A Brief Analysis of the Relationship Between Free Radicals and Animal Nutrition
A Brief Discussion of Free Radicals and Animal Nutrition
A Brief Discussion of Free Radicals and Animal Nutrition
"Life is a chemical process." This famous assertion put forward by the chemist Lavoisier in 1783 laid the theoretical foundation for animal nutrition research. In the more than 200 years of animal nutrition research carried out since then, many new theories and methods have continuously penetrated this field, enabling animal nutrition research methods to be continuously improved and developed, and its content to become richer and more in-depth. Free radical biology, meanwhile, has developed extremely rapidly over the past dozen years, expanding its scope of research and its application to other life sciences at a very fast pace. As an aerobic organism, the animal body's production, scavenging, utilization and harm of reactive oxygen species, along with the repair of the biomolecular damage they cause, as well as the metabolism and effects of nitric oxide (NO) and the derived reactive nitrogen species, are not only the main content of free radical biology research, but must also be given attention in animal nutrition and health research. The vitamins that are studied and applied more often in nutrition science: beta-carotene as a source of vitamin A, vitamin C, vitamin E, and some other antioxidants, are also indispensable important components within the scope of free radical biology research. Research on free radicals and nutrition has surged year by year, and its progress reveals a new academic field and a new direction of development combining the molecular level with the submolecular level.
1. Free radicals exist in the animal body
As early as 1931, Michalis proposed that the intermediate products of certain enzymatic redox reactions are free radicals, and his experimental evidence also indicated that free radicals may exist in organisms; however, it was not until the rapid development of free radical biology in the last 30 years that the production and scavenging of free radicals in the body were given attention. Today, the increase in endogenous free radical production and the weakening of its scavenging capacity have been confirmed as important mechanisms in the development and aggravation of radiation damage, and it has been recognized that free radicals are closely related to the occurrence and development of many diseases.
A large number of studies have shown that biomolecules in the animal body include both non-radicals and free radicals. Reactive oxygen species are oxygen free radicals and their reactive derivatives. Their production, scavenging, utilization and harm were the main content of research in the early stages of the development of free radical biology. In 1986, the biological effects of nitric oxide were discovered [Palmerm et al., 1987], and reactive nitrogen species also became a major research subject in free radical biology. The biological effects of free radicals centered on O, N, C, S and other elements and their derivatives involve not only reactions between free radicals, but also reactions between free radicals and non-radicals [Wink DA et al., 1998]. For example: NO combines with superoxide free radicals to form ONOO-, a substance whose activity is far higher than that of NO or superoxide free radicals; ONOO- can also react with CO2 to generate highly active substances, and can even undergo homolysis into free radicals and non-radicals [Squadrito GL et al., 1998].
2 The relationship between nutrients and free radicals
2.1. Nutrients in the animal body are the material basis for free radical production
Free radicals in the animal body are produced by enzymatic or non-enzymatic reactions, and apart from O2, their sources can all be traced back to nutrients. The process of nitric oxide formation in the body (see Figure 1) [Marletta MA, 1993] can very intuitively demonstrate that nutrients are the material basis for free radical generation. This process is mainly an enzymatic reaction catalyzed by nitric oxide synthase (NOS), with arginine as the substrate and NADPH as a cofactor. Moreover, the biosynthesis of nitric oxide synthase requires amino acids, riboflavin, purines and other substances, and requires ATP to provide energy. The production of ATP inevitably involves nutrients: the metabolism of carbohydrates, lipids and proteins (amino acids), as well as the participation of certain vitamins. When studying free radicals, one cannot ignore this natural connection with nutrients.
2.2. Nutrients are the material source for scavenging free radicals in the animal body
Free radicals in the animal body are constantly produced and constantly scavenged; under normal conditions, free radicals are always scavenged and maintained at an extremely low equilibrium level. For example, under the action of various antioxidant enzymes, endogenous antioxidants and exogenous antioxidants, reactive oxygen species can be scavenged to an extremely low level. The body needs to maintain these antioxidant enzymes, endogenous antioxidants and exogenous antioxidants at certain concentrations, which inevitably involves protein synthesis and the metabolism of various nutrients. Superoxide dismutase (Cu,Zn-SOD; Mn-SOD), catalase (containing Fe), glutathione peroxidase (containing Fe) and other antioxidant enzymes and macromolecular antioxidants such as metallothionein and ceruloplasmin, as well as small-molecule antioxidants such as glutathione, require the participation of amino acids, mineral elements and ATP for their biosynthesis. The essential antioxidant vitamins in the body are themselves nutrients. And some endogenous selenium, copper and manganese are trace elements essential for the biosynthesis of glutathione peroxidase (GSH-Px) and superoxide dismutase (Cu,Zn-SOD; Mn-SOD). When the animal body is deficient in selenium, myocardial GSH-Px activity decreases, and even decreases; antioxidants such as uric acid are derived from the metabolic products of nutrients in the body.
