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Correlation between Nutrition, Oxidative Stress and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (31 May 2017) | Viewed by 183024

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Guest Editor
Department of Physiology, Institute of Nutrition and Food Technology “Jose Mataix”, Biomedical Research Center, University of Granada, Avda. Conocimiento s/n, 18100 Armilla, Granada, Spain
Interests: cancer biology; antioxidants; oxidative stress; food chemistry; nutrition; reactive oxygen species
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Special Issue Information

Dear Colleagues,

When the regulation of homeostasis of radicals in tissues or cells do not function correctly, a situation of stress can come about, due to the increased presence of oxidative radicals. In these cases, the term “oxidative stress” is often used to indicate an imbalance towards major oxidation of tissue, measured by the appearance of oxidized species present in the main elements of a cell, that is, lipids, proteins, DNA, and carbohydrates. A strong relationship exists between nutrition and oxidative stress. Works that have been published in recent years, in the field of human health, demonstrate that the production, transformation, and metabolism of free radicals are finely regulated processes, and that the malfunction of these inevitably leads to inflammatory tissue damage. On the other hand, oxidative stress does not only have to be considered as a negative event, as it also has physiological functions: For example, a transient situation of oxidative stress constitutes one of the fundamental mechanisms of functioning to answer or to send many types of signals (hormones, neurotransmitters, cytokine, etc.), to defend oneself from infective agents and to alter the redox state, which is necessary to start up a differentiated process. On the other hand, the chronicity of oxidative stress constitutes a condition of risk for degenerative processes and can lead to a pathological situation. A varied, balanced, and good-quality diet can produce a majority of antioxidant substances that can act in synergy to obstruct the excessive presence of free radicals. In addition, it is essential that diet be rich in foods of vegetable origin, which are the true allies in tackling the damages associated with an alteration of the redox cellular state.

Prof. Dr. Lorenza Speranza
Prof. Dr. Josè L. Quiles
Dr. Sara Franceschelli
Guest Editors

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Keywords

  • nutrition
  • oxidative stress
  • disease
  • antioxidant
  • bioactive vegetable molecules
  • superoxide dismutase
  • catalase
  • vegetable food
  • polyphenol
  • α-mangostin

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Published Papers (17 papers)

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Research

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3739 KiB  
Article
Effect of Angelica sinensis Root Extract on Cancer Prevention in Different Stages of an AOM/DSS Mouse Model
by Bochen Zhao, Qian Kang, Yu Peng, Yuanping Xie, Cheng Chen, Bingshao Li and Qing Wu
Int. J. Mol. Sci. 2017, 18(8), 1750; https://doi.org/10.3390/ijms18081750 - 11 Aug 2017
Cited by 18 | Viewed by 6024
Abstract
Angelica sinensis root (ASR) extract was obtained to investigate its effects on colorectal carcinogenesis in different stages of an Azoxymethane/Dextran sodium sulphate (AOM/DSS) model. In this study, we showed that ASR extract administration in the initial stage of the AOM/DSS model had cancer [...] Read more.
Angelica sinensis root (ASR) extract was obtained to investigate its effects on colorectal carcinogenesis in different stages of an Azoxymethane/Dextran sodium sulphate (AOM/DSS) model. In this study, we showed that ASR extract administration in the initial stage of the AOM/DSS model had cancer preventive effects with decreasing tumor incidence and a high-grade of intraepithelial neoplasia incidence. With respect to DNA damage, the amounts of 8-oxoguanine and γ-H2AX were suppressed in colon tissue. The balance of apoptosis and proliferation was approaching the normal state. In contrast, ASR extract administration in the promotion stage of the AOM/DSS model accelerated the progression of carcinogenesis. The maximum tumor size reached 49.85 ± 25.04 mm3. High-grade pathological changes were significantly increased. Decreased DNA damage and P53 level reflected the disrupted reactive oxygen species (ROS) concentration in colorectal tissue, which led to an imbalance of proliferative and apoptotic relationships. These findings suggested that the cancer-preventive effect of ASR extract may be stage-dependent in the process of carcinogenesis. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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Article
A Novel Therapeutic Approach in the Treatment of Pulmonary Arterial Hypertension: Allium ursinum Liophylisate Alleviates Symptoms Comparably to Sildenafil
by Mariann Bombicz, Daniel Priksz, Balazs Varga, Andrea Kurucz, Attila Kertész, Akos Takacs, Aniko Posa, Rita Kiss, Zoltan Szilvassy and Bela Juhasz
Int. J. Mol. Sci. 2017, 18(7), 1436; https://doi.org/10.3390/ijms18071436 - 4 Jul 2017
Cited by 14 | Viewed by 6694
Abstract
Right-sided heart failure—often caused by elevated pulmonary arterial pressure—is a chronic and progressive condition with particularly high mortality rates. Recent studies and our current findings suggest that components of Wild garlic (Allium ursinum, AU) may play a role in reducing blood [...] Read more.
