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1.
Vitamin A and beta (β)-carotene supplementation for cystic fibrosis.
de Vries, JJ, Chang, AB, Bonifant, CM, Shevill, E, Marchant, JM
The Cochrane database of systematic reviews. 2018;(8):CD006751
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Abstract
BACKGROUND People with cystic fibrosis (CF) and pancreatic insufficiency are at risk of a deficiency in fat-soluble vitamins, including vitamin A. Vitamin A deficiency predominantly causes eye and skin problems, while excessive levels of vitamin A can harm the respiratory and skeletal systems in children and interfere with the metabolism of other fat-soluble vitamins. Most CF centres administer vitamin A as supplements to reduce the frequency of vitamin A deficiency in people with CF and to improve clinical outcomes such as growth, although the recommended dose varies between different guidelines. Thus, a systematic review on vitamin A and vitamin A-like supplementation (carotenes or other retinoids) in people with CF would help guide clinical practice. This is an update of an earlier Cochrane Review. OBJECTIVES To determine if supplementation with vitamin A, carotenes or other retinoid supplements in children and adults with CF reduces the frequency of vitamin A deficiency disorders, improves general and respiratory health and affects the frequency of vitamin A toxicity. SEARCH METHODS We searched the Cochrane Cystic Fibrosis and Genetic Disorders Group Cystic Fibrosis Trials Register compiled from electronic database searches and handsearching of journals and conference abstract books. Additionally we searched several ongoing trials registries, including ClinicalTrials.gov, the WHO International Clinical Trials Registry Platform and the International Standard Randomised Controlled Trial Number Registry.Most recent database searches: 01 June 2018. SELECTION CRITERIA All randomised or quasi-randomised controlled studies comparing all preparations of oral vitamin A, carotenes or retinoids (or in combination), used as a supplement compared to placebo at any dose, for at least three months, in people with CF (diagnosed by sweat tests or genetic testing) with and without pancreatic insufficiency. DATA COLLECTION AND ANALYSIS Two authors individually assessed study quality and extracted data on outcome measures. The authors assessed the quality of the evidence using the GRADE system. Investigators were contacted to retrieve missing quantitative data. MAIN RESULTS No studies of vitamin A or other retinoid supplementation were eligible for inclusion. However, one randomised study of beta (β)-carotene supplementation involving 24 people with CF who were receiving pancreatic enzyme substitution was included. The study compared successive β-carotene supplementation periods (high dose followed by low dose) compared to placebo. The results for the low-dose supplementation period should be interpreted with caution, due to the lack of a wash-out period after the high-dose supplementation.The included study did not report on two of the review's primary outcomes (vitamin A deficiency disorders and mortality); results for our third primary outcome of growth and nutritional status (reported as z score for height) showed no difference between supplementation and placebo, mean difference (MD) -0.23 (95% confidence interval (CI) -0.89 to 0.43) (low-quality evidence). With regards to secondary outcomes, supplementation with high-dose β-carotene for three months led to significantly fewer days of systemic antibiotics required to treat pulmonary exacerbations, compared to controls, MD -15 days (95% CI -27.60 to -2.40); however, this was not maintained in the second three-month section of the study when the level of β-carotene supplementation was reduced, MD -8 days (95% CI -18.80 to 2.80) (low-quality evidence). There were no statistically significant effects between groups in lung function (low-quality evidence) and no adverse events were observed (low-quality evidence). Supplementation affected levels of β-carotene in plasma, but not vitamin A levels. The study did not report on quality of life or toxicity. AUTHORS' CONCLUSIONS Since no randomised or quasi-randomised controlled studies on retinoid supplementation were identified, no conclusion on the supplementation of vitamin A in people with CF can be drawn. Additionally, due to methodological limitations in the included study, also reflected in the low-quality evidence judged following the specific evidence grading system (GRADE), no clear conclusions on β-carotene supplementation can be drawn. Until further data are available, country- or region-specific guidelines regarding these practices should be followed.
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2.
Antioxidant effects of β-carotene, but not of retinol and vitamin E, in orbital fibroblasts from patients with Graves' orbitopathy (GO).
