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ENHANCE your ANTIOXIDANT ABSORPTION with this scientific TECHNIQUE - The cure for FREE RADICALSAntioxidant protection against diseases -
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.
The majority of CVD is correlated with atherosclerosis development, in which OS play a causal role Madamanchi et al. Excessive ROS can be generated in vascular cells from NAD P H oxidase Nox , nitric oxide synthases NOS uncoupling, and mitochondria, which cause oxidative modifications of low density lipoprotein LDL Azumi et al.
The oxidized LDL ox-LDL transported through the arterial lumens induces apoptosis of endothelial cells and smooth muscle cells SMCs. 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.
Considering the implications of ROS in CVD development, numerous studies have been performed to evaluate the effects of nutritional antioxidants in CVD patients. 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.
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.
Another study involving patients with coronary atherosclerosis showed that supplementation of natural α-tocopherol RRR-AT can significantly reduce the incidence of CVD-related death and non-fatal myocardial infarction Table 1 Stephens et al.
However, different results are present suggesting no beneficial effect of vitamin supplementation on CVD mortality or morbidity Kris-Etherton et al. For example, a meta-analysis study, which involved 81, participants, reported that daily supplementation of either vitamin E at a dose of 50— IU or β carotene at a dose of 15—80 mg did not decrease the mortality associated with CVD Vivekananthan et al.
Therefore, vitamin E and β carotene may not be the only active constituent of fruits and vegetables that exert cardiovascular protective effects. 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. Most of the trials reporting inefficacy of vitamin E have used all-racemic α tocopherol, which is a major constituent of synthetic vitamin E Hoppe and Krennrich, ; Madamanchi et al.
By contrast, RRR-AT, the natural form of vitamin E has been associated with better treatment effects Hoppe and Krennrich, ; Madamanchi et al. Thus, further research is needed to address the difference between RRR-AT and all-racemic α tocopherol in terms of their therapeutic efficacy.
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.
An early population-based study was conducted to evaluate the relationship between the risk of myocardial infarction and the status of three types of carotenoids including lycopene, α carotene, and β carotene, respectively.
It was found that only lycopene had significant protective effects Kohlmeier et al. 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.
Evidence has suggested that oxidative events occur prior to the onset of plaque pathology and amyloid-β Aβ accumulation, which further supports the critical roles of OS in the initiating stage of AD Lin and Beal, ; Wang et al.
OS is not the initiation factor of HD. However, severe OS is a typical feature of HD and may contribute to the increased DNA oxidation in the HD brain Browne and Beal, 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, As a result, OS is responsible for the metabolic defects seen in HD 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. However, excessive ROS production is a critical component of the mechanisms underlying PD progression Jenner, Loss of antioxidant defense, especially glutathione GSH content is found early in PD although the cause remains unknown Jenner, High levels of oxidation of protein, DNA, and lipids are observed in PD.
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.
In ALS, superoxide dismutase SOD 1 mutation and mitochondrial degeneration represent one of the major mechanisms underlying ALS pathology Rotunno and Bosco, 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.
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. Rutin, resveratrol, and vitamin E, which target ROS-mediated cascades such as JNK and NF-κB, have yielded some positive outcomes in improving neurodegeneration both in vitro and in vivo Zuo et al.
In a rat brain, vitamin E was found to be more effective in modulating OS than vitamins A and C Zaidi and Banu, 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.
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 the initiation stage, ROS-induced DNA mutations can accumulate if they are not repaired in cancerous tissues Poulsen et al. Excessive ROS production may lead to oncogenic mutation of DNA, potentially contributing to the onset of cancer Valko 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. IBD, which is comprised of CD and ulcerative colitis UC , is characterized by chronic and prominent inflammation associated with OS in the GI tract 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, FIGURE 2.
Schematic illustrating the roles of OS and nutrient antioxidants in IBD. IBD, inflammatory bowel diseases; OS, oxidative stress; Se, selenium; Zn, zinc. 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. For example, studies have shown that CuZn-SOD and 5-aminosalicylic acid effectively alleviate mucosal injuries in CD by scavenging or inducing rapid decomposition of ROS Emerit 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. Foods rich in micronutrients such as α-tocopherol vitamin E and minerals have been reported to be beneficial in alleviating ROS damage.
For example, selenium and zinc interact with GPx and SOD, respectively, to combat OS. 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, Excessive ROS accumulation can directly damage DNA, protein, and lipids, which disturbs normal cellular function Zuo et al.
Mitochondrial DNA mtDNA is particularly susceptible to OS and the mutation of mtDNA has been closely linked with the aging process Trifunovic et al. 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.
Additionally, aging-associated OS could be responsible for the chronic systematic inflammation as commonly seen in the elderly via the activation of NF-κB Chung et al.
NF-κB is a key regulator for inflammatory factors such as tumor necrosis factor-alpha TNF-α , interleukin IL -1β, and IL-6 Chung et al. OS-induced NF-κB signaling is short-lived under normal conditions in contrast to chronic activation during aging Chung 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.
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.
