Concurrency limit. Sign out. Search: Keyword Advanced Browse all content Thesaurus. Please use quotation marks for searching phrases e. Your products All Products. Browse by : Author Author Serial Subject. Enter author surname:. Display : 25 50 Previous record Next record.
Actions Tools Choose a colour. This book reviews the role of functional foods in helping to prevent a number of degenerative conditions such as osteoporosis, obesity, immune system disorders and neoplasms. The book begins with discussions on the regulation of functional foods in the EU and the role of diet in preventing Functional foods, ageing and degenerative disease.
The book begins with discussions on the regulation of functional foods in the EU and the role of diet in preventing degenerative disease. The final part of the book reviews research on functional foods and cancer, with chapters on synbiotics synbiotics Subject Category: Miscellaneous see more details , anti-angiogenic functional foods, glucosinolates glucosinolates Subject Category: Chemicals and Chemical Groups see more details , dietary fibre fibre Subject Category: Miscellaneous see more details fibre Subject Category: Miscellaneous see more details and phytoestrogens.
Back to top. Edit annotation. Cancel Edit annotation. Add annotation. Cancel Add annotation. Print citation. Cancel Print. Email citation. Please enter a valid email address. Cancel Send. Export citation list. Records to Export: Export upto 10, records per session in batches of max. Cancel Export. Remove search.
Are you sure you want to remove this search from Saved Searches? Cancel Remove search. Add to project. Select project. Cancel Add to project. Create a project. Name your project Please enter project name. Project already exists. Malnutrition-induced antioxidant deficiency may contribute to increased risks of disease occurrence and poor treatment outcomes Ames and Wakimoto, ; Evatt et al.
Currently, the clinical awareness of nutritional balance in disease occurrence, progression, and outcomes is limited. In this review, we will outline the roles of ROS in common OS-associated diseases and aging as well as discuss the effects of nutritional antioxidants as treatments or adjuvants. Respiratory diseases such as COPD and asthma have been identified as major health problems due to increased prevalence and mortality worldwide Masoli et al. The toxicity of oxidants directly damages alveoli and connective tissues of the lungs, exacerbating the development of COPD van Eeden and Sin, OS is also implicated in the pathophysiology of asthma Comhair and Erzurum, Although it remains inconclusive regarding whether increased OS in asthma is a causative factor of the disease or a consequence of inflammation, OS is suggested to play a pivotal role in asthma progression Cho and Moon, Moreover, it enhances airway hyper-responsiveness and stimulates mucin secretion, both of which are associated with severe asthma Fitzpatrick et al.
OS-induced damages in the respiratory system and the reduced antioxidant defenses further lead to an increase in endogenous ROS formation Jiang et al. Underweight COPD patients tend to experience more pulmonary damage, exercise intolerance, and increased mortality rates, in comparison to individuals with normal weights King et al. Malnutrition can lead to respiratory muscle mass reduction, which lowers the strength and endurance of these muscles Ferreira et al.
In addition, decreased intake or availability of dietary antioxidants such as vitamins C and E, carotenoids, and polyphenols, can weaken the antioxidant system and exacerbate disease progression Figure 1 and Table 1 Sies et al. A dietary pattern that is rich in vegetables, fruits, fish, and whole grains has been associated with improved pulmonary function and a lower risk of COPD Varraso et al. It is suggested that nutritional supplementation enhances respiratory muscle function in malnourished COPD patients, thereby improving their quality of life Ferreira et al.
For example, Hornikx et al. Furthermore, melatonin, a powerful antioxidant and a regulator of the sleep-wake cycle, can also attenuate OS-related lung deterioration Figure 1 and Table 1 Gumral et al. These findings support the potential use of nutritional antioxidants as an adjuvant to COPD treatment.
Similarly, several observational studies suggest that nutritional antioxidants from diets or supplements can improve asthma control and lung function in asthmatic patients Moreno-Macias and Romieu, A systematic review has proposed that there is an inverse association between dietary intake of vitamins A and C and incidence of asthma Table 1 Allen et al.