Rotondo Dottore, G, Ionni, I, Menconi, F, Casini, G, Sellari-Franceschini, S, Nardi, M, Vitti, P, Marcocci, C, Marinò, M
Journal of endocrinological investigation. 2018;(7):815-820
Abstract
BACKGROUND Oxidative stress is involved in the pathogenesis of Graves' orbitopathy (GO) and several antioxidant agents, namely, selenium, quercetin, enalapril, vitamin C, N-acetyl-L-cysteine, and melatonin, have been shown to reduce oxidative stress and its consequences in primary culture of orbital fibroblasts. In addition, selenium is effective for the treatment of mild GO. Here, we investigated the action of three additional antioxidants in orbital fibroblasts, namely, retinol, β-carotene, and vitamin E. METHODS Primary cultures of orbital fibroblasts were established from GO patients and control subjects. To induce oxidative stress, cells were treated with H2O2, after which glutathione disulfide (GSSG) (a parameter of oxidative stress), cell proliferation, hyaluronic acid, TNFα, IFNγ, and IL1β were measured. RESULTS H2O2-dependent oxidative stress (augmented GSSG) was associated with increased cell proliferation and cytokine release. All the three antioxidant substances reduced GSSG in both GO and control fibroblasts. β-carotene reduced proliferation in GO, but not in control fibroblasts. IL1β was reduced by all three substances. Retinol reduced IFNγ in GO and control fibroblasts. CONCLUSIONS Our study supports an antioxidant role of retinol, β-carotene, and vitamin E in orbital fibroblasts from patients with GO and provides a basis for a possible clinical use these substances.
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3.
ROS production and glutathione response in keratinocytes after application of β-carotene and VIS/NIR irradiation.
Lohan, SB, Vitt, K, Scholz, P, Keck, CM, Meinke, MC
Chemico-biological interactions. 2018;:1-7
Abstract
The skin is exposed to many stress factors which, in turn, can promote a shift of the antioxidant (AO) network towards the prooxidative side, supporting the development of various skin disorders. A balanced diet, in combination with a healthy lifestyle could reduce oxidative stress. Carotenoids are essential nonenzymatic AOs and main components of the exogenous AO system. To examine the interdependence between endogenous and exogenous AOs, secondary keratinocytes (HaCaT) were treated with various Beta (β-)-carotene concentrations with subsequent stress treatment by moderate irradiation (700-2000 nm). To facilitate the uptake of β-carotene, an innovative nanocrystal solution was used. Cell viability assay was applied to HaCaT cells to evaluate suitable concentration of β-carotene, whereby the uptake was measured by resonant Raman spectroscopy. The redox status was determined before and after supplementation with two selected β-carotene concentrations (0.02 and 0.1 μg/ml) and irradiation. Reactive oxygen species (ROS) were measured by electron paramagnetic resonance spectroscopy and the AO glutathione (GSH) by a fluorescent-based assay for evaluating the endogenous redox status. An increase of ROS and a reduction of GSH after irradiation was observed. Interestingly, the applied β-carotene, already induce oxidative stress. Nevertheless, an effective protection against irradiation could be observed for the lower dose. The high dose turned pro-oxidative.
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Effect of β-Carotene Supplementation on the Risk of Pneumonia Is Heterogeneous in Males: Effect Modification by Cigarette Smoking.
Hemilä, H
Journal of nutritional science and vitaminology. 2018;(5):374-378
Abstract
Beta-carotene has been suggested to be a factor for improving the immune system, which implies that it might decrease the risk of infections. We therefore analyzed whether beta-carotene supplementation influenced pneumonia risk in 14,564 Finnish male smokers of the Alpha-Tocopherol Beta-Carotene (ATBC) Study. There were 231 pneumonia cases in the beta-carotene group and 217 cases in the placebo group. Thus, beta-carotene had no effect on the average incidence of pneumonia, RR=1.07 (95% CI: 0.89-1.29). However, cigarette smoking exposure significantly modified the effect. Beta-carotene increased pneumonia risk by RR=4.0 (95% CI: 1.63-10) among 990 participants who started to smoke at the age of ≥21 y and smoked ≥21 cigarettes per day at the study baseline. However, beta-carotene had no influence on pneumonia risk for the remaining participants. We also analyzed the effect of beta-carotene on participants who quit smoking during the ATBC Study. Among 4,290 participants who quit smoking, the 58 pneumonia cases were evenly distributed between the beta-carotene and placebo groups with RR=0.93 (95% CI: 0.55-1.55). Accordingly, no evidence was found that beta-carotene decreased pneumonia risk; instead, it significantly increased the incidence of pneumonia in a subgroup that covered 7% of the study population.
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5.
[Meta-analysis of vitamin C, vitamin E and β-carotene levels in the plasma of Alzheimer's disease patients].
