Free radicals and cancer -
As a result of this unpaired electron, free radicals seek out and take electrons from other molecules, which oftentimes causes damage to the second molecule. Like many things that occur in nature, free radicals are not only impossible to avoid, but necessary for life.
Free radicals help us fight infection, begin the inflammation process that helps repair tissue injury, and short-term oxidative stress may inhibit aging. At the same time, excessive amounts are harmful to humans.
Free radicals are thought to be one cause of cancer, as well as the cause of some auto-immune diseases, heart diseases, neurological diseases, and the aging process in general.
can cause cell mutations which increases breast cancer risk. of cancer cells. Antioxidants are molecules that can safely interact with free radicals. Unlike other molecules, antioxidants can donate an electron to a free radical and still remain stable, therefore stopping the cycle A persistent and recurring way.
of cell damage. Examples of antioxidants are:. One of the best ways to reduce free radical damage in the body, and therefore decrease your risk of breast cancer, is to increase your intake of these vitamins.
One of the best sources? The increase of ROS level of intracellular by activating signaling pathways in cancer cells represents that these cells very more vulnerable than normal cells to ROS-caused cell death.
As a result, these cells in comparison to normal cells very more dependent on the capacity of the antioxidant system and more vulnerable to major oxidative stress induced through exogenous ROS-generating agents or compounds that inhibit the antioxidant system.
This might constitute a biochemical basis to plan therapeutic strategies to selectively death cancer cells using ROS-moderated mechanisms [ 4 — 6 ]. As described above, the increase of ROS in cancer cells was induced several biological responses.
These biological responses including adaptation, increase in cellular proliferation, cell damage, and cell death are likely to be dependent on the cellular genetic background, the types of the specific ROS involved, and the levels of ROS at the duration of the oxidative stress [ 7 ].
The regulation of ROS level by ROS inducers and ROS scavengers. Oxidative stress plays an important role in cell signaling as a sensor and regulator. It was reported that a lot of regulator agents have a considerable effect on up-expression and down-expression of antioxidant genes.
In the following, we explain some of the major factors that act directly in the expression of antioxidant genes Figure 2.
On the other hand, good understanding of the particular pathways that are affected by these regulators is important before designing therapeutic approaches to the adjustment of ROS levels [ 4 ]. NRF2 is an important regulator of the antioxidant system and cellular stress responses in the several cancers.
From the support on the function of Nrf2 target genes, one can easily conclude that activation of Nrf2 may protect cells from several stresses imposed through toxic exposure. Actually, it is recognized that NRF2 regulate various anti-oxidative stress responses and for detoxification reactions, its expression in the tissues increases [ 8 , 9 ].
NRF2 adjust the common various different antioxidant pathways such as GSH production and regeneration, GSH utilization, NADPH production, thioredoxin TXN production, regeneration and utilization, Quinone detoxification and Iron sequestration Figure 2. It is directly through GSH metabolism and indirectly controlling free Fe II homeostasis involved in ROS detoxification.
NRF2 decreases the generation of harmful hydroxyl radicals from ROS by increasing the release of Fe II from haem molecules [ 4 ].
It was suggested that phytochemical compounds such as dietary and medicinal plants through the effect on NRF2 pathway played a key role in cancer therapy [ 8 , 9 ].
FOXO, as a transcription factors, are involved in different signaling pathways and play key roles in some physiological and pathological processes such as cancer. It could play and act as a self-regulatory mechanism, which protects cells from an oxidative damages, via keep in good condition a balance of ROS and antioxidant productions.
FOXO and p53 as a tumor suppressor have a key role in inhibiting oxidative stress process through inducing antioxidant gene expression [ 4 ]. It was reported that an increase of ROS level leads to up-regulation of anti-oxidative proteins, such as MnSOD and catalase through FOXO3a- and FOXO1 [ 10 ].