Right-sided heart failure—often caused by elevated pulmonary arterial pressure—is a chronic and progressive condition with particularly high mortality rates. Recent studies and our current findings suggest that components of Wild garlic (Allium ursinum, AU) may play a role in reducing blood pressure, inhibiting angiotensin-converting enzyme (ACE), as well as improving right ventricle function in rabbit models with heart failure. We hypothesize that AU may mitigate cardiovascular damage caused by pulmonary arterial hypertension (PAH) and has value in the supplementary treatment of the complications of the disease. In this present investigation, PAH was induced by a single dose of monocrotaline (MCT) injection in Sprague-Dawley rats, and animals were divided into 4 treatment groups as follows: I. healthy control animals (Control group); II. pulmonary hypertensive rats (PAH group); III. pulmonary hypertensive rats + daily sildenafil treatment (Sildenafil group); and IV. pulmonary hypertensive rats + Wild garlic liophylisate-enriched chow (WGLL group), for 8 weeks. Echocardiographic measurements were obtained on the 0 and 8 weeks with fundamental and Doppler imaging. Isolated working heart method was used to determinate cardiac functions ex vivo after thoracotomy on the 8th week. Histological analyses were carried out on excised lung samples, and Western blot technique was used to determine Phosphodiesterase type 5 enzyme (PDE5) expression in both myocardial and pulmonary tissues. Our data demonstrate that right ventricle function measured by echocardiography was deteriorated in PAH animals compared to controls, which was counteracted by AU treatment. Isolated working heart measurements showed elevated aortic flow in WGLL group compared to PAH animals. Histological analysis revealed dramatic increase in medial wall thickness of pulmonary arteries harvested from PAH animals, but arteries of animals in sildenafil- and WGLL-treated groups showed physiological status. Our results suggest that bioactive compounds in Allium ursinum could have beneficial effects in pulmonary hypertension. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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Article
Loss of Bone Mineral Density Associated with Age in Male Rats Fed on Sunflower Oil Is Avoided by Virgin Olive Oil Intake or Coenzyme Q Supplementation
by Alfonso Varela-López, Julio J. Ochoa, José M. Llamas-Elvira, Magdalena López-Frías, Elena Planells, Lorenza Speranza, Maurizio Battino and José L. Quiles
Int. J. Mol. Sci. 2017, 18(7), 1397; https://doi.org/10.3390/ijms18071397 - 29 Jun 2017
Cited by 18 | Viewed by 4909
Abstract
The role of dietary fat unsaturation and the supplementation of coenzyme Q have been evaluated in relation to bone health. Male Wistar rats were maintained for 6 or 24 months on two diets varying in the fat source, namely virgin olive oil, rich [...] Read more.
The role of dietary fat unsaturation and the supplementation of coenzyme Q have been evaluated in relation to bone health. Male Wistar rats were maintained for 6 or 24 months on two diets varying in the fat source, namely virgin olive oil, rich in monounsaturated fatty acids, or sunflower oil, rich in n-6 polyunsaturated fatty acids. Both dietary fats were supplemented or not with coenzyme Q10 (CoQ10). Bone mineral density (BMD) was evaluated in the femur. Serum levels of osteocalcin, osteopontin, receptor activator of nuclear factor κB ligand (RANKL), osteoprotegerin (OPG), adrenocorticotropin (ACTH) and parathyroid hormone (PTH), as well as urinary F2-isoprostanes were measured. Aged animals fed on virgin olive oil showed higher BMD than those fed on sunflower oil. In addition, CoQ10 prevented the age-related decline in BMD in animals fed on sunflower oil. Urinary F2-isoprostanes analysis showed that sunflower oil led to the highest oxidative status in old animals, which was avoided by supplementation with CoQ10. In conclusion, lifelong feeding on virgin olive oil or the supplementation of sunflower oil on CoQ10 prevented, at least in part mediated by a low oxidative stress status, the age-related decrease in BMD found in sunflower oil fed animals. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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Article
The Roles of Reactive Oxygen Species and Nitric Oxide in Perfluorooctanoic Acid-Induced Developmental Cardiotoxicity and l-Carnitine Mediated Protection
by Meng Zhao, Qixiao Jiang, Wencheng Wang, Min Geng, Meng Wang, Yantao Han and Chunbo Wang
Int. J. Mol. Sci. 2017, 18(6), 1229; https://doi.org/10.3390/ijms18061229 - 8 Jun 2017
Cited by 15 | Viewed by 5664
Abstract
Perfluorooctanoic acid (PFOA) is an environmental contaminant that could induce developmental cardiotoxicity in a chicken embryo, which may be alleviated by l-carnitine. To explore the roles of reactive oxygen species (ROS) and nitric oxide (NO) in such changes and the potential effects [...] Read more.
