10.2478/v10102-009-0026-y] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/02/2009] [Revised: 07/20/2009] [Accepted: 07/21/2009] [Indexed: 11/20/2022] Open
Abstract
One of the very complex structures in the vertebrates is the joint. The main component of the joint is the synovial fluid with its high-molar-mass glycosaminoglycan hyaluronan, which turnover is approximately twelve hours. Since the synovial fluid does not contain any hyaluronidases, the fast hyaluronan catabolism is caused primarily by reductive-oxidative processes.Eight transition metals - V(23), Mn(25), Fe(26), Co(27), Ni(28), Cu(29), Zn(30), and Mo(42) - naturally occurring in living organism are essential for the control of various metabolic and signaling pathways. They are also the key elements in catabolism of hyaluronan in the joint.In this overview, the role of these metals in physiological and pathophysiological catabolism of hyaluronan is described. The participation of these metals in the initiation and propagation of the radical degradation hyaluronan is critically reviewed.
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Affiliation(s)
- Ladislav Šoltés
- Institute of Experimental Pharmacology, Slovak Academy of Sciences, SK-84104 Bratislava, Slovakia
| | - Grigorij Kogan
- Directorate Health, Directorate General Research, European Commission, B-1049, Brussels, Belgium
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12
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Abstract
Recommended Nutrient Intakes (RNIs) are set for healthy individuals living in clean environments. There are no generally accepted RNIs for those with moderate malnutrition, wasting, and stunting, who live in poor environments. Two sets of recommendations are made for the dietary intake of 30 essential nutrients in children with moderate malnutrition who require accelerated growth to regain normality: first, for those moderately malnourished children who will receive specially formulated foods and diets; and second, for those who are to take mixtures of locally available foods over a longer term to treat or prevent moderate stunting and wasting. Because of the change in definition of severe malnutrition, much of the older literature is pertinent to the moderately wasted or stunted child. A factorial approach has been used in deriving the recommendations for both functional, protective nutrients (type I) and growth nutrients (type II).
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Steinert JR, Wyatt AW, Jacob R, Mann GE. Redox modulation of Ca2+ signaling in human endothelial and smooth muscle cells in pre-eclampsia. Antioxid Redox Signal 2009; 11:1149-63. [PMID: 19125611 DOI: 10.1089/ars.2008.2303] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/13/2022]
Abstract
Pre-eclampsia (PE) is a leading cause of maternal hypertension in pregnancy and is associated with fetal growth restriction, premature birth, and fetal and maternal mortality. Activation and dysfunction of the maternal and fetal endothelium in PE appears to be a consequence of increased oxidative stress, resulting from elevated levels of circulating lipid peroxides. Accumulating evidence implicates reactive oxygen species (ROS) in the pathogenesis of vascular dysfunction in PE, perhaps involving a disturbance in intracellular Ca(2+) signaling. Several ion-transport pathways are highly sensitive to oxidative stress, and the resulting modulation of ion transport by ROS will affect intracellular Ca(2+) homeostasis. We review the evidence that changes in ion transport induced by ROS may be linked with abnormalities in Ca(2+)-mediated signal transduction, leading to endothelial and smooth muscle dysfunction in maternal and fetal circulations in PE. As dysregulation of Ca(2+) signaling in fetal umbilical endothelial cells is maintained in culture and embryonic, fetal, and postnatal development is affected by the cellular redox state, we hypothesize that impaired redox signaling in PE may influence "programming" of the fetal cardiovascular system and endothelial function in adulthood.
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Affiliation(s)
- Joern R Steinert
- Cardiovascular Division, School of Medicine, King's College London, London, England
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Soltés L, Kogan G, Stankovska M, Mendichi R, Rychlý J, Schiller J, Gemeiner P. Degradation of High-Molar-Mass Hyaluronan and Characterization of Fragments. Biomacromolecules 2007; 8:2697-705. [PMID: 17691842 DOI: 10.1021/bm070309b] [Citation(s) in RCA: 53] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/17/2023]
Abstract
A sample of high-molar mass hyaluronan was oxidized by seven oxidative systems involving hydrogen peroxide, cupric chloride, ascorbic acid, and sodium hypochlorite in different concentrations and combinations. The process of the oxidative degradation of hyaluronan was monitored by rotational viscometry, while the fragments produced were investigated by size-exclusion chromatography, matrix-assisted laser desorption ionization-time-of-flight mass spectrometry, and non-isothermal chemiluminometry. The results obtained imply that the degradation of hyaluronan by these oxidative systems, some of which resemble the chemical combinations present in vivo in the inflamed joint, proceeds predominantly via hydroxyl radicals. The hyaluronan fragmentation occurred randomly and produced species with rather narrow and unimodal distribution of molar mass. Oxidative degradation not only reduces the molecular size of hyaluronan but also modifies its component monosaccharides, generating polymer fragments that may have properties substantially different from those of the original macromolecule.