The p53, as a final transcription factor, has an important role in regulating antioxidant gene expression is p53 and a double-edged as a pro- and antioxidant role in ROS controlling. Hypoxic conditions caused by the imbalance between intake and oxygen consumption [ 4 ].
The production of ROS through the mitochondrial complex I and III, xanthine oxidase, and NADPH oxidase related to hypoxia is recognized as one of the most harmful causes of oxidative process. Some studies have shown that hypoxia condition-caused superoxide generation occurs through the activation of NADPH oxidase placed in the cell membrane and under moderate condition, NO is generated in mitochondria.
Studies suggested that hypoxia-induced loss in mitochondria membrane potential and this and this event is related to raising ROS [ 11 ]. Studies have shown that the mitochondria complex III at the Qo site at during the transfer of electrons from ubisemiquinone to molecular oxygen is the main source for ROS generation under hypoxia.
In addition, it has shown that activation the transcription factor hypoxia-inducible factor HIF dependent on ROS level.
HIFs regulate physiological responses to hypoxia, such as pathophysiological processes especially in cancer [ 4 ]. It was reported that, there is a relation between an increase in the level of H 2 O 2 generation of mitochondria and an increase in susceptible cancer cells to apoptosis.
This susceptibility caused cytotoxicity and also to oxidative stress-induced apoptosis when compared to normal cells [ 12 ]. In the cancer cells, oxidative stress due to increase ROS level and decrease antioxidant level is higher than normal cells.
At a time when equivalent levels of oxidative stress are added by the administration of exogenous ROS-inducing agents, oxidative stress levels in cancer cells but not normal cells can readily over the threshold of cell death.
Hence, cancer cells in compared normal cells are expected to be more vulnerable to cell damage caused by ROS-inducing agents and this vulnerability can be exploited to selectively kill these cells [ 11 ].
A model for increase ROS and apoptosis signaling by oncogenes such as c-MYC. The activation of MYC in cancer cells leads to an elevating in intracellular ROS through mechanisms such as changes in scavenging process, metabolic rate, and eventual activation of intracellular oxidases Figure 3.
The previous investigations show that the increased expression of c-MYC and E2F1 induces accumulation of ROS and increases ROS by c-MYC and E2F1 sensitizes host cells to apoptosis. Hypoxia, on the one hand, as a ROS inducer, can also directly induce the raised expression of oncogenes such as MYC and RAS through HIF-2α.
On the other hand, MYC increases mitochondrial biogenesis, which adds to the raised ROS generation under hypoxic conditions and the raised mitochondrial ROS generation elevate the oxidative stress process [ 12 ].
It has been suggested that RAS, p53, and c-MYC through the mitochondria to regulate ROS generation, thereby affecting apoptosis.
RAS in K-Ras-transformed fibroblast cell under the condition that glucose deprivation induces apoptosis through changes in mitochondrial complex gene expression. It has also been reported that RAS in p66SHC overexpression condition in the transformed cells increase ROS generation through mitochondria and p53, MPTP opening and mitochondrial swelling could induce apoptosis Figure 3 [ 12 ].
In recent decades, several studies have shown that mitochondria organelle plays an important role in human health and disease.
These studies led to the emergence of a new field of study named "mitochondrial medicine. It has been confirmed that these organelles are the principal intracellular source of ROS production in most tissues. Studies have shown that under physiological condition, complex II respiratory chain could also be a main regulator of ROS generation from mitochondria [ 13 ].
In eukaryotic cells, the mitochondrion is an important organelle that plays a main role in several critical processes. The important role of mitochondria is mentioned in the physiology of cancer, such as in energy metabolism and cell cycle regulation.
There is powerful documentary evidence to support the rationale for the expansion of anticancer strategies based on mitochondrial targets.
This organelle is recognizing to play an important role in the apoptosis mechanism and initiate cell death through various mechanisms that comprise disrupting electron transport and energy metabolism in the respiratory chain, releasing agents or proteins such as cytochrome c that mediate apoptosis signaling, and changing the cellular redox status by ROS generation.