Perfluorooctanoic acid (PFOA) is an environmental contaminant that could induce developmental cardiotoxicity in a chicken embryo, which may be alleviated by l-carnitine. To explore the roles of reactive oxygen species (ROS) and nitric oxide (NO) in such changes and the potential effects of l-carnitine, fertile chicken eggs were exposed to PFOA via an air cell injection, with or without l-carnitine co-treatment. The ROS and NO levels in chicken embryo hearts were determined with electron spin resonance (ESR), and the protein levels of the nuclear factor κ-light chain-enhancer of activated B cells (NF-κB) p65 and inducible nitric oxide synthase (iNOS) in chicken embryo hearts were assessed with western blotting. The results of ESR indicated that PFOA exposure induced an elevation in the ROS levels in ED19 chicken embryo hearts and hatchling chicken hearts, while l-carnitine could alleviate such changes. Meanwhile, increased NO levels were observed in ED19 embryo hearts and hatchling hearts following PFOA exposure, while l-carnitine co-treatment exerted modulatory effects. Western blotting revealed that p65 translocation in ED19 embryo hearts and hatchling hearts was enhanced by PFOA, while l-carnitine co-treatment alleviated such changes. iNOS expression levels in ED19 embryo hearts followed the same pattern as NO levels, while a suppression of expression was observed in hatchling hearts exposed to PFOA. ROS/NF-κB p65 and iNOS/NO seem to be involved in the late stage (ED19 and post hatch) of PFOA-induced developmental cardiotoxicity in a chicken embryo. l-carnitine could exert anti-oxidant and NO modulatory effects in the developing chicken embryo hearts, which likely contribute to its cardioprotective effects. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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Article
Molecular Pathways Involved in the Amelioration of Myocardial Injury in Diabetic Rats by Kaempferol
by Kapil Suchal, Salma Malik, Sana Irfan Khan, Rajiv Kumar Malhotra, Sameer N. Goyal, Jagriti Bhatia, Shreesh Ojha and Dharamvir Singh Arya
Int. J. Mol. Sci. 2017, 18(5), 1001; https://doi.org/10.3390/ijms18051001 - 15 May 2017
Cited by 85 | Viewed by 6862
Abstract
There is growing evidence that chronic hyperglycemia leads to the formation of advanced glycation end products (AGEs) which exerts its effect via interaction with the receptor for advanced glycation end products (RAGE). AGE-RAGE activation results in oxidative stress and inflammation. It is well [...] Read more.
There is growing evidence that chronic hyperglycemia leads to the formation of advanced glycation end products (AGEs) which exerts its effect via interaction with the receptor for advanced glycation end products (RAGE). AGE-RAGE activation results in oxidative stress and inflammation. It is well known that this mechanism is involved in the pathogenesis of cardiovascular disease in diabetes. Kaempferol, a dietary flavonoid, is known to possess antioxidant, anti-apoptotic, and anti-inflammatory activities. However, little is known about the effect of kaempferol on myocardial ischemia-reperfusion (IR) injury in diabetic rats. Diabetes was induced in male albino Wistar rats using streptozotocin (70 mg/kg; i.p.), and rats with glucose level >250 mg/dL were considered as diabetic. Diabetic rats were treated with vehicle (2 mL/kg; i.p.) and kaempferol (20 mg/kg; i.p.) daily for a period of 28 days and on the 28th day, ischemia was produced by one-stage ligation of the left anterior descending coronary artery for 45 min followed by reperfusion for 60 min. After completion of surgery, rats were sacrificed and the heart tissue was processed for biochemical, morphological, and molecular studies. Kaempferol pretreatment significantly reduced hyperglycemia, maintained hemodynamic function, suppressed AGE-RAGE axis activation, normalized oxidative stress, and preserved morphological alterations. In addition, there was decreased level of inflammatory markers (tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and NF-κB), inhibition of active c-Jun N-terminal kinase (JNK) and p38 proteins, and activation of Extracellular signal regulated kinase 1/2 (ERK1/2) a prosurvival kinase. Furthermore, it also attenuated apoptosis by reducing the expression of pro-apoptotic proteins (Bax and Caspase-3), Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) positive cells, and increasing the level of anti-apoptotic protein (Bcl-2). In conclusion, kaempferol attenuated myocardial ischemia-reperfusion injury in diabetic rats by reducing AGE-RAGE/ mitogen activated protein kinase (MAPK) induced oxidative stress and inflammation. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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4184 KiB  
Article
Folic Acid Supplementation Delays Atherosclerotic Lesion Development by Modulating MCP1 and VEGF DNA Methylation Levels In Vivo and In Vitro
by Shanshan Cui, Wen Li, Xin Lv, Pengyan Wang, Yuxia Gao and Guowei Huang
Int. J. Mol. Sci. 2017, 18(5), 990; https://doi.org/10.3390/ijms18050990 - 5 May 2017
Cited by 39 | Viewed by 6595
Abstract
The pathogenesis of atherosclerosis has been partly acknowledged to result from aberrant epigenetic mechanisms. Accordingly, low folate levels are considered to be a contributing factor to promoting vascular disease because of deregulation of DNA methylation. We hypothesized that increasing the levels of folic [...] Read more.