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Affiliation(s)
- L Soltés
- Institute of Experimental Pharmacology, Slovak Academy of Sciences, SK-84104 Bratislava, Slovakia
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15
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Soltés L, Valachová K, Mendichi R, Kogan G, Arnhold J, Gemeiner P. Solution properties of high-molar-mass hyaluronans: the biopolymer degradation by ascorbate. Carbohydr Res 2007; 342:1071-7. [PMID: 17362893 DOI: 10.1016/j.carres.2007.02.018] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/16/2006] [Revised: 01/31/2007] [Accepted: 02/16/2007] [Indexed: 11/24/2022]
Abstract
An accurate molecular characterization, molar mass and size distributions, of 10 hyaluronan (HA) samples was performed by using a multi-angle light scattering detector connected on-line to a size exclusion chromatographic system. The dynamic viscosity eta of the HA solutions was investigated using a rotational viscometer. On monitoring the sample dynamic viscosity for up to 5h, a small however constant increase of the eta value was observed, indicating rheopectic behavior of all 10 HA solutions. Addition of ascorbic acid to the HA solutions caused significant changes in the rheological properties of the samples investigated. The change of eta values in the course of time was explained by the redox reactions (caused by the added ascorbate) that occur during the dynamic viscosity monitoring.
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Affiliation(s)
- Ladislav Soltés
- Institute of Experimental Pharmacology, Slovak Academy of Sciences, SK-84104 Bratislava, Slovakia.
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16
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Grano A, De Tullio MC. Ascorbic acid as a sensor of oxidative stress and a regulator of gene expression: the Yin and Yang of vitamin C. Med Hypotheses 2007; 69:953-4. [PMID: 17376607 DOI: 10.1016/j.mehy.2007.02.008] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/05/2007] [Accepted: 02/09/2007] [Indexed: 11/21/2022]
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Abstract
Multiple sclerosis (MS) is an immune-mediated disease, with inflammation and neurodegeneration contributing to neuronal demyelination and axonal injury. Current therapies for MS are directed toward modulation of the immune response; however, there is increasing evidence that oxidative stress is an important component in the pathogenesis of MS. The inflammatory environment in demyelinating lesions is conducive to the generation of reactive oxygen species. When these species are generated in MS and animal models of MS, products such as peroxynitrite and superoxide are formed that are highly toxic to cells. There are several examples of potential beneficial effects from various antioxidants in animal models of MS, but the efficacy may vary between different agents and, in some instances, may yield deleterious effects. Despite these promising results in animal models, there is limited and conflicting evidence of potential therapeutic effects of antioxidants such as vitamins C and E in treating MS. However, clinical trials in MS patients with more potent antioxidants, identified in animal studies, have been initiated.
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Affiliation(s)
- Noel G Carlson
- GRECC, VASLCHCS, Department of Neurobiology and Anatomy, University of Utah, Salt Lake City, Utah, USA
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Trommer H, Böttcher R, Huschka C, Wohlrab W, Neubert RHH. Further investigations on the role of ascorbic acid in stratum corneum lipid models after UV exposure. J Pharm Pharmacol 2005; 57:963-72. [PMID: 16102251 DOI: 10.1211/0022357056703] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/31/2022]
Abstract
This study is the continuation of our research into vitamin C and its possible effects on human skin after topical administration. The effects of ascorbic acid, iron ions and UV irradiation on stratum corneum lipid models were investigated. The lipid models used were: a simple system (linolenic acid dispersion), a complex system (liposomes consisting of dipalmitoylphosphatidylcholine, cholesterol and linolenic acid) and complex systems with additionally incorporated ceramides (types III and IV). The lipid peroxidation was quantified by the thiobarbituric acid assay. A human adult low-calcium high-temperature (HaCaT) keratinocytes cell culture was used as a second in-vitro model. The amount of intracellular peroxides was determined by measuring the fluorescence intensity using the dihydrorhodamine 123 assay. Electron paramagnetic resonance spectroscopy was used to study the influence of ascorbic acid and iron ions on the signal intensity of 5-doxylstearic acid during UV exposure. Ascorbic acid showed prooxidative properties in the thiobarbituric acid assay whereas cell protection was measured in the HaCaT keratinocytes experiments. Electron paramagnetic resonance investigations revealed different extents of free radical production generated by iron ions, ascorbic acid and UV irradiation. In evaluating the results from this study new aspects of the mechanism of lipid damage caused by these three factors were suggested, transcending the simple redox behaviour of ascorbic acid.