The therapeutic targeting of cancer cells based on mitochondria have often depended on the intrinsic various differences between mitochondria in normal and cancer cells, which allow for better options, manipulation different pathways, and destruction of these cancer cells.
These differences are including bioenergetics change, disturbance of the mitochondrial DNA mtDNA , and morphological and physiological changes in the cancer cell Table 1.
The mtDNA is one main target of ROS and the lack of sufficient protective histones surrounding the mtDNA in cancer cells makes the mtDNA more easily tending to ROS-caused DNA damage.
In addition, various researches have shown that the mitochondria were different in cancer cells than in normal cells, such as grow faster, fewer and smaller, and also had the morphological transformed [ 13 ].
Some differences between cancer and normal cells such as bioenergetics process, MMP and ROS level, and morphological and physiological differences. Today, several mitochondria targeted strategies for cancer therapy have been focused on the development of agents that manage increased the ROS generation in mitochondria from the cancer cells without effect on the normal cells.
It has been shown that ROS generation in the mitochondria is evaluated through the rates of both mitochondria ROS mtROS disposal and production, and ROS levels in mitochondria are regulated by several agents, including mitochondria O 2 levels, mitochondrial membrane potential MMP or Δψm , the metabolic condition of mitochondria, and other factors Figure 4.
A number of recent researches reveal the fact that mtROS at low to high levels act as several functions. That is it at low levels, involved in the hypoxia adaptation process, at moderate levels, involved in controlling inflammatory response, and at high level involved in regulating apoptosis signaling.
Adjustment of mitochondria ROS mtROS generation. Several agents such as MMP, the metabolic state of mitochondrial, O 2 level and STAT3 adjust the generation of mtROS. As mentioned in the previous section, the increase of ROS level of intracellular by sever agents through activating signaling pathways in cancer cells represents that these cells are more vulnerable than normal cells to ROS-caused cell death.
The results of the studies suggest that ROS such as H 2 O 2 could affect the extrinsic apoptosis pathway through changing the intracellular space. The up-regulation of receptor shows in various systems with increase ROS by exogenous ROS and ROS causing agents.
It has also been found to sensitize cancer cells, but not normal cells to TRAIL-caused apoptosis. Adenine nucleotide translocator ANT , as an inner mitochondrial protein, is also a target of ROS regulation by integrity of its redox-sensitive cysteines, supplying an extra mechanism by which drug-caused ROS generation may activate mitochondrial apoptosis signaling.
On the other hand, ROS also could regulate protein complexes inner place the mitochondrial electron transport chain mETC , activate caspases-3 and initiate apoptosis signaling.
Today, agents that are used in the treatment of cancer through the mechanism of ROS generation are known as an important drug class.
Some studies have shown that several mitochondria-targeted drugs have potency useful in selective cancer cell killing and no effect on normal cells in pre-clinical and clinical testing, such as ROS regulators. It has been shown that cancer cells in comparison with normal cells are more vulnerable to irreversible damage induced by stress oxidative and subsequent apoptosis.
Researchers in previous studies have been used of the differences between the mitochondria between cancer and normal cells as a means to kill cancer cells by anti-cancer drugs.
Developing cancer therapies based on increasing further the high ROS level in cancer cells to a toxic level by the several mechanisms such as triggering ROS accumulation directly and inhibiting the antioxidant systems display powerful phenomenon of selectively killing cancer cells [ 6 ].
A number of drugs class have been recognized as increasing ROS production. It is well documented that some of chemotherapeutic agents can induce ROS generation through mitochondrial respiratory chain complexes in patients during cancer therapy. These compounds can be separated into various categories such as alkylating agents, anthracycline antibiotics, platinum compounds, mitotic inhibitors, antimetabolites, biological response modifiers, and hormone therapies.
Arsenic trioxide ATO is used in the treatment of acute promyelocytic leukemia APL. It was reported that ATO induces apoptosis signaling in several cancer cells such as lung, leukemia, and myeloma cancer through the induction of ROS.