The pathogenesis of atherosclerosis has been partly acknowledged to result from aberrant epigenetic mechanisms. Accordingly, low folate levels are considered to be a contributing factor to promoting vascular disease because of deregulation of DNA methylation. We hypothesized that increasing the levels of folic acid may act via an epigenetic gene silencing mechanism to ameliorate atherosclerosis. Here, we investigated the atheroprotective effects of folic acid and the resultant methylation status in high-fat diet-fed ApoE knockout mice and in oxidized low-density lipoprotein-treated human umbilical vein endothelial cells. We analyzed atherosclerotic lesion histology, folate concentration, homocysteine concentration, S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), and DNA methyltransferase activity, as well as monocyte chemotactic protein-1 (MCP1) and vascular endothelial growth factor (VEGF) expression and promoter methylation. Folic acid reduced atherosclerotic lesion size in ApoE knockout mice. The underlying folic acid protective mechanism appears to operate through regulating the normal homocysteine state, upregulating the SAM: SAH ratio, elevating DNA methyltransferase activity and expression, altering MCP1 and VEGF promoter methylation, and inhibiting MCP1 and VEGF expression. We conclude that folic acid supplementation effectively prevented atherosclerosis by modifying DNA methylation through the methionine cycle, improving DNA methyltransferase activity and expression, and thus changing the expression of atherosclerosis-related genes. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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5420 KiB  
Article
Protective Effect of Fragaria ananassa Crude Extract on Cadmium-Induced Lipid Peroxidation, Antioxidant Enzymes Suppression, and Apoptosis in Rat Testes
by Mohammed I. Y. Elmallah, Manal F. Elkhadragy, Ebtesam M. Al-Olayan and Ahmed E. Abdel Moneim
Int. J. Mol. Sci. 2017, 18(5), 957; https://doi.org/10.3390/ijms18050957 - 5 May 2017
Cited by 64 | Viewed by 6490
Abstract
Cadmium is a deleterious environmental pollutant that threats both animals and human health. Oxidative stress and elevated levels of reactive oxygen species (ROS) have recently been reported to be the main cause of cellular damage as a result of cadmium exposure. We investigate, [...] Read more.
Cadmium is a deleterious environmental pollutant that threats both animals and human health. Oxidative stress and elevated levels of reactive oxygen species (ROS) have recently been reported to be the main cause of cellular damage as a result of cadmium exposure. We investigate, here, the protective effect of strawberry crude extracts on cadmium-induced oxidative damage of testes in rats. Four groups (n = 8) of 32 adult male Wistar rats weighing 160–180 g were used. The control group received 0.9% saline solution all over the experimental period (5 days). Group 2 was intraperitoneally injected with 6.5 mg/kg CdCl2. Group 3 was provided only with an oral administration of strawberry methanolic extract (SME) at a dose of 250 mg/kg. Group 4 was treated with SME before cadmium injection with the same mentioned doses. It was shown that cadmium exposure results in a significant decrease in both relative testicular weight and serum testosterone level. Analyzing the oxidative damaging effect of cadmium on the testicular tissue revealed the induction of oxidative stress markers represented in the elevated level of lipid peroxidation (LPO), nitric oxide (NO), and a decrease in the reduced glutathione (GSH) content. Considering cadmium toxicity, the level of the antioxidant enzyme activities including catalase (CAT), superoxide dismutase (SOD2), glutathione peroxidase (GPx1), and glutathione reductase (GR) were markedly decreased. Moreover, gene expression analysis indicated significant upregulation of the pro-apoptotic proteins, bcl-2-associated-X-protein (BAX), and tumor necrosis factor-α (TNFA) in response to cadmium intoxication, while significant downregulation of the anti-apoptotic, B-cell lymphoma 2 (BCL2) gene was detected. Immunohistochemistry of the testicular tissue possessed positive immunostaining for the increased level of TNF-α, but decreased number of proliferating cell nuclear antigen (PCNA) stained cells. Administration of SME debilitated the deleterious effect of cadmium via reduction of both LPO and NO levels followed by a significant enhancement in the gene expression level of CAT, SOD2, GPX1, GR, nuclear factor-erythroid 2-related factor 2 (NFE2L2), heme oxygenase-1 (HMOX1), Bcl-2, and PCNA. In addition, the SME treated group revealed a significant increase in the level of testosterone and GSH accompanied by a marked decrease in the gene expression level of Bax and TNF-α. In terms of the summarized results, the SME of Fragaria ananassa has a protective effect against cadmium-induced oxidative damage of testes. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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1666 KiB  
Article
Biological Effect of Licochalcone C on the Regulation of PI3K/Akt/eNOS and NF-κB/iNOS/NO Signaling Pathways in H9c2 Cells in Response to LPS Stimulation
by Sara Franceschelli, Mirko Pesce, Alessio Ferrone, Daniela Maria Pia Gatta, Antonia Patruno, Maria Anna De Lutiis, José Luis Quiles, Alfredo Grilli, Mario Felaco and Lorenza Speranza
Int. J. Mol. Sci. 2017, 18(4), 690; https://doi.org/10.3390/ijms18040690 - 23 Mar 2017
Cited by 56 | Viewed by 5508
Abstract
Polyphenols compounds are a group molecules present in many plants. They have antioxidant properties and can also be helpful in the management of sepsis. Licochalcone C (LicoC), a constituent of Glycyrrhiza glabra, has various biological and pharmacological properties. In saying this, the [...] Read more.