When animals are malnourished, it may lead to an increase in free radical production in the body, and malnutrition may also affect the biosynthesis of various antioxidant enzymes and the level of endogenous antioxidant production, thereby further increasing free radicals in the body. Some scholars have observed (Robinson et al., 1997) that in nutritionally deficient rats, O2 production in the liver increases while glutathione (GSH) levels decrease. Dabbagh et al. (1994) found that excessive iron intake can reduce antioxidant levels and increase reactive oxygen species in experimental rats, and cause lipid peroxidation induced by reactive oxygen species. Hammrmueller et al. (1984) pointed out that zinc and copper deficiency can increase the activity of NADPH-dependent cytochrome P-450 reductase in the microsomes of rat liver and lung, leading to increased production of reactive oxygen species and thus lipid peroxidation. Malnutrition or nutritional deficiency may also induce inflammation or other complications, causing the production of NO and its derived reactive nitrogen species and reactive oxygen species [Wepnir, 2000]. 95%, therefore oxidative damage and mitochondrial dysfunction occur. If selenium is supplemented, the degree of decrease in GSH-Px activity is reduced, and thus selenium deficiency symptoms can also improve. Chow et al. (1973) observed that GSH-Px activity in animal tissues is parallel to the dietary selenium supply. Experiments have proven that in copper-deficient animals, Cu,Zn-SOD activity in the body decreases; manganese deficiency will lead to a decrease in Mn-SOD activity in animal tissues. Dietary vitamin deficiency also affects the biosynthesis of antioxidant enzymes; for example: Housewirsh et al. (1975) found that in experimental rats fed a diet deficient in vitamin E, catalase activity in the liver decreased.
The levels of non-enzymatic antioxidants in the animal body mainly depend on their production and decomposition in the body. The levels of metallothionein, ceruloplasmin, selenoprotein and redox proteins are determined by their biosynthetic amount and their metabolic decomposition rate; the amount of uric acid changes with metabolic changes. Glutathione (GSH) is a very important antioxidant in the body, and its oxidation product is GSSH. The GSH/GSSH ratio can reflect the body's antioxidant defense capacity. During malnutrition, GSH levels decrease and the GSH/GSSH ratio decreases; the reasons may be: protein deficiency weakens the ability to synthesize GSH; during malnutrition, glutathione reductase activity in the body decreases, and the ability to catalyze the reduction of GSSH to GSH weakens; the NADPH/NADP ratio in the body decreases under the influence of nutritional status, reducing glutathione reductase activity. The diet can provide a considerable amount of GSH to the body, and insufficient food supply can aggravate the decrease in GSH levels in the body. In addition, experiments have proven that vitamin B2 deficiency in animals can cause a decrease in glutathione reductase activity (Beutler, 1969).
2.3 Nutrients are the material basis for repairing biomolecular damage caused by free radicals
Usually, the free radicals produced in the animal body are not scavenged to the range required for physiology, but can only be maintained at an extremely low steady-state level of normal equilibrium; therefore, they can still damage important biomolecules such as DNA, proteins (enzymes) and biological membranes. However, the body can repair or replace damaged biomolecules. Damaged proteins can be degraded, and their metabolic products can enter the amino acid pool to participate in the resynthesis of proteins. The substances needed in the process of repairing or replacing damaged biomolecules, such as nucleotides, amino acids, fatty acids, enzyme systems and cofactors, as well as energy sources, all ultimately have nutrients as their material basis. Certain natural antioxidants and some non-nutrient active components in feed or food may also directly or indirectly play the role of material basis in the repair or replacement of biomolecules.