The mechanism by which ATO cause increased ROS generation is not completely well known. The most recent investigations indicated that ATO can impair the function of respiratory chain in the mitochondria, leading to increased generation of superoxide, likely by causing leakage of electrons from the mitochondrial respiratory chain complexes Figure 5.
On the other hand, ATO could be used in mixture with several anticancer drugs, which play a role through increasing ROS production. Mechanism of ROS generation and apoptosis induction by the ATO, doxorubicin, daunorubicin and bleomycin anthracycline antibiotics and cisplatin.
These drugs, leading to increased generation of ROS, likely by causing leakage of electrons from the mitochondrial respiratory chain complexes.
The doxorubicin, daunorubicin, and bleomycin are an anthracycline antibiotics, cisplatin is a platinum compound, and amitriptyline as a tricyclic antidepressant are used in the treatment of several types of cancer. The mechanism of doxorubicin bleomycin, cisplatin, and amitriptyline in the ROS production is the same of ATO.
These drugs with impair the function of respiratory chain in the mitochondria, leading to increase generation of superoxide. These compounds due to this mechanism ROS generation are used for the treatment of several types of cancers Figure 5. Studies have shown that other drugs such as dequalinium chloride preclinical and metformin preclinical and clinical, Phase I through inhibition of mitochondrial complex 1 have the ability to produce ROS.
VDACs, also known as mitochondrial porins, show high similarity between some animals especially mice and humans. VDAC play an important role in the cell, such as regulating mitochondrial shape and structural changes, regulating apoptosis signaling, regulating ATP and calcium transport.
Several studies have demonstrated the role of VDAC in the regulation of apoptosis signaling and VDAC is being studied as a cancer-specific target. As has been mentioned, these drugs promote ROS production through the disturbance of VDAC and cause non-apoptotic form of cell death in KRAS. Several studies have shown that some drugs and agents including, paclitaxel taxol , ionizing radiation, niclosamide, AGX, AG with effect on NOX induces ROS generation.
The recent results from both in vitro and in vivo studies have shown that this drug causes the translocation of Rac1, which favorably regulates the activity of NOX, thereby furthering ROS H 2 O 2 production.
It was reported that taxol can raise the levels of ROS in the extracellular and subsequently induced cancer cell death resulting in the release of cytochrome c from the mitochondria. P53 act as a transcription factor to regulate the expression of many pro-oxidant genes. The 5-fluorouracil 5-FU is an antimetabolites and pyrimidine analog.
It is used for therapies for several types of cancers, such as gastrointestinal, colon, rectal, and head and neck cancer, through inducing intracellular increase in superoxide.
The mechanism by which 5-FU cause increased ROS generation from mitochondria is through a pdependent pathway [ 4 ]. The two pathways GSH through enzymes such as GPX and GST and catalase can act directly on scavenging ROS in cells. For that reason, oxidative stress can be promoted with methods based on the loss of the reduced GSH storage and other antioxidant sources.
A number of drugs class have been recognized as increasing oxidative stress process and ROS generation through targeting antioxidant system [ 4 , 5 ]. These drugs are, including buthionine sulfoximine BSO , imexon, phenylethyl isothiocyanate, mangafodipir, 2-methoxyestradiol, tetrathiomolybdate ATN , and auranofin, used in the treatment of various types of cancer.
For example, BSO through inhibition of the antioxidant system especially GSH in cancer cells such as ovarian and breast cancers can induce an accumulation of ROS due to the high basal ROS output in ovarian and breast cancers, and initiate cell death [ 4 , 5 ].
Other studies have shown that imexon through decrease GSH pool and subsequently increase the production of ROS and decrease mitochondria function was induced apoptosis. Other studies have shown that some other drugs, including ascorbic acid and diethylmaleate are able effects on GSH GSH depletion.
One the other hand, mercaptosuccinic acid, aminotriazol, and 2-Methoxyoestradiol were able to inhibit of GPx, catalase, and SOD, respectively, and thereby increase ROS production [ 7 ].