Polyphenols compounds are a group molecules present in many plants. They have antioxidant properties and can also be helpful in the management of sepsis. Licochalcone C (LicoC), a constituent of Glycyrrhiza glabra, has various biological and pharmacological properties. In saying this, the effect of LicoC on the inflammatory response that characterizes septic myocardial dysfunction is poorly understood. The aim of this study was to determine whether LicoC exhibits anti-inflammatory properties on H9c2 cells that are stimulated with lipopolysaccharide. Our results have shown that LicoC treatment represses nuclear factor-κB (NF-κB) translocation and several downstream molecules, such as inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Moreover, LicoC has upregulated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/endothelial nitric oxide synthase (eNOS) signaling pathway. Finally, 2-(4-Morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride (LY294002), a specific PI3K inhibitor, blocked the protective effects of LicoC. These findings indicate that LicoC plays a pivotal role in cardiac dysfunction in sepsis-induced inflammation. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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1541 KiB  
Article
Combined Effects of Curcumin and Lycopene or Bixin in Yoghurt on Inhibition of LDL Oxidation and Increases in HDL and Paraoxonase Levels in Streptozotocin-Diabetic Rats
by Renata Pires Assis, Carlos Alberto Arcaro, Vânia Ortega Gutierres, Juliana Oriel Oliveira, Paulo Inácio Costa, Amanda Martins Baviera and Iguatemy Lourenço Brunetti
Int. J. Mol. Sci. 2017, 18(4), 332; https://doi.org/10.3390/ijms18040332 - 23 Mar 2017
Cited by 64 | Viewed by 7926
Abstract
Combination therapy using natural antioxidants to manage diabetes mellitus and its complications is an emerging trend. The aim of this study was to investigate the changes promoted by treatment of streptozotocin (STZ)-diabetic rats with yoghurt enriched with the bioactives curcumin, lycopene, or bixin [...] Read more.
Combination therapy using natural antioxidants to manage diabetes mellitus and its complications is an emerging trend. The aim of this study was to investigate the changes promoted by treatment of streptozotocin (STZ)-diabetic rats with yoghurt enriched with the bioactives curcumin, lycopene, or bixin (the latter two being carotenoids). Antioxidants were administered individually, or as mixtures, and biomarkers of metabolic and oxidative disturbances, particularly those associated with cardiovascular risk, were assessed. Treatment of STZ-diabetic rats with natural products individually decreased glycemia, triacylglycerol, total-cholesterol, oxidative stress biomarkers, including oxidized low-density lipoprotein (ox-LDL), and increased the activities of antioxidant enzymes. Individual carotenoids increased both high-density lipoprotein (HDL) and paraoxonase levels, whereas curcumin increased only paraoxonase. Treatments with mixtures of curcumin and lycopene or bixin had combined effects, decreasing biomarkers of carbohydrate and lipid disturbances (curcumin effect), increasing the HDL levels (carotenoids effects) and mitigating oxidative stress (curcumin and carotenoids effects). The combined effects also led to prevention of the LDL oxidation, thereby mitigating the cardiovascular risk in diabetes. These findings provide evidence for the beneficial effect of curcumin and carotenoid mixtures as a supplementation having antioxidant and antiatherogenic potentials, thus appearing as an interesting strategy to be studied as a complementary therapy for diabetic complications. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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Review

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585 KiB  
Review
Nutritional and Acquired Deficiencies in Inositol Bioavailability. Correlations with Metabolic Disorders
by Simona Dinicola, Mirko Minini, Vittorio Unfer, Roberto Verna, Alessandra Cucina and Mariano Bizzarri
Int. J. Mol. Sci. 2017, 18(10), 2187; https://doi.org/10.3390/ijms18102187 - 20 Oct 2017
Cited by 78 | Viewed by 13328
Abstract
Communities eating a western-like diet, rich in fat, sugar and significantly deprived of fibers, share a relevant increased risk of both metabolic and cancerous diseases. Even more remarkable is that a low-fiber diet lacks some key components—as phytates and inositols—for which a mechanistic [...] Read more.