2.4. Certain nutrients help animals adapt to oxidative stress and prevent and treat certain animal diseases
Exogenous or endogenous stimuli can shift the redox state in the body toward oxidation. Oxidative stress often brings many problems, such as decreased livestock and poultry production performance (for example: heat stress reduces the laying rate of laying hens), decreased quality of animal products (for example: slaughter stress produces PSE pork), and even the occurrence of animal diseases (for example: environmental stress and nutritional stress trigger ascites in broilers). In production practice, in order to reduce the harm caused by oxidative stress, the amount of antioxidants (such as vitamin C and vitamin E) is often greatly increased in the diet or drinking water. And an appropriate nutritional level can also reduce and prevent damage caused by physiological oxidative stress.
Oxidative stress is often accompanied by a great increase in reactive oxygen species in the body, an increase in lipid peroxides, protein oxidative modification products and DNA damage products in the body, while the consumption of antioxidant vitamins (such as vitamin E) and GSH also increases, so the supply of antioxidant vitamins (such as vitamins E and C) and GSH should be increased accordingly. Experiments and production practice both prove that under stress conditions, adding large amounts of antioxidants such as vitamin E and ascorbic acid to animals helps animals resist oxidative damage in the body, thereby reducing the harm brought by oxidative stress. Bray (1993) proposed that attention should be paid to tissue GSH levels, nutritional status and oxidative stress. He believed that appropriate nutrition can increase the exogenous GSH supply, regulate tissue GSH levels, increase antioxidant capacity and prevent damage caused by reactive oxygen species.
3 Pay attention to the harm of oxidative stress to livestock production and strengthen research on animal nutrition and free radicals
As an applied science, animal nutrition research mainly targets problems that need to be solved in production practice; however, forward-looking research and basic research often have more important and broader guiding significance. The harm of oxidative stress already exists in large quantities in livestock production, but people have studied it very superficially, have not fully recognized the connection between phenomena and essence, and have been even less able to find the key to solving the problem. On the other hand, we can also draw inspiration from the large number of studies determining animal vitamin requirements. The development of animal nutrition must also be further combined with more new disciplines and new technologies, and research on animal nutrition and free radicals should become an important part of animal nutrition research.
--------------------------------------
Hehe, something new in animal nutrition
--------------------------------------
This is very good material, it should be bumped up. I have always been paying attention to material on free radicals.
--------------------------------------
Thanks a lot, it has practical value
"Life is a chemical process." This famous assertion put forward by the chemist Lavoisier in 1783 laid the theoretical foundation for animal nutrition research. In the more than 200 years of animal nutrition research carried out since then, many new theories and methods have continuously penetrated this field, enabling animal nutrition research methods to be continuously improved and developed, and its content to become richer and more in-depth. Free radical biology, meanwhile, has developed extremely rapidly over the past dozen years, expanding its scope of research and its application to other life sciences at a very fast pace. As an aerobic organism, the animal body's production, scavenging, utilization and harm of reactive oxygen species, along with the repair of the biomolecular damage they cause, as well as the metabolism and effects of nitric oxide (NO) and the derived reactive nitrogen species, are not only the main content of free radical biology research, but must also be given attention in animal nutrition and health research. The vitamins that are studied and applied more often in nutrition science: beta-carotene as a source of vitamin A, vitamin C, vitamin E, and some other antioxidants, are also indispensable important components within the scope of free radical biology research. Research on free radicals and nutrition has surged year by year, and its progress reveals a new academic field and a new direction of development combining the molecular level with the submolecular level.
1. Free radicals exist in the animal body
As early as 1931, Michalis proposed that the intermediate products of certain enzymatic redox reactions are free radicals, and his experimental evidence also indicated that free radicals may exist in organisms; however, it was not until the rapid development of free radical biology in the last 30 years that the production and scavenging of free radicals in the body were given attention. Today, the increase in endogenous free radical production and the weakening of its scavenging capacity have been confirmed as important mechanisms in the development and aggravation of radiation damage, and it has been recognized that free radicals are closely related to the occurrence and development of many diseases.