Cancer is a multistage disease including initiation, promotion, and progression. The increased ROS causes DNA damage, which may lead to DNA damage or gene mutation, resulting in the progression of cancer. Increased generation of ROS and an altered redox status have observed in cancer cells, and investigations suggest that this biochemical property of cancer cells can be exploited for cancer therapy.
For treatment of cancer, since high levels of ROS can induce cell death, treatment of radiation, chemotherapy, and molecule compounds all can increase the level of intracellular ROS to induce cancer cell death and apoptosis. The increased intracellular ROS levels could make cancer cells more vulnerable than normal cells to oxidative stress-induced cell death.
Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3. Edited by Rizwan Ahmad. Open access peer-reviewed chapter Role of Oxygen Free Radicals in Cancer Development and Treatment Written By Jalal Pourahmad, Ahmad Salimi and Enaytollah Seydi.
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Chapter metrics overview 3, Chapter Downloads View Full Metrics. Impact of this chapter. Abstract It is well known that species derived from oxygen are cytotoxic and are involved in the etiology of cancer. Keywords cancer reactive oxygen species oxidation therapy mitochondria.
pourahmadjaktaji utoronto. Mechanisms of free radical-induced DNA base modification and mutagenesis It has been appraised that in one human cell is exposed to nearly 10 5 oxidative hits such as hydroxyl radical and other such species in a day.
Role of ROS in genotoxicity and DNA damage ROS-caused DNA lesion may be characterized both structurally and chemically and displays a typical schema of modifications. Lipid peroxidation and DNA damage While major consideration has centralized on direct DNA lesion by oxygen free radicals because of the genetic outcomes of such lesion, reactive radical species may also induce damage to other cellular members.
Functions of ROS in the cancer cells. Antioxidant and oxidation pathways regulate ROS generation. NRF2 nuclear factor, erythroid-derived 2, like 2 NRF2 is an important regulator of the antioxidant system and cellular stress responses in the several cancers. FOXO Forkhead box O and p53 FOXO, as a transcription factors, are involved in different signaling pathways and play key roles in some physiological and pathological processes such as cancer.
Hypoxia and hypoglycemia Hypoxic conditions caused by the imbalance between intake and oxygen consumption [ 4 ]. Mitochondria In recent decades, several studies have shown that mitochondria organelle plays an important role in human health and disease.
Cancer cells Normal cell Bioenergetics process Aerobic glycolysis condition "Warburg Effect" Aerobic condition Mitochondrial DNA mtDNA mtDNA is mutated mtDNA is normal Morphological and physiological differences shape and count Size and shape: smaller Size and shape: larger MMP level Higher ~60 mV Lower ROS level Higher Lower Intracellular pH Acidic No acidic Metabolic rates Higher Lower.
Table 1. Targeting mitochondrial respiratory chain Arsenic trioxide ATO is used in the treatment of acute promyelocytic leukemia APL. Targeting VDACs VDACs, also known as mitochondrial porins, show high similarity between some animals especially mice and humans.
Targeting NOX Several studies have shown that some drugs and agents including, paclitaxel taxol , ionizing radiation, niclosamide, AGX, AG with effect on NOX induces ROS generation.
Targeting p53 P53 act as a transcription factor to regulate the expression of many pro-oxidant genes. References 1. Dizdaroglu M, Jaruga P, Birincioglu M, Rodriguez H.
Free radical-induced damage to DNA: mechanisms and measurement 1, 2. Free Radical Biology and Medicine. Waris G, Ahsan H. Reactive oxygen species: role in the development of cancer and various chronic conditions. Journal of Carcinogenesis. Marnett LJ. Oxy radicals, lipid peroxidation and DNA damage.
Gorrini C, Harris IS, Mak TW. Modulation of oxidative stress as an anticancer strategy. Nature Reviews Drug Discovery. Trachootham D, Alexandre J, Huang P.
Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach? Nogueira V, Hay N. Molecular pathways: reactive oxygen species homeostasis in cancer cells and implications for cancer therapy.
The Ohio State University. Rdaicals new study in animal models shows that the presence of a Evaluating fluid volume tumor alone can gadicals Free radicals and cancer cardiac damage, and suggests the Ftee are raidcals called free radicals interacting cancwr specific Free radicals and cancer in the heart. Adding specific types of antioxidants to food consumed by fruit flies with tumors reversed the damage to their hearts — a finding suggesting that harm caused by free radicals was the likely link between cancer and cardiac dysfunction. The researchers found that different cancer-associated genes affect the heart in different ways — a sign that genetic information could one day guide heart-protective treatment decisions in cancer patients. The study is published in the journal Antioxidants. However, emerging research has suggested that heart problems can surface before cancer treatment or muscle wasting occur.Free radicals and cancer -
She and Singh also emphasized that reactive oxygen species are just one identified mechanism of tumor-related heart damage, and that there is still a lot to learn about how antioxidants might fit into a treatment regimen. Though this research zeroed in on one cancer-causing gene to study the mechanism of heart damage in fruit flies, the researchers initially tested the effects of several cancer-causing genes in the flies.
The heart function affected and the intensity of the effects on the heart varied, depending on the gene. Singh is collaborating with clinicians at Ohio State and other institutions to collect blood samples from cancer patients who have heart failure.
Second, we want to see what the message is and whether we can prescribe antioxidants. Additional co-authors include Priyanka Karekar, Haley Jensen, Kathryn Russart, Devasena Ponnalagu, Shridhar Sanghvi, Sakima Smith and Leah Pyter from Ohio State and Sarah Seeley from Ohio Northern University ONU.
The work was supported by Commonwealth Universal Research Enhancement Program grants, the W. Lane Ave. Columbus, Ohio OHIO.
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Vitamin E supplements, as well as the antioxidants CoQ10 and GSH, reversed heart damage in fruit flies caused by a tumor. Study links free radicals to heart damage caused by cancer. In fruit flies, antioxidants reverse tumor-related cardiac dysfunction.
Follow me on X opens in new window. Add me on LinkedIn opens in new window. Share this. Share on: Twitter. Share on: Facebook. Food is one of the few things you can be in control of during your treatment. The oncology certified registered dietitians at the Stanford Cancer Center are here to help you make informed choices about nutrition, answer your nutrition-related questions, and help you to achieve and maintain good health.
Antioxidants are substances that inhibit the oxidation process and act as protective agents. They protect the body from the damaging effects of free radicals by-products of the body's normal chemical processes. Free radicals attack healthy cells, which changes their DNA, allowing tumors to grow. Research is underway to investigate the role of antioxidants in decreasing the risk of developing cancer.
According to the National Cancer Institute NCI , vitamin C may protect against cancer of the oral cavity, stomach, and esophagus and may also reduce the risk of developing cancers of the rectum, pancreas, and cervix.
Also known as ascorbic acid, vitamin C may provide protection against breast and lung cancer. According to the American Dietetic Association and USDA Nutrient Database for Standard Reference, the following foods are good sources of vitamin C:. The recommended dietary allowance RDA for vitamin C has recently been increased to 75 milligrams per day for women and 90 milligrams per day for men.
If you smoke cigarettes, it is recommended to increase your intake of vitamin C to milligrams per day. Beta carotene, also known as provitamin A, may help decrease the risk of developing cancer. According to the American Cancer Society, this nutrient may prevent certain cancers by enhancing the white blood cells in your immune system.
White blood cells work to block cell-damaging free radicals. Good sources of beta carotene are dark green leafy and yellow-orange fruits and vegetables. In the body, beta carotene is converted to vitamin A. Eating foods rich in beta carotene is recommended to possibly decrease the risk of developing stomach, lung, prostate, breast, and head and neck cancer.