Dong, R, Yang, Q, Zhang, Y, Li, J, Zhang, L, Zhao, H
Wei sheng yan jiu = Journal of hygiene research. 2018;(4):648-654
Abstract
OBJECTIVE To systematically evaluate the levels of vitamin C, vitamin E and β-carotene in the plasma of Alzheimer's disease( AD) patients. METHODS In this study, literature of the levels of vitamin C, vitamin E and β-carotene in the plasma of AD patients were collected by retrieving the database of Pub Med, Science Direct, CNKI and Wan Fang( from they were built to July 2017). RESULTS Meta-analysis result showed that, compared with the control group, the level of vitamin E in the plasma of AD patients declined significantly( SMD =-1. 49 μmol/L, 95% CI-2. 08--0. 89 μmol/L, P <0. 001). However, no differences were determined in the levels of the plasma vitamin C and β-carotene between the two groups( vitamin C: SMD =-1. 43 μmol/L, 95% CI-3. 05-0. 19 μmol/L, P = 0. 083; β-carotene: SMD =-0. 61 μmol/L, 95% CI-1. 40-0. 18 μmol/L, P = 0. 131). CONCLUSION Increasing vitamin E level in the plasma through vitamin E riched diet may be useful to prevent AD. However it is not yet believed the benefical role on AD to increase vitamin C and β-carotene.
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Lack of Association Between Heart Failure and Incident Cancer.
Selvaraj, S, Bhatt, DL, Claggett, B, Djoussé, L, Shah, SJ, Chen, J, Imran, TF, Qazi, S, Sesso, HD, Gaziano, JM, et al
Journal of the American College of Cardiology. 2018;(14):1501-1510
Abstract
BACKGROUND Several recent studies have suggested an increased cancer risk among patients with heart failure (HF). However, these studies are constrained by limited size and follow-up, lack of comprehensive data on other health attributes, and adjudicated cancer outcomes. OBJECTIVES This study sought to determine whether HF is associated with cancer incidence and cancer-specific mortality. METHODS The study assembled a cohort from the Physicians' Health Studies I and II, 2 randomized controlled trials of aspirin and vitamin supplements conducted from 1982 to 1995 and from 1997 to 2011, respectively, that included annual health evaluations and determination of cancer and HF diagnoses. In the primary analysis, the study excluded participants with cancer or HF at baseline and performed multivariable-adjusted Cox models to determine the relationship between HF and cancer, modeling HF as a time-varying exposure. In a complementary analysis, the study used the landmark method and identified cancer-free participants at 70 years of age, distinguishing between those with and without HF, and likewise performed Cox regression. Sensitivity analyses were performed at 65, 75, and 80 years of age. RESULTS Among 28,341 Physicians' Health Study participants, 1,420 developed HF. A total of 7,363 cancers developed during a median follow-up time of 19.9 years (25th to 75th percentile: 11.0 to 26.8 years). HF was not associated with cancer incidence in crude (hazard ratio: 0.92; 95% confidence interval: 0.80 to 1.08) or multivariable-adjusted analysis (hazard ratio: 1.05; 95% confidence interval: 0.86 to 1.29). No association was found between HF and site-specific cancer incidence or cancer-specific mortality after multivariable adjustment. Results were similar when using the landmark method at all landmark ages. CONCLUSIONS HF is not associated with an increased risk of cancer among male physicians.
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β-carotene at physiologically attainable concentration induces apoptosis and down-regulates cell survival and antioxidant markers in human breast cancer (MCF-7) cells.
Sowmya Shree, G, Yogendra Prasad, K, Arpitha, HS, Deepika, UR, Nawneet Kumar, K, Mondal, P, Ganesan, P
Molecular and cellular biochemistry. 2017;(1-2):1-12
Abstract
Although β-carotene is known for its anti-carcinogenic and antioxidant properties, a few recent epidemiological and experimental evidence show that at higher concentration it acts as pro-oxidant and induces cancer. Since the global burden of breast cancer exceeds all other types of cancer, and its incidence rates is also in increasing trend, the present study attempted to evaluate the anti-cancer molecular mechanism of β-carotene (at 1 µM concentration) isolated from Spinacia oleracea in human breast cancer (MCF-7) cells. The carotenoid was purified by open column chromatography and identified by LC-MS. The anti-proliferative effect of β-carotene at different concentrations was evaluated by WST-1 assay and the changes in cell morphology were examined by microscopic observation. The induction of apoptosis by β-carotene was observed by DAPI staining and colorimetric caspase-3 assay. The expression of cell survival, apoptotic, and antioxidant marker proteins was measured by western blot analysis. Purified β-carotene inhibited the viability of MCF-7 cells in a dose-dependent manner, which was well correlated with changes in cell morphology. Increased apoptotic cells were observed in β-carotene (1 µM)-treated cells. This apoptosis induction was associated with increased caspase-3 activity. The protein expression studies showed that β-carotene at 1 µM concentration effectively decreases the expression of the anti-apoptotic protein, Bcl-2 and PARP, and survival protein, NF-kB. It also inhibited the activation of intracellular growth signaling proteins, Akt and ERK1/2. The inhibition of Akt activation by β-carotene results in decreased phosphorylation of Bad. Further, it down-regulated antioxidant enzyme, SOD-2, and its transactivation factor (Nrf-2), and endoplasmic reticulum (ER) stress marker, XBP-1, at protein levels. These findings exhibit the key role of β-carotene even at a low physiological concentration in MCF-7 cells which further explains its predominant anti-cancer activity.