A large number of studies have shown that biomolecules in the animal body include both non-radicals and free radicals. Reactive oxygen species are oxygen free radicals and their reactive derivatives. Their production, scavenging, utilization and harm were the main content of research in the early stages of the development of free radical biology. In 1986, the biological effects of nitric oxide were discovered [Palmerm et al., 1987], and reactive nitrogen species also became a major research subject in free radical biology. The biological effects of free radicals centered on O, N, C, S and other elements and their derivatives involve not only reactions between free radicals, but also reactions between free radicals and non-radicals [Wink DA et al., 1998]. For example: NO combines with superoxide free radicals to form ONOO-, a substance whose activity is far higher than that of NO or superoxide free radicals; ONOO- can also react with CO2 to generate highly active substances, and can even undergo homolysis into free radicals and non-radicals [Squadrito GL et al., 1998].
2 The relationship between nutrients and free radicals
2.1. Nutrients in the animal body are the material basis for free radical production
Free radicals in the animal body are produced by enzymatic or non-enzymatic reactions, and apart from O2, their sources can all be traced back to nutrients. The process of nitric oxide formation in the body (see Figure 1) [Marletta MA, 1993] can very intuitively demonstrate that nutrients are the material basis for free radical generation. This process is mainly an enzymatic reaction catalyzed by nitric oxide synthase (NOS), with arginine as the substrate and NADPH as a cofactor. Moreover, the biosynthesis of nitric oxide synthase requires amino acids, riboflavin, purines and other substances, and requires ATP to provide energy. The production of ATP inevitably involves nutrients: the metabolism of carbohydrates, lipids and proteins (amino acids), as well as the participation of certain vitamins. When studying free radicals, one cannot ignore this natural connection with nutrients.
2.2. Nutrients are the material source for scavenging free radicals in the animal body
Free radicals in the animal body are constantly produced and constantly scavenged; under normal conditions, free radicals are always scavenged and maintained at an extremely low equilibrium level. For example, under the action of various antioxidant enzymes, endogenous antioxidants and exogenous antioxidants, reactive oxygen species can be scavenged to an extremely low level. The body needs to maintain these antioxidant enzymes, endogenous antioxidants and exogenous antioxidants at certain concentrations, which inevitably involves protein synthesis and the metabolism of various nutrients. Superoxide dismutase (Cu,Zn-SOD; Mn-SOD), catalase (containing Fe), glutathione peroxidase (containing Fe) and other antioxidant enzymes and macromolecular antioxidants such as metallothionein and ceruloplasmin, as well as small-molecule antioxidants such as glutathione, require the participation of amino acids, mineral elements and ATP for their biosynthesis. The essential antioxidant vitamins in the body are themselves nutrients. And some endogenous selenium, copper and manganese are trace elements essential for the biosynthesis of glutathione peroxidase (GSH-Px) and superoxide dismutase (Cu,Zn-SOD; Mn-SOD). When the animal body is deficient in selenium, myocardial GSH-Px activity decreases, and even decreases; antioxidants such as uric acid are derived from the metabolic products of nutrients in the body.
When animals are malnourished, it may lead to an increase in free radical production in the body, and malnutrition may also affect the biosynthesis of various antioxidant enzymes and the level of endogenous antioxidant production, thereby further increasing free radicals in the body. Some scholars have observed (Robinson et al., 1997) that in nutritionally deficient rats, O2 production in the liver increases while glutathione (GSH) levels decrease. Dabbagh et al. (1994) found that excessive iron intake can reduce antioxidant levels and increase reactive oxygen species in experimental rats, and cause lipid peroxidation induced by reactive oxygen species. Hammrmueller et al. (1984) pointed out that zinc and copper deficiency can increase the activity of NADPH-dependent cytochrome P-450 reductase in the microsomes of rat liver and lung, leading to increased production of reactive oxygen species and thus lipid peroxidation. Malnutrition or nutritional deficiency may also induce inflammation or other complications, causing the production of NO and its derived reactive nitrogen species and reactive oxygen species [Wepnir, 2000]. 95%, therefore oxidative damage and mitochondrial dysfunction occur. If selenium is supplemented, the degree of decrease in GSH-Px activity is reduced, and thus selenium deficiency symptoms can also improve. Chow et al. (1973) observed that GSH-Px activity in animal tissues is parallel to the dietary selenium supply. Experiments have proven that in copper-deficient animals, Cu,Zn-SOD activity in the body decreases; manganese deficiency will lead to a decrease in Mn-SOD activity in animal tissues. Dietary vitamin deficiency also affects the biosynthesis of antioxidant enzymes; for example: Housewirsh et al. (1975) found that in experimental rats fed a diet deficient in vitamin E, catalase activity in the liver decreased.