ZL, ZR, and JZ summarized the literature and wrote the manuscript. LZ, EK, C-CC, and TZ critically revised the manuscript. 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.
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Heidenreich, P. Forecasting the future of cardiovascular disease in the United States a policy statement from the American heart association. Circulation , — Holick, M. Antioxidants inhibit a process called oxidation, which generates free radicals that leads to cellular damage.
Antioxidants safely interact with free radicals, neutralizing them before they can cause damage to proteins, lipids, and DNA. Oxidative stress occurs when there are too many free radicals in the body.
This imbalance can occur due to increased production of free radicals or decreased antioxidant defenses. For example, many chronic diseases , including heart disease and cancer, have links to progressive damage from free radicals.
For example, cells contain antioxidant enzymes that help reduce free radical levels. The primary antioxidant enzymes in the cells include superoxide dismutase SOD , catalase CAT , glutathione peroxidase GPx , and glutathione reductase GRx. These antioxidant enzymes are known as first-line defense antioxidants.
They help regulate free radical levels by neutralizing both free radicals and other molecules that have the potential to become free radicals. The body also produces metabolic antioxidants through metabolism.
These include lipoic acid, glutathione, coenzyme Q10, melatonin, uric acid, L-arginine, metal-chelating proteins, bilirubin, and transferrin. However, there are some antioxidants that the body cannot produce, which means a person must consume them through food or by taking dietary supplements.
These nutrient antioxidants include carotenoids, antioxidant vitamins, including vitamins C and E, selenium, manganese, zinc, flavonoids, and omega-3 and omega-6 fats.
Unraveling the intricacies of dietary antioxidants can be challenging and confusing. Foods such as fruits, vegetables, spices, and nuts contain thousands of different compounds that act as antioxidants.
For example, grapes, apples, pears, cherries, and berries contain a group of plant chemicals called polyphenol antioxidants. There are over 8, different polyphenol antioxidants in nature. Brightly colored fruits and vegetables also contain high concentrations of carotenoids , another class of antioxidants.
However, these natural food-derived antioxidants are very different from those found in dietary supplements. For example, there are many forms of vitamin E, including synthetic vitamin E and natural vitamin E, such as alpha-tocopherol esters.
All these forms of vitamin E may have different effects on the body. This may be why studies investigating the potential health benefits of vitamin E supplements have produced conflicting results. Additionally, supplements typically contain concentrated doses of isolated antioxidant compounds that can impact health differently than antioxidant-rich foods.
Although antioxidant-rich foods are extremely nutritious and important for health, taking a very high-dose antioxidant supplement may not suit everyone and may even be harmful to some people. It is clear that a diet concentrated in antioxidant-rich foods, especially fruits and vegetables, is beneficial for overall health.
However, the relationship between supplemental antioxidants and disease prevention is less clear. Many studies have shown that taking supplements that contain concentrated doses of antioxidants may benefit certain aspects of health. For example, researchers have linked antioxidant supplements — including omega-3 fats , curcumin , selenium , resveratrol , and vitamin C — with various beneficial health outcomes.
However, although certain antioxidants may deliver health benefits when a person takes them for a specific reason, this does not mean that taking supplemental antioxidants is always safe or necessary.
For example, scientists have linked vitamin E supplementation with an increased risk of prostate cancer in healthy men. Similarly, studies have linked beta carotene supplementation with an increased risk of lung cancer in smokers. Research has also found no clear benefit of antioxidant supplements on disease risk.
Some evidence suggests that high-dose supplementation with vitamin E, vitamin A, and beta-carotene may increase mortality risk. Conversely, research has consistently linked antioxidant-rich diets high in vegetables, fruits, spices, and other natural sources of antioxidants with decreased disease risk and have found no associations with any adverse health outcomes.
For this reason, experts suggest that people should focus on consuming antioxidants through the foods they eat. They do not recommend that people take high-dose antioxidants supplements unless specifically recommended by a healthcare provider.
There is no doubt that consuming a diet high in antioxidant-rich foods is beneficial for health and may help prevent disease development. It is best to avoid high-dose antioxidant supplements unless a trusted healthcare provider prescribes or recommends them. The best way to take in antioxidants is through foods and beverages, such as vegetables, fruits, nuts, fish, spices, and tea.
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Free radicals are highly reactive chemicals that have Antioxidsnt potential aggainst Antioxidant-rich fruit muffins Natural Coconut Oil. They are Antkoxidant when an Performance nutrition plan or a molecule a chemical Antioxidant protection against diseases agaijst two or Antioxidant protection against diseases atoms either gains or Antioxidant protection against diseases an electron a small negatively charged Anyioxidant found in atoms. Free diseasees are formed naturally in the body and play an important role in many normal cellular processes 12. At high concentrations, however, free radicals can be hazardous to the body and damage all major components of cells, including DNA, proteins, and cell membranes. The damage to cells caused by free radicals, especially the damage to DNA, may play a role in the development of cancer and other health conditions 12. Abnormally high concentrations of free radicals in the body can be caused by exposure to ionizing radiation and other environmental toxins.
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