However, more research is needed before a definite recommendation on beta carotene consumption can be made. Overdosing on beta carotene is not recommended. Large doses can cause the skin to turn a yellow-orange color, a condition called carotenosis.
High intakes of beta carotene in supplement form may actually cause lung cancer in people at risk, such as smokers. While there is a recommended dietary allowance for vitamin A, there is not one for beta carotene. Examples of some foods high in beta carotene include the following:.
Vitamin E is essential for our bodies to work properly. Vitamin E helps to build normal and red blood cells, as well as working as an antioxidant. Research is finding evidence that vitamin E may protect against prostate and colorectal cancer.
The recommended dietary allowance for vitamin E is 15 milligrams per day. The adult upper limit for vitamin E is 1, milligrams per day.
Good sources of vitamin E and the amount each serving contains include the following:. Since some sources of vitamin E are high in fat. A synthetic form of a vitamin E is available as a supplement. Vitamin E supplementation is probably not needed for most individuals because vitamin E is a fat-soluble vitamin and is stored in our bodies.
Very high doses of vitamin E can also interfere with the way other fat-soluble vitamins work. Also, large doses of vitamin E from supplements are not recommended for people taking blood thinners and some other medications, as the vitamin can interfere with the action of the medication.
To make sure you are meeting your needs, eat a varied diet that includes whole-wheat breads and cereals. There is no recommended dietary allowance for antioxidants. Eat a variety of foods, including plenty of fruits and vegetables, to ensure you are getting adequate amounts in your diet.
In honor of Colon Cancer Awareness month , we'll be featuring four colorectal cancer friendly recipes each week during the month of March.
Broccoli, cabbage, collard greens, kale, cauliflower and Brussels sprouts are all cruciferous vegetables. This vegetable family contains powerful phytochemicals, including carotenoids, indoles and glucosinolates and isothiocyanates, which have been studied and shown to slow the growth of many cancers.
Get the recipe ». Apple Muffins. Baked Oatmeal. Banana Bran Muffins. Banana-Oatmeal Hot Cakes. Multigrain Pancakes with Strawberry Sauce. Orange Bran Flax Muffins. Spring Vegetable Frittata. Whole Wheat Blueberry Muffins.
Pesto Toastini. Fiesta Quesadillas with Black Beans. Skewered Shrimp, Chicken and Pineapple with Honey Orange Dipping Sauce. Zucchini Bites. Asparagus and Scallion Soup with Almonds. Black Bean and Corn Salad. Broccoli Sunflower Salad. Butternut Squash Soup.
California Citrus Greens Salad with Garlic Dressing. Carrot and Apple Soup. Creamy Irish Soup. Crunchy Chicken Salad. Curried Chicken Salad. Curried Chickpea Salad with Walnuts. Easy Pea Soup with Tarragon. Egyptian Red Lentil Soup. Fall Stew in a Pumpkin with Poblano-Cucumber Salsa.
Golden Fruit Salad. Hawaiian Star Soup. Hearty Vegetable and Brown Rice Soup. Hot and Sour Soup. Lentil Sweet Potato Soup.
Marinated Artichoke Potato Salad. Melon Salad. Minty Cucumber-Quinoa-Grape Salad. Mulligatawny Soup. Papaya, Chicken and Pecan Salad. Pluot Summer Salad. Pomegranate Salad.
Pumpkin Bisque. Roasted Asparagus Salad. Salmon Salad with Pimento and Herbs. Shredded Carrot and Beet Salad. Spicy Black Bean Salad. Spinach Salad with Strawberry Vinaigrette.
Spinach, Red Bell Pepper and Feta Cheese Salad with Yogurt Dressing. Spring Pea Soup. Summer Rice Salad.
Sweet and Spicy Carrot Salad. Vegetable Soup. Whole Grain Salad. Anytime Burrito. Baked Tofu Kabobs.