Communities eating a western-like diet, rich in fat, sugar and significantly deprived of fibers, share a relevant increased risk of both metabolic and cancerous diseases. Even more remarkable is that a low-fiber diet lacks some key components—as phytates and inositols—for which a mechanistic link has been clearly established in the pathogenesis of both cancer and metabolic illness. Reduced bioavailability of inositol in living organisms could arise from reduced food supply or from metabolism deregulation. Inositol deregulation has been found in a number of conditions mechanistically and epidemiologically associated to high-glucose diets or altered glucose metabolism. Indeed, high glucose levels hinder inositol availability by increasing its degradation and by inhibiting both myo-Ins biosynthesis and absorption. These underappreciated mechanisms may likely account for acquired, metabolic deficiency in inositol bioavailability. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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759 KiB  
Review
Dietary Modulation of Oxidative Stress in Alzheimer’s Disease
by Arjun Thapa and Nick J. Carroll
Int. J. Mol. Sci. 2017, 18(7), 1583; https://doi.org/10.3390/ijms18071583 - 21 Jul 2017
Cited by 70 | Viewed by 10301
Abstract
Cells generate unpaired electrons, typically via oxygen- or nitrogen-based by-products during normal cellular respiration and under stressed situations. These pro-oxidant molecules are highly unstable and may oxidize surrounding cellular macromolecules. Under normal conditions, the reactive oxygen or nitrogen species can be beneficial to [...] Read more.
Cells generate unpaired electrons, typically via oxygen- or nitrogen-based by-products during normal cellular respiration and under stressed situations. These pro-oxidant molecules are highly unstable and may oxidize surrounding cellular macromolecules. Under normal conditions, the reactive oxygen or nitrogen species can be beneficial to cell survival and function by destroying and degrading pathogens or antigens. However, excessive generation and accumulation of the reactive pro-oxidant species over time can damage proteins, lipids, carbohydrates, and nucleic acids. Over time, this oxidative stress can contribute to a range of aging-related degenerative diseases such as cancer, diabetes, macular degeneration, and Alzheimer’s, and Parkinson’s diseases. It is well accepted that natural compounds, including vitamins A, C, and E, β-carotene, and minerals found in fruits and vegetables are powerful anti-oxidants that offer health benefits against several different oxidative stress induced degenerative diseases, including Alzheimer’s disease (AD). There is increasing interest in developing anti-oxidative therapeutics to prevent AD. There are contradictory and inconsistent reports on the possible benefits of anti-oxidative supplements; however, fruits and vegetables enriched with multiple anti-oxidants (e.g., flavonoids and polyphenols) and minerals may be highly effective in attenuating the harmful effects of oxidative stress. As the physiological activation of either protective or destructive pro-oxidant behavior remains relatively unclear, it is not straightforward to relate the efficacy of dietary anti-oxidants in disease prevention. Here, we review oxidative stress mediated toxicity associated with AD and highlight the modulatory roles of natural dietary anti-oxidants in preventing AD. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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3462 KiB  
Review
Correlation between Oxidative Stress, Nutrition, and Cancer Initiation
by Subbroto Kumar Saha, Soo Bin Lee, Jihye Won, Hye Yeon Choi, Kyeongseok Kim, Gwang-Mo Yang, Ahmed Abdal Dayem and Ssang-goo Cho
Int. J. Mol. Sci. 2017, 18(7), 1544; https://doi.org/10.3390/ijms18071544 - 17 Jul 2017
Cited by 280 | Viewed by 20444
Abstract
Inadequate or excessive nutrient consumption leads to oxidative stress, which may disrupt oxidative homeostasis, activate a cascade of molecular pathways, and alter the metabolic status of various tissues. Several foods and consumption patterns have been associated with various cancers and approximately 30–35% of [...] Read more.