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Antioxidants Taken Orally prior to Diagnostic Radiation Exposure Can Prevent DNA Injury.
Velauthapillai, N, Barfett, J, Jaffer, H, Mikulis, D, Murphy, K
Journal of vascular and interventional radiology : JVIR. 2017;(3):406-411
Abstract
PURPOSE To evaluate efficacy of oral antioxidant treatment given to patients before radiologic procedures in reducing x-ray-induced DNA damage. MATERIALS AND METHODS In a single-center prospective controlled trial, antioxidant treatment with 2 g ascorbate, 1.2 g N-acetylcysteine, 600 mg lipoic acid, and 30 mg beta carotene was given to 5 consecutive participants before undergoing clinically indicated technetium-99m methylene diphosphonate (99mTc MDP) bone scans for cancer staging. These participants were compared with 5 participants without antioxidant treatment. DNA damage was visualized in peripheral blood mononuclear cells (PBMCs) before and after bone scans using three-dimensional microscopy and fluorescently labeled gamma-H2AX protein. Wilcoxon rank sum test was used to determine whether there was a statistically significant difference in the radiation received between the control and antioxidant groups, the number of foci/cell before and after bone scan within groups, and foci/cell after bone scan between groups. RESULTS There was a significantly higher number of gamma-H2AX foci/cell after ionization radiation in the control group compared with the antioxidant group (P = .009). There was no statistically significant difference in number of gamma-H2AX foci/cell before or after exposure in the antioxidant group; the number of gamma-H2AX foci/cell was statistically significantly higher (P = .009) in the control group after exposure to 99mTc MDP. CONCLUSIONS In patients undergoing 99mTc MDP bone scans, treatment with oral antioxidants before scanning significantly prevented DNA damage in PBMCs. Antioxidants may provide an effective means to protect patients and health care professionals from radiation-induced DNA damage during imaging studies.
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[Progress in metabolic engineering of β-carotene synthesis].
Wang, Y, Xing, J, Chen, H
Sheng wu gong cheng xue bao = Chinese journal of biotechnology. 2017;(4):578-590
Abstract
β-carotene is an important natural plant pigment and has various physiological functions in organisms. With the proposition of systematic biology and progress in carotenoids biosynthesis since the 1960s, metabolic engineering has played a significant role in enhancing carotenoid production. In this review, we present β-carotene's traditional production methods and metabolic engineering strategies for constructing β-carotene-producing strains. Meanwhile, main problems and corresponding solutions to improve β-carotene yield of engineered strains were further analyzed, for further efficient microbial production of β-carotene.
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β-carotene treatment alters the cellular death process in oxidative stress-induced K562 cells.
Akçakaya, H, Tok, S, Dal, F, Cinar, SA, Nurten, R
Cell biology international. 2017;(3):309-319
Abstract
Oxidizing agents (e.g., H2 O2 ) cause structural and functional disruptions of molecules by affecting lipids, proteins, and nucleic acids. As a result, cellular mechanisms related to disrupted macro molecules are affected and cell death is induced. Oxidative damage can be prevented at a certain point by antioxidants or the damage can be reversed. In this work, we studied the cellular response against oxidative stress induced by H2 O2 and antioxidant-oxidant (β-carotene-H2 O2 ) interactions in terms of time, concentration, and treatment method (pre-, co-, and post) in K562 cells. We showed that co- or post-treatment with β-carotene did not protect cells from the damage of oxidative stress furthermore co- and post-β-carotene-treated oxidative stress induced cells showed similar results with only H2 O2 treated cells. However, β-carotene pre-treatment prevented oxidative damage induced by H2 O2 at concentrations lower than 1,000 μM compared with only H2 O2 -treated and co- and post-β-carotene-treated oxidative stress-induced cells in terms of studied cellular parameters (mitochondrial membrane potential [Δψm ], cell cycle and apoptosis). Prevention effect of β-carotene pre-treatment was lost at concentrations higher than 1,000 μM H2 O2 (2-10 mM). These findings suggest that β-carotene pre-treatment alters the effects of oxidative damage induced by H2 O2 and cell death processes in K562 cells.