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Affiliation(s)
- Hagen Trommer
- Martin-Luther-University Halle-Wittenberg, School of Pharmacy, Institute of Pharmaceutics and Biopharmaceutics, Wolfgang-Langenbeck-Strasse 4, D-06120 Halle (Saale), Germany.
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Ko WS, Guo CH, Yeh MS, Lin LY, Hsu GSW, Chen PC, Luo MC, Lin CY. Blood micronutrient, oxidative stress, and viral load in patients with chronic hepatitis C. World J Gastroenterol 2005; 11:4697-702. [PMID: 16094713 PMCID: PMC4615414 DOI: 10.3748/wjg.v11.i30.4697] [Citation(s) in RCA: 71] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: To assess the extent of micronutrient and oxidative stress in blood and to examine their linkages with viral loads in chronic hepatitis C patients.
METHODS: Hepatitis C virus (HCV)-RNA levels were quantified in the serum from 37 previously untreated patients with chronic hepatitis C. The plasma and erythrocyte micronutrients (zinc, selenium, copper, and iron) were estimated, and malondialdehyde (MDA) contents were determined as a marker to detect oxidative stress. Antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPX) and glutathione reductase (GR) activities in blood were also measured. The control group contained 31 healthy volunteers.
RESULTS: The contents of zinc (Zn), and selenium (Se) in plasma and erythrocytes were significantly lower in hepatitis C patients than in the controls. On the contrary, copper (Cu) levels were significantly higher. Furthermore, plasma and erythrocyte MDA levels, and the SOD and GR activities in erythrocytes significantly increased in hepatitis C patients compared to the controls. However, the plasma GPX activity in patients was markedly lower. Plasma Se (r = -0.730, P < 0.05), Cu (r = 0.635), and GPX (r = -0.675) demonstrated correlations with HCV-RNA loads. Significant correlation coefficients were also observed between HCV-RNA levels and erythrocyte Zn (r = -0.403), Se (r = -0.544), Cu (r = 0.701) and MDA (r = 0.629) and GR (r = 0.441).
CONCLUSION: The levels of Zn, Se, Cu, and oxidative stress (MDA), as well as related anti-oxidative enzymes (GR and GPX) in blood have important impact on the viral factors in chronic hepatitis C. The distribution of these parameters might be significant biomarkers for HCV.
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Affiliation(s)
- Wang-Sheng Ko
- Department of Food and Nutrition, Hung Kuang University, Taichung, Taiwan, China
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Dhar-Mascareño M, Cárcamo JM, Golde DW. Hypoxia-reoxygenation-induced mitochondrial damage and apoptosis in human endothelial cells are inhibited by vitamin C. Free Radic Biol Med 2005; 38:1311-22. [PMID: 15855049 DOI: 10.1016/j.freeradbiomed.2005.01.017] [Citation(s) in RCA: 111] [Impact Index Per Article: 5.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/22/2004] [Revised: 01/20/2005] [Accepted: 01/20/2005] [Indexed: 10/25/2022]
Abstract
Hypoxia and hypoxia-reperfusion (H-R) play important roles in human pathophysiology because they occur in clinical conditions such as circulatory shock, myocardial ischemia, stroke, and organ transplantation. Reintroduction of oxygen to hypoxic cells during reperfusion causes an increase in generation of reactive oxygen species (ROS), which can alter cell signaling, and cause damage to lipids, proteins, and DNA leading to ischemia-reperfusion injury. Since vitamin C is a potent antioxidant and quenches ROS, we investigated the role of intracellular ascorbic acid (iAA) in endothelial cells undergoing hypoxia-reperfusion. Intracellular AA protected human endothelial cells from H-R-induced apoptosis. Intracellular AA also prevents loss of mitochondrial membrane potential and the release of cytochrome C and activation of caspase-9 and caspase-3 during H-R. Additionally, inhibition of caspase-9 activation prevented H-R-induced apoptosis, suggesting a mitochondrial site of initiation of apoptosis. We found that H-R induced an increase in ROS in endothelial cells that was abrogated in the presence of iAA. Our results indicate that vitamin C prevents hypoxia and H-R-induced damage to human endothelium.
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Affiliation(s)
- Manya Dhar-Mascareño
- Molecular Pharmacology and Chemistry Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.
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