Inadequate or excessive nutrient consumption leads to oxidative stress, which may disrupt oxidative homeostasis, activate a cascade of molecular pathways, and alter the metabolic status of various tissues. Several foods and consumption patterns have been associated with various cancers and approximately 30–35% of the cancer cases are correlated with overnutrition or malnutrition. However, several contradictory studies are available regarding the association between diet and cancer risk, which remains to be elucidated. Concurrently, oxidative stress is a crucial factor for cancer progression and therapy. Nutritional oxidative stress may be induced by an imbalance between antioxidant defense and pro-oxidant load due to inadequate or excess nutrient supply. Oxidative stress is a physiological state where high levels of reactive oxygen species (ROS) and free radicals are generated. Several signaling pathways associated with carcinogenesis can additionally control ROS generation and regulate ROS downstream mechanisms, which could have potential implications in anticancer research. Cancer initiation may be modulated by the nutrition-mediated elevation in ROS levels, which can stimulate cancer initiation by triggering DNA mutations, damage, and pro-oncogenic signaling. Therefore, in this review, we have provided an overview of the relationship between nutrition, oxidative stress, and cancer initiation, and evaluated the impact of nutrient-mediated regulation of antioxidant capability against cancer therapy. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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313 KiB  
Review
Naturally Occurring Compounds: New Potential Weapons against Oxidative Stress in Chronic Kidney Disease
by Lorenzo Signorini, Simona Granata, Antonio Lupo and Gianluigi Zaza
Int. J. Mol. Sci. 2017, 18(7), 1481; https://doi.org/10.3390/ijms18071481 - 10 Jul 2017
Cited by 25 | Viewed by 5553
Abstract
Oxidative stress is a well-described imbalance between the production of reactive oxygen species (ROS) and the antioxidant defense system of cells and tissues. The overproduction of free radicals damages all components of the cell (proteins, lipids, nucleic acids) and modifies their physiological functions. [...] Read more.
Oxidative stress is a well-described imbalance between the production of reactive oxygen species (ROS) and the antioxidant defense system of cells and tissues. The overproduction of free radicals damages all components of the cell (proteins, lipids, nucleic acids) and modifies their physiological functions. As widely described, this condition is a biochemical hallmark of chronic kidney disease (CKD) and may dramatically influence the progression of renal impairment and the onset/development of major systemic comorbidities including cardiovascular diseases. This state is exacerbated by exposure of the body to uremic toxins and dialysis, a treatment that, although necessary to ensure patients’ survival, exposes cells to non-physiological contact with extracorporeal circuits and membranes with consequent mitochondrial and anti-redox cellular system alterations. Therefore, it is undeniable that counteracting oxidative stress machinery is a major pharmacological target in medicine/nephrology. As a consequence, in recent years several new naturally occurring compounds, administered alone or integrated with classical therapies and an appropriate lifestyle, have been proposed as therapeutic tools for CKD patients. In this paper, we reviewed the recent literature regarding the “pioneering” in vivo testing of these agents and their inclusion in small clinical trials performed in patients affected by CKD. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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1042 KiB  
Review
Hypotheses on the Potential of Rice Bran Intake to Prevent Gastrointestinal Cancer through the Modulation of Oxidative Stress
by Bernard M. H. Law, Mary M. Y. Waye, Winnie K. W. So and Sek Ying Chair
Int. J. Mol. Sci. 2017, 18(7), 1352; https://doi.org/10.3390/ijms18071352 - 24 Jun 2017
Cited by 24 | Viewed by 7168
Abstract
Previous studies have suggested the potential involvement of oxidative stress in gastrointestinal cancers. In light of this, research efforts have been focused on the potential of dietary antioxidant intake to prevent gastrointestinal cancer through the modulation of oxidative stress. Rice bran, a by-product [...] Read more.
Previous studies have suggested the potential involvement of oxidative stress in gastrointestinal cancers. In light of this, research efforts have been focused on the potential of dietary antioxidant intake to prevent gastrointestinal cancer through the modulation of oxidative stress. Rice bran, a by-product of rice milling, has been shown to contain an abundance of phytochemicals, which are dietary antioxidants. To date, a number of studies have shown the antioxidative effect of rice bran intake, and some demonstrated that such an effect may contribute to gastrointestinal cancer prevention, largely through the antioxidative properties of rice bran phytochemicals. In addition, these phytochemicals were shown to provide protection against cancer through mechanisms linked to oxidative stress, including β-catenin-mediated cell proliferation and inflammation. The present article provides an overview of current evidence for the antioxidative properties of rice bran and its phytochemicals, and for the potential of such properties in cancer prevention through the oxidative-stress-linked mechanisms mentioned above. The article also highlights the need for an evaluation of the effectiveness of rice bran dietary interventions among cancer survivors in ameliorating oxidative stress and reducing the level of gastrointestinal cancer biomarkers, thereby establishing the potential of such interventions among these individuals in the prevention of cancer recurrence. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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936 KiB  
Review
Therapeutic Applications of Rose Hips from Different Rosa Species
by Inés Mármol, Cristina Sánchez-de-Diego, Nerea Jiménez-Moreno, Carmen Ancín-Azpilicueta and María Jesús Rodríguez-Yoldi
Int. J. Mol. Sci. 2017, 18(6), 1137; https://doi.org/10.3390/ijms18061137 - 25 May 2017
Cited by 117 | Viewed by 30010
Abstract
Rosa species, rose hips, are widespread wild plants that have been traditionally used as medicinal compounds for the treatment of a wide variety of diseases. The therapeutic potential of these plants is based on its antioxidant effects caused by or associated with its [...] Read more.