In addition, dietary carotenoids have been shown to correlate with improved asthma outcomes and lung function Wood et al. The linkage between OS and the development of respiratory diseases suggests a pivotal role of nutritional antioxidants Romieu, Vulnerable populations include those with deficiency in dietary antioxidants, increased exposure to environmental sources of oxidants, and poor access to nutritional antioxidants Moreno-Macias and Romieu, It is important to note that although antioxidants may help to mitigate the progression of respiratory diseases, antioxidant supplements can act as pro-oxidants or OS inducers if consumed at levels that significantly surpass the recommended dietary intake Pham-Huy et al.
The potential benefits and risks of nutritional antioxidant supplementation trials in respiratory diseases should be considered on a case-by-case basis. Furthermore, it remains unknown whether OS is a consequence or the causative factor for some pulmonary diseases. Therefore, antioxidant treatment may not be an effective approach to modify disease progression although it may be able to alleviate OS-related symptoms Margaritelis, Cardiovascular diseases CVD are the leading cause of mortality in the United States, resulting in nearly one million deaths each year Madamanchi et al.
By taking up ox-LDL, macrophages may transform into foam cells, which secrete growth mediators to attract SMCs into the intima. SMCs can secret extracellular matrix that forms a thin fibrous cap surrounding the fatty streak Madamanchi et al. With the continuous propagation of SMCs, monocytes, and macrophages, fatty streaks are ultimately converted into more advanced fibrous plaque Madamanchi et al.
Further, OS has also been implicated in the development cardiac hypertrophy, ischemic-reperfusion injury, and myocyte apoptosis, all of which may contribute to heart failure Madamanchi et al. Consumption of fruit and vegetable is found to increase the levels of antioxidants such as carotene and vitamin C in the blood as well as decrease the cholesterol oxidation Zino et al.
Functional Foods, Ageing and Degenerative Disease
Therefore, the potential benefits of fruits and vegetables in CVD have been broadly investigated. In a meta-analysis consisting of 16 prospective cohort studies and , participants, CVD-related mortality was found to be inversely correlated with fruit and vegetable consumption Wang et al. However, different results are present suggesting no beneficial effect of vitamin supplementation on CVD mortality or morbidity Kris-Etherton et al. Instead, other antioxidant compounds such as lycopene and polyphenols could play a more important role in the protection against CVD as will be discussed below Ignarro et al.
Furthermore, the inconsistency in treatment outcomes are likely associated with antioxidant formulation. Additionally, the complicated redox mechanisms of antioxidant are far from clear now. Some of the antioxidant such as vitamin C may exhibit prooxidant properties when administrated at high doses Madamanchi et al. This could partially explain why some of the trials using antioxidant supplementation failed to show any protective effect. Lycopene is a natural dietary antioxidant most abundant in tomatoes. An inverse association was found between CVD incidence and consumption of either tomatoes or lycopene Kohlmeier and Hastings, ; Arab and Steck, ; Rao and Agarwal, This could be attributed to the protective effects of lycopene against LDL oxidation by inhibiting cholesterol synthesis and improving LDL degradation Table 1 Ignarro et al.
It was found that only lycopene had significant protective effects Kohlmeier et al.
- Eat Right 4 Your Type Personalized Cookbook Type A: 150+ Healthy Recipes For Your Blood Type Diet.
- Search again!
- Higher Levels of Carotenoids for Increased Vitamin A?
- Islam and Public Controversy in Europe.
- The Theory and Practice of Econometrics, Second Edition (Wiley Series in Probability and Statistics)!
Therefore, lycopene may be one of the primary contributors that underlie the protective mechanisms of vegetable consumption against CVD Kohlmeier et al. Epidemiologic studies found a significantly reduced risk for CVD with higher polyphenol intake Table 1 Vita, Beverages rich in flavonoid such as tea can markedly improve endothelial function. However, tea consumption did not reduce the oxidative markers in the blood.
So it remains elusive whether this beneficial effect of tea is elicited by its antioxidant effects Vita, Indeed, increasing evidence has suggested that the protective effects of polyphenols are not solely contributed by their antioxidant ability but more likely correlated with their anti-inflammatory effects as well as the regulation of vasodilation and apoptosis of endothelial cells Quinones et al. Neurons are particularly vulnerable to OS-induced damage due to their weakened antioxidant defense system, high demand for oxygen consumption, and abundant polyunsaturated fatty acid content in their cell membranes Rego and Oliveira, AD is a major cause of dementia in elderly Harman, Although the exact pathogenesis of AD remains elusive, aging-related progressive increase in OS has been considered a chief contributor to the formation of AD lesions Harman, ; Pimplikar et al.