The levels of non-enzymatic antioxidants in the animal body mainly depend on their production and decomposition in the body. The levels of metallothionein, ceruloplasmin, selenoprotein and redox proteins are determined by their biosynthetic amount and their metabolic decomposition rate; the amount of uric acid changes with metabolic changes. Glutathione (GSH) is a very important antioxidant in the body, and its oxidation product is GSSH. The GSH/GSSH ratio can reflect the body's antioxidant defense capacity. During malnutrition, GSH levels decrease and the GSH/GSSH ratio decreases; the reasons may be: protein deficiency weakens the ability to synthesize GSH; during malnutrition, glutathione reductase activity in the body decreases, and the ability to catalyze the reduction of GSSH to GSH weakens; the NADPH/NADP ratio in the body decreases under the influence of nutritional status, reducing glutathione reductase activity. The diet can provide a considerable amount of GSH to the body, and insufficient food supply can aggravate the decrease in GSH levels in the body. In addition, experiments have proven that vitamin B2 deficiency in animals can cause a decrease in glutathione reductase activity (Beutler, 1969).
2.3 Nutrients are the material basis for repairing biomolecular damage caused by free radicals
Usually, the free radicals produced in the animal body are not scavenged to the range required for physiology, but can only be maintained at an extremely low steady-state level of normal equilibrium; therefore, they can still damage important biomolecules such as DNA, proteins (enzymes) and biological membranes. However, the body can repair or replace damaged biomolecules. Damaged proteins can be degraded, and their metabolic products can enter the amino acid pool to participate in the resynthesis of proteins. The substances needed in the process of repairing or replacing damaged biomolecules, such as nucleotides, amino acids, fatty acids, enzyme systems and cofactors, as well as energy sources, all ultimately have nutrients as their material basis. Certain natural antioxidants and some non-nutrient active components in feed or food may also directly or indirectly play the role of material basis in the repair or replacement of biomolecules.
2.4. Certain nutrients help animals adapt to oxidative stress and prevent and treat certain animal diseases
Exogenous or endogenous stimuli can shift the redox state in the body toward oxidation. Oxidative stress often brings many problems, such as decreased livestock and poultry production performance (for example: heat stress reduces the laying rate of laying hens), decreased quality of animal products (for example: slaughter stress produces PSE pork), and even the occurrence of animal diseases (for example: environmental stress and nutritional stress trigger ascites in broilers). In production practice, in order to reduce the harm caused by oxidative stress, the amount of antioxidants (such as vitamin C and vitamin E) is often greatly increased in the diet or drinking water. And an appropriate nutritional level can also reduce and prevent damage caused by physiological oxidative stress.
Oxidative stress is often accompanied by a great increase in reactive oxygen species in the body, an increase in lipid peroxides, protein oxidative modification products and DNA damage products in the body, while the consumption of antioxidant vitamins (such as vitamin E) and GSH also increases, so the supply of antioxidant vitamins (such as vitamins E and C) and GSH should be increased accordingly. Experiments and production practice both prove that under stress conditions, adding large amounts of antioxidants such as vitamin E and ascorbic acid to animals helps animals resist oxidative damage in the body, thereby reducing the harm brought by oxidative stress. Bray (1993) proposed that attention should be paid to tissue GSH levels, nutritional status and oxidative stress. He believed that appropriate nutrition can increase the exogenous GSH supply, regulate tissue GSH levels, increase antioxidant capacity and prevent damage caused by reactive oxygen species.
3 Pay attention to the harm of oxidative stress to livestock production and strengthen research on animal nutrition and free radicals
As an applied science, animal nutrition research mainly targets problems that need to be solved in production practice; however, forward-looking research and basic research often have more important and broader guiding significance. The harm of oxidative stress already exists in large quantities in livestock production, but people have studied it very superficially, have not fully recognized the connection between phenomena and essence, and have been even less able to find the key to solving the problem. On the other hand, we can also draw inspiration from the large number of studies determining animal vitamin requirements. The development of animal nutrition must also be further combined with more new disciplines and new technologies, and research on animal nutrition and free radicals should become an important part of animal nutrition research.
--------------------------------------
Hehe, something new in animal nutrition
--------------------------------------
This is very good material, it should be bumped up. I have always been paying attention to material on free radicals.
--------------------------------------
Thanks a lot, it has practical value