Rosa species, rose hips, are widespread wild plants that have been traditionally used as medicinal compounds for the treatment of a wide variety of diseases. The therapeutic potential of these plants is based on its antioxidant effects caused by or associated with its phytochemical composition, which includes ascorbic acid, phenolic compounds and healthy fatty acids among others. Over the last few years, medicinal interest in rose hips has increased as a consequence of recent research that has studied its potential application as a treatment for several diseases including skin disorders, hepatotoxicity, renal disturbances, diarrhoea, inflammatory disorders, arthritis, diabetes, hyperlipidaemia, obesity and cancer. In this review, the role of different species of Rosa in the prevention of treatment of various disorders related to oxidative stress, is examined, focusing on new therapeutic approaches from a molecular point of view. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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Review
Interplay between Oxidative Stress and Nutrient Sensing Signaling in the Developmental Origins of Cardiovascular Disease
by You-Lin Tain and Chien-Ning Hsu
Int. J. Mol. Sci. 2017, 18(4), 841; https://doi.org/10.3390/ijms18040841 - 15 Apr 2017
Cited by 61 | Viewed by 7176
Abstract
Cardiovascular disease (CVD) presents a global health burden, despite recent advances in management. CVD can originate from early life by so-called “developmental origins of health and disease” (DOHaD). Epidemiological and experimental evidence supports that early-life insults can induce programming of later CVD. Underlying [...] Read more.
Cardiovascular disease (CVD) presents a global health burden, despite recent advances in management. CVD can originate from early life by so-called “developmental origins of health and disease” (DOHaD). Epidemiological and experimental evidence supports that early-life insults can induce programming of later CVD. Underlying the DOHaD concept, early intervention may offset programming process to prevent the development of CVD, namely reprogramming. Oxidative stress and nutrient sensing signals have been considered to be major mechanisms of cardiovascular programming, while the interplay between these two mechanisms have not been examined in detail. This review summarizes current evidence that supports the link between oxidative stress and nutrient sensing signaling to cardiovascular programming, with an emphasis on the l-arginine–asymmetric dimethylarginine (ADMA)–nitric oxide (NO) pathway. This review provides an overview of evidence from human studies supporting fetal programming of CVD, insight from animal models of cardiovascular programming and oxidative stress, impact of the l-arginine–ADMA–NO pathway in cardiovascular programming, the crosstalk between l-arginine metabolism and nutrient sensing signals, and application of reprogramming interventions to prevent the programming of CVD. A greater understanding of the mechanisms underlying cardiovascular programming is essential to developing early reprogramming interventions to combat the globally growing epidemic of CVD. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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247 KiB  
Review
Effects and Mechanisms of Fruit and Vegetable Juices on Cardiovascular Diseases
by Jie Zheng, Yue Zhou, Sha Li, Pei Zhang, Tong Zhou, Dong-Ping Xu and Hua-Bin Li
Int. J. Mol. Sci. 2017, 18(3), 555; https://doi.org/10.3390/ijms18030555 - 4 Mar 2017
Cited by 109 | Viewed by 30928
Abstract
Many studies have indicated that consumption of vegetables and fruits are positively related to lower incidence of several chronic noncommunicable diseases. Although composition of fruit and vegetable juices is different from that of the edible portion of fruits and vegetables, they contain polyphenols [...] Read more.
Many studies have indicated that consumption of vegetables and fruits are positively related to lower incidence of several chronic noncommunicable diseases. Although composition of fruit and vegetable juices is different from that of the edible portion of fruits and vegetables, they contain polyphenols and vitamins from fruits and vegetables. Drinking vegetable and fruit juices is very popular in many countries, and also an efficient way to improve consumption of fruits and vegetables. The studies showed that fruit and vegetable juices affect cardiovascular risk factors, such as lowering blood pressure and improving blood lipid profiles. The main mechanisms of action included antioxidant effects, improvement of the aspects of the cardiovascular system, inhibition of platelet aggregation, anti-inflammatory effects, and prevention of hyperhomocysteinemia. Drinking juices might be a potential way to improve cardiovascular health, especially mixtures of juices because they contain a variety of polyphenols, vitamins, and minerals from different fruits and vegetables. This review summarizes recent studies on the effects of fruit and vegetable juices on indicators of cardiovascular disease, and special attention is paid to the mechanisms of action. Full article
(This article belongs to the Special Issue Correlation between Nutrition, Oxidative Stress and Disease)
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