OS is not the initiation factor of HD. OS-induced mitochondrial dysfunction is commonly observed in HD and the impairment of respiratory chain can exacerbate ROS formation Browne and Beal, Furthermore, mitochondrial aconitase, an important tricarboxylic acid TCA -cycle enzyme, is significantly impaired in HD. The decline in aconitase activity is thought to be caused by ROS-induced oxidation of Fe-S cluster within aconitase Browne and Beal, In HD, OS is also related to decreased expression of glucose transporter GLUT -3, which results in the inhibition of glucose uptake and the over-accumulation of lactate Covarrubias-Pinto et al.
It remains inconclusive whether OS is an initiator or consequence of neurodegeneration in PD. Loss of antioxidant defense, especially glutathione GSH content is found early in PD although the cause remains unknown Jenner, The toxic products from the oxidative damage may lead to neural cell death Jenner, In the substantia nigra pars compacta SNc of PD patients, reduced activity of Complex I in the mitochondrial respiratory chain contributes to excessive ROS generation and consequently induces the apoptosis of dopaminergic neurons Blesa et al.
Specifically, significant vacuolar degeneration of mitochondria was observed just before the death of neuron in SOD1 mutant mice, indicating that mitochondrial dysfunction initiates the onset of ALS Lin and Beal, Mutant SOD1 has been shown to abnormally interact with mitochondria, leading to cytochrome c release and activation of apoptosis Lin and Beal, A decline in antioxidant capability due to SOD1 mutation is potentially associated with motor neuron degeneration Zuo et al.
Furthermore, marked mitochondrial alterations caused by OS have been suggested to be involved in the development of SCA Stucki et al.
Anti-Ageing Nutrients: Evidence-Based Prevention of Age-Associated Diseases
Considering the complex roles of OS in neurodegenerative disorders, the regulation of cellular ROS levels may represent a potential treatment to impede neurodegeneration and alleviate associated symptoms Uttara et al. Clinical evidence indicates that neurodegenerations can be ameliorated upon proper intake of natural or supplementary antioxidants Zandi et al.
On the other hand, a lack of major antioxidants due to malnutrition, which is implicated in various neurodegenerative diseases, can worsen the progress of neurological conditions Brambilla et al. For example, vitamin D deficiency has recently emerged as one of the contributing factors leading to aberrant neurological development. Vitamin D is an essential antioxidant that regulates calcium-mediated neuronal excitotoxicity and the induction of neurotransmitters and synaptic structural proteins Mpandzou et al. Wang et al. Neurological impairments have also been manifested in individuals with a vitamin B deficiency.
Multiple vitamin B e. Accordingly, a 2-year administration of vitamin E at a dose of IU per day has been shown to reduce the functional decline associated with AD Sano et al. The combination of vitamin E and coenzyme Q10 improves energy generation in some cases of Friedreich ataxia by attenuating OS and restoring mitochondrial function Lodi et al. In addition to vitamins, phytochemicals, another type of bioactive compounds that can be found in fruits and vegetables, exhibit high antioxidant capacity with potential neuroprotective effects against PD Mazo et al.
Anthocyanin derived from strawberries possesses anti-oxidative, anti-inflammatory, and anti-apoptotic abilities. It has been reported to alleviate astrogliosis and preserve neuromuscular junctions and muscle function, serving as a possible therapeutic agent for ALS and other neurodegenerative diseases Winter et al.
Lipoic acid LA is shown to enhance GSH generation and deplete lipid peroxide, thus protecting neurons against OS-induced mitochondrial dysfunction Table 1 Moreira et al. Long-term administration of MitoQ, a mitochondria-target antioxidant, also significantly restores mitochondrial functions in Purkinje cells and alleviates SCA1-related symptoms such as motor incoordination Stucki et al. Numerous studies have been performed to investigate the therapeutic effects of natural antioxidants on neurodegenerative disorders; however, mixed results have been yielded Dias et al.