Bean and Vegetable Enchilada Casserole. Bean Surprise. Broiled Portobello Mushrooms. Cajun Salmon over Polenta. Chicken Chili. Chicken Enchilada Casserole. Cranberry Salmon. Cranberry-Turkey Salad Sandwiches. Crispy Parmesan Turkey Cutlets. Crunchy Veggie Wrap.
Easy Spinach Lasagna. Eating Well Sloppy Joe. Egg, Spinach, and Bacon Sandwiches. Fish Filet with Squash and Herbs. Greek-Style Scallops. Grilled Ginger Tuna. Grilled Halibut with a Tomato-Herb Sauce. Grilled Portobello Burgers. Grilled Vegetable Polenta with Pan Roasted Red Pepper and Tomato Sauce.
Halibut with Citrus and Garlic. Healthy Jambalaya. Hearty Beef Stew with Winter Vegetables. Hearty Mediterranean Stew. Herbed Polenta with Grilled Portobello Mushrooms.
Indonesian Salmon. Lasagna Rolls. Lemon Dijon Salmon. Mediterranean Grilled Veggie Pockets. Molasses-Cured Pork Loin with Apples. Mushroom Goulash. New American Plate "Tetrazzini" Casserole. New Tuna Salad. Peppers Stuffed with Barley, Parmesan and Onion. Pizza Meat Loaf. Pumpkin Gnocchi. Quinoa and Mushroom Pilaf with Dill.
Quinoa Stuffed Peppers. Roasted Pork Tenderloin with Maple Mustard Sauce. Scallion Crusted Arctic Char. Seared Scallops with Beet Puree and Arugula Salad. Soft Tacos with Southwestern Vegetables. Spaghetti alla Carbonara. Speedy Summer Ratatouille. Spicy Broccoli, Cauliflower and Tofu. Steamed Halibut on Spinach with Lemon Sauce.
Stuffed Cornish Hens. Summer Tofu Kebab with Peanut Sauce. Sweet and Sour Chicken. Sweet and Sour Tofu. Tofu Cutlets Marsala. Turkey Reuben Grilled Sandwiches. Udon Noodles with Spicy Peanut Ginger Sauce. Veggie Pita Pizzas.
White Wine Coq au Vin. Whole Wheat Pasta with Fennel, Peas and Arugula. Zesty Roasted Chicken. Asian Green Bean Stir-Fry. Asian Pilaf. Avocado and Mango Salsa. Baked Sweet Potato Wedges.
Bok Choy with Sautéed Mushrooms and Shallots. Braised Kale with Black Beans and Tomatoes. Broccoli with Hazelnuts.
Brussels Sprouts with Pecans and Dried Cranberries. Butternut Squash Pilaf. Garlicky Greens.
There is increasing Free radicals and cancer that the progress of biologic aging results from radicqls free radical damage, and tadicals a significant fraction of cancer is also caused by deleterious free radical reactions. Free radicals originate Refreshment Services for Weddings the utilization of oxygen and anc metabolism of organic Free radicals and cancer, cnacer can be scavenged in living organisms by a range of enzymes and small antioxidant molecules. In this review, the various theories of aging are examined, as are the possible origins of cancer. The mitochondrion is proposed as the common link between cancer and aging, and the free radical reactions that occur in the mitochondrion are explained. Some of the important free radical reactions, both essential and deleterious, that occur continuously in a living organism, are discussed, and an outline is given of the multi-layered defense system that all aerobic organisms have against excess free radicals. SpringerPlus volume radocalsArticle number: Cite this article. Rdicals details. Researchers Free radicals and cancer recently shown an increased Pumpkin Seed Coffee in free radicals and Fres role in the tumor microenvironment. Free radicals Radical molecules with rxdicals instability and reactivity due to the presence of an odd number of electrons in the outermost orbit of their atoms. Free radicals include reactive oxygen and nitrogen species, which are key players in the initiation and progression of tumor cells and enhance their metastatic potential. In fact, they are now considered a hallmark of cancer. However, both reactive species may contribute to improve the outcomes of radiotherapy in cancer patients.
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