For instance, despite the seeming effectiveness of vitamin E, a study has showed that vitamin E intake for 5 months failed to elevate vitamin E levels in ventricular cerebrospinal fluid of PD patients Pappert et al. ROS formation is subtly regulated by antioxidant defense systems within the human body Zuo et al. Hence, single antioxidant intake could not be sufficient to resist OS under pathophysiological conditions and could result in cellular damage Murphy, In this regard, a combined use of various nutritional antioxidants should be considered.
Shop Functional Foods, Ageing, And Degenerative Disease
Importantly, the simple dichotomy in redox biology comprised of good antioxidants and bad ROS is regarded as untenable. It is now well accepted that a small amount of ROS is essential to activate redox-sensitive signaling pathways, while excessive ROS can lead to detrimental effects Margaritelis et al. The different characteristics and sources of ROS may define their specific roles in regulating cellular activities Winterbourn and Hampton, ; Margaritelis et al. Numerous studies have stressed the need for a more precise description of the metabolism of ROS in aspects of quantity, reactivity, location, and reaction kinetics Winterbourn and Hampton, ; Forman et al.
However, most of the exogenously administrated antioxidants are non-selective and distributed uniformly across various parts of the cells or tissues Margaritelis et al. The lack of specificity of antioxidants may account for their inefficacy in treating OS-related diseases. It is thus imperative that researchers focus on developing novel and targeted antioxidants such as mitoQ and Nox inhibitors to improve the precise therapeutic effects of antioxidants in future studies Altenhofer et al.
ROS are involved in all three stages of cancer development, namely initiation, promotion, and progression Khandrika et al.
In addition, cancer cells are characterized by more ROS production than normal cells due to an altered metabolism and increased energy demand Sosa et al. ROS-induced OS in carcinoma cells may promote cancer growth by triggering cell growth signaling, enhancing tumor resistance to therapies, increasing blood supply to tumors, and promoting metastasis Brown and Bicknell, ROS promote the expansion of cancerous cells by modifying the genes related to apoptosis, cell proliferation and transcription factors Trueba et al.
In the progression stage of cancer development, ROS contribute to the upregulation of matrix metalloproteinases, inhibiting the action of anti-proteases and angiogenesis, eventually leading to metastasis Maulik, ; Mori et al. A depletion of endogenous antioxidants or a disruption of redox equilibrium may lead to cancer development.
Fruits and vegetables, which are rich in antioxidants, exert a protective effect against several different types of cancers Soerjomataram et al. Plant foods that contain polyphenols have proven to be effective antioxidant agents for the body Barrajon-Catalan et al. They have been shown to possess anti-cancer activity which is effective against lung, breast, tongue, gastric, larynx, colon, and prostate cancers Table 1 Manikandan et al.
Fruits containing higher phenolic content have stronger antioxidant properties since they can induce hydroxyl group substitution in the aromatic rings of phenol compounds Sun et al. Polyphenols induce apoptosis of cancer cells, inhibit proliferation of mutated cells, reduce production of cyclooxygenase-2 COX-2 , and downregulate cancer gene expression Gloria et al.
Moreover, nutrients such as vitamins and minerals can reduce cancer risk by eliciting antioxidant action, inhibiting proliferation of cancerous cells, maintaining DNA methylation, and promoting cell-cycle arrest Pathak et al. In individuals previously treated for cancer, a healthy diet rich in fruits and vegetables can modify biologic markers of cancer progression Jones and Demark-Wahnefried, Healthy plant foods have shown to reduce the risk of death after being diagnosed with breast Vrieling et al. A high vegetable diet has been shown to be effective in reducing breast cancer recurrence for patients on tamoxifen Gold et al.
Vitamins such as Vitamin A and E have a preventive effect against oral cancer Garewal, However, limited evidence supports the effectiveness of vitamins and minerals in cancer prevention Fortmann et al. Additionally, there is a lack of randomized control trials investigating diets and cancer due to difficulty in whole diet interventions as well as ethical issues in the proposed research Norat et al. Hence, current recommendations are based on the effectiveness of a healthy diet rich in fruits, vegetables, and grains, and low on red meat and alcohol and lifestyle on reducing cancer risk Norat et al.
It is well established that intestinal inflammation-associated OS plays an essential role in the pathophysiology of various gastrointestinal GI diseases, such as inflammatory bowel diseases IBD Balmus et al. Although the exact etiology of IBD remains unclear, the underlying pathologies can be partially attributed to excess ROS formation Zhu and Li, ; Bhattacharyya et al.
Due to the presence of food particles, pathogens, or microbiota imbalance, the GI tract may become irritated, generating excess ROS and compromising endogenous antioxidant defenses Moura et al. OS disrupts the intestinal epithelial barrier and increases intestinal permeability, further exacerbating inflammation Figure 2 Balmus et al.
Elevated levels of pro-inflammatory mediators such as platelet activating factor PAF and leukotriene B 4 LTB 4 observed in the mucosal samples from active IBD patients have been shown to trigger the release of cytotoxic reactive oxygen metabolites by overstimulating phagocytes Ingraham et al. Moreover, myeloperoxidases are released during the massive infiltration of polymorphonuclear neutrophils and macrophages into the inflamed mucosa, producing hypochlorous acid, a potent oxidizing agent, via the metabolism of H 2 O 2. Other sources of ROS include enzymes such as cyclooxygenase, xanthine oxidase, and 5-lipoxygenase that reside in the intestinal mucosa Alzoghaibi, Despite ROS overproduction, a deficiency in dietary and enzymatic antioxidants also contributes to the development of OS Alzoghaibi, For example, low levels of enzymatic antioxidants and vitamins have been observed in patients with CD, which is partly due to malnutrition Buffinton and Doe, ; Alzoghaibi, In malnourished IBD patients, the reduced dietary intakes of fruits and vegetables greatly influence the concentration of carotenoid vitamin A Balmus et al.
Vitamin C, which helps to repair and protect mucosal lining against detrimental insults, is depleted in peptic ulcers and gastritis Aditi and Graham, Notably, the increased incidence of vitamin D deficiency in CD patients is highly associated with skeletal morbidity and a worsened quality of life Figure 2 van Hogezand and Hamdy, ; Alastair et al. Persistent OS can damage the intestinal barrier and increase the permeability of GI epithelium via lipid peroxidation and tight junction disruption. This alters the composition of commensal microbiota in the GI tract and interrupts their ability to establish colonization resistance, thus promoting the invasion of pathogenic bacteria Buffie and Pamer, ; Moura et al.
Such infections further aggravate ROS production and inflammation and potentially increase the risk of inflammatory bowel syndrome Zhu and Li, Considering a strong indication of ROS elevation in IBD and other GI diseases, the adjuvant or treatment potential of antioxidants are largely investigated. Antioxidant applications have been shown to restore redox balance, thereby attenuating intestinal damages and maintaining GI health Bhattacharyya et al. In a randomized placebo-controlled study, 3 months of oral antioxidant supplementation markedly improved the serum antioxidant status in CD patients in remission.
The combination of antioxidants with n -3 fatty acids further attenuated pro-inflammatory activities, thus serving as a potential treatment for CD Geerling et al. Compared to supplements, dietary intakes of antioxidants from natural fruits and vegetables may be a safer approach to avoid overconsumption. Inappropriate antioxidant application can be harmful by scavenging of physiological ROS Bjelakovic et al. The combination of selenium and vitamin E has demonstrated protective effects against oxidative damage in the colon of UC rats Figure 2 and Table 1 Bitiren et al.
Several functional foods may be beneficial for IBD without undesirable effects. Free radical theory, which was first proposed by Harman in , suggests that aging is process related with progressive and irreversible accumulation of oxidative damage in the cells Harman, ; Mariani et al. This alteration of redox profile may blunt cellular capability of buffering ROS produced both under physiological conditions and in response to external stress Kregel and Zhang, It was reported that mice with somatic mtDNA mutation exhibited an earlier onset of aging-related features such as hair loss, osteoporosis, and decreased subcutaneous fat as well as a shorter lifespan Trifunovic et al.
Exposure to high levels of ROS can also accelerate telomere shortening, which ultimately triggers cellular senescence Kregel and Zhang, For example, fibroblast cells cultured under high OS showed increased rate of telomere shortening and a reduced lifespan Vonzglinicki et al. The persistent low-level inflammation could be responsible for the development of age-related diseases such as atherosclerosis, cancer, and dementia Chung et al. Aging population are at a higher risk of suffering from malnutrition due to a general decline in body function including decreased metabolic rate, digestive and absorptive capability Brownie, Therefore, the elderly are more likely to be affected by diseases associated with nutritional inadequacy.
For example, aging-related vitamin D deficiency has been shown to result in bone loss, susceptibility to fracture, and hyperparathyroidism Lips, Therefore, appropriate supplementation with vitamin D can reduce the risk of hip and other fractures in housebound elderly Table 1 Lips, In recent years, focus on the diet has increased due to the diet being an essential source of exogenously obtained antioxidants. It appears that dietary antioxidants have the anti-aging activity by their ability to suppress the generation of free radicals Kandola et al.
Cognitive decline represents a major health concern in aging population Kang et al. A key study by Kang et al. It was found that women who consumed more green leafy or cruciferous vegetables demonstrated the lowest cognitive decline; while fruit consumption did not affect their cognitive function Kang et al. Interestingly, higher intake of green and yellow vegetables was also correlated with a slower rate of skin aging in Japanese women after adjustment for age, BMI, smoking status, and sun exposure Nagata et al. Energy restriction ER has recently been put up as a potential way to extend life expectancy.
This was partially due to the favorable effects of ER on redox management. Various natural antioxidants, nutraceuticals, and functional foods have been identified as free radical or progressive oxygen hunters. Therefore, functional foods and nutraceuticals which control the antioxidant activity may represent an important role in slowing the aging process Peng et al.
- Gravitation, Electromagnetism and Cosmology : Toward a New Synthesis.
- All Products;
A diet rich in antioxidant has been shown to increase lifespan in animal models Miquel, ; Peng et al. For instance, a diet supplemented blueberry extract was found to markedly improve the lifespan in fruit flies and Caenorhabditis elegans Wilson et al. This was accompanied by an increased expression of SOD and catalase.
The prolongevity induced by blueberry extract was not observed in SOD or catalase-mutated fruit flies. These results suggest that the beneficial effects of blueberry to extend lifespan are potentially linked with boosted endogenous antioxidant system Peng et al. Other nutritional antioxidants including apple polyphenols, black rice anthocyanin extract, and black tea theaflavins all demonstrated prominent prolongevity effects by upregulating the endogenous antioxidant levels in animal models Table 1 Peng et al.
Further research is needed to evaluate the potential effects of natural antioxidants on life expectancy in human beings. The implication of OS in the etiology of several chronic and inflammatory diseases indicates that antioxidant-based therapy could be promising for these disorders. However, many problems remain elusive regarding antioxidant supplements in disease prevention. It remains to be elucidated about the precise roles of ROS in the pathogenesis of various diseases. Current recommendations are based on the intake of a healthy diet rich in fruits, vegetables, and grains and low on red meat and alcohol and healthy lifestyle, which has demonstrated the ability to reduce the risk for diseases.
Further research is warranted before using antioxidant supplements as an adjuvant therapy. In the meantime, avoiding oxidant sources such as cigarette smoke and alcohol must be considered when taking dietary antioxidants. LZ conceptualized and designed the review. TZ prepared the figures and abstract. All authors agreed to be accountable for the content of this work. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. We thank Paige Henry, Alicia Simpson, and Denethi Wijegunawardana for their assistance during the manuscript preparation.
Aditi, A. Vitamin C, gastritis, and gastric disease: a historical review and update. Alastair, F. Nutrition in inflammatory bowel disease. JPEN J. Enteral Nutr. Allen, S. Association between antioxidant vitamins and asthma outcome measures: systematic review and meta-analysis. Thorax 64, — Altenhofer, S. Redox Signal. Alzoghaibi, M. World J. Ambrose, J. The pathophysiology of cigarette smoking and cardiovascular disease: an update. Ames, B. Are vitamin and mineral deficiencies a major cancer risk? Cancer 2, — Anekonda, T. Brain Res. Arab, L.
Lycopene and cardiovascular disease. Arthur, A. Pretreatment dietary patterns, weight status, and head and neck squamous cell carcinoma prognosis. Asplund, K. Antioxidant vitamins in the prevention of cardiovascular disease: a systematic review. Azumi, H. Superoxide generation in directional coronary atherectomy specimens of patients with angina pectoris - Important role of NAD P H oxidase.
Balmus, I. The implications of oxidative stress and antioxidant therapies in inflammatory bowel disease: clinical aspects and animal models. Saudi J. Barrajon-Catalan, E. Cistaceae aqueous extracts containing ellagitannins show antioxidant and antimicrobial capacity, and cytotoxic activity against human cancer cells. Food Chem. Bellaver, B. Resveratrol increases antioxidant defenses and decreases proinflammatory cytokines in hippocampal astrocyte cultures from newborn, adult and aged Wistar rats. In Vitro 28, — Bhattacharyya, A.
Oxidative stress: an essential factor in the pathogenesis of gastrointestinal mucosal diseases. Bitiren, M. Protective effects of selenium and vitamin E combination on experimental colitis in blood plasma and colon of rats. Trace Elem. Bjelakovic, G. Antioxidant supplements for prevention of gastrointestinal cancers: a systematic review and meta-analysis. Lancet , — Blesa, J. Block, K. Impact of antioxidant supplementation on chemotherapeutic toxicity: a systematic review of the evidence from randomized controlled trials.
Functional Foods, Ageing and Degenerative Disease edited by C. Remacle and B. Reusens
Cancer , — Bonnefont-Rousselot, D. Melatonin: action as antioxidant and potential applications in human disease and aging. Toxicology , 55— Brambilla, D. Brown, N. Hypoxia and oxidative stress in breast cancer - Oxidative stress: its effects on the growth, metastatic potential and response to therapy of breast cancer. Breast Cancer Res. Browne, S. Brownie, S. Why are elderly individuals at risk of nutritional deficiency?
Buffie, C. Microbiota-mediated colonization resistance against intestinal pathogens. Buffinton, G. Altered ascorbic acid status in the mucosa from inflammatory bowel disease patients. Free Radic. Cachofeiro, V. Oxidative stress and inflammation, a link between chronic kidney disease and cardiovascular disease. Kidney Int. Cho, Y. The role of oxidative stress in the pathogenesis of asthma. Allergy Asthma Immunol. Chung, H. Molecular inflammation: underpinnings of aging and age-related diseases. Ageing Res. Comhair, S. Redox control of asthma: molecular mechanisms and therapeutic opportunities.
Cordero-Herrera, I. Epicatechin gallate induces cell death via p53 activation and stimulation of p38 and JNK in human colon cancer SW cells. Cancer 65, — Couto, D. Scavenging of reactive oxygen and nitrogen species by the prodrug sulfasalazine and its metabolites 5-aminosalicylic acid and sulfapyridine. Redox Rep. Covarrubias-Pinto, A. Davila, D. Neuronal death by oxidative stress involves activation of FOXO3 through a two-arm pathway that activates stress kinases and attenuates insulin-like growth factor I signaling.
Cell 19, — Dias, V. Parkinsons Dis. Doll, R. The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. Cancer Inst. Emerit, J. Evatt, M. Prevalence of vitamin D insufficiency in patients with Parkinson disease and Alzheimer disease. Ferreira, I. Nutritional supplementation for stable chronic obstructive pulmonary disease. Cochrane Database Syst. The influence of 6 months of oral anabolic steroids on body mass and respiratory muscles in undernourished COPD patients.
Chest , 19— Fitzpatrick, A. Airway glutathione homeostasis is altered in children with severe asthma: evidence for oxidant stress. Allergy Clin. Forman, H. An overview of mechanisms of redox signaling. Cell Cardiol. Fortmann, S. Vitamin and mineral supplements in the primary prevention of cardiovascular disease and cancer: an updated systematic evidence review for the U. Preventive Services Task Force. Garewal, H.
Antioxidants in oral cancer prevention. Geerling, B. Bowel Dis. George, S. Cancer Epidemiol. Biomarkers Prev. Gilgun-Sherki, Y. Oxidative stress induced-neurodegenerative diseases: the need for antioxidants that penetrate the blood brain barrier.