The homeostasis of free radicals is vital to the evolution and life of oxygen-requiring organisms. Under normal physiological conditions, rates of the production of free radicals are virtually equal to rates of their ...The homeostasis of free radicals is vital to the evolution and life of oxygen-requiring organisms. Under normal physiological conditions, rates of the production of free radicals are virtually equal to rates of their removal. The cytotoxic effect of free radicals is deleterious to cells and mediates the pathogenesis of a wide array of diseases. Therefore, antioxidants (e.g. vitamin C, vitamin E, β-carotene, and glutathione) are essential to the survival, health, and reproduction of animals, including humans. Antioxidants may be classified as nutritionally essential (e.g. vitamin antioxidants), indirectly essential (e.g., dietary fibre), conditionally essential (e.g. flavonoids and other effective phytochemicals) or non-essential. In the body, appropriate nutrition should not only prevent diseases, but also promote free radical homeostasis. Thus, it is crucial to develop useful indicators of oxidative stress, such as the cellular ratio of /, lipid peroxidation, oxidative modification of protein and DNA damage. On the basis of the recent report that the improper therapy of iron deficiency results in free radical-mediated dysfunction of the gastrointestinal tract, it is important to verify whether the formulated requirement of nutrients meet the need of maintaining the homeostasis of free radicals. The recommended intake of vitamin E, vitamin C and other antioxidants may need to be revised so as to protect the body against oxidative stress brought about by endogenous and exogenous factors. In order to delay aging and promote health in humans of all ages, and eliminate oxidative damage in response to the treatment of certain diseases, special nutritional measures should be taken. These measures may include the control of caloric intake, reduction in the absorption of free radicals and electrophilic substances, and adequate provision of antioxidant nutrients as well as effective phytochemicals and nutraceuticals. We predict that the concept of free radical biology will continue to greatly advance life sciences, inclu展开更多
Oxidative stress is increased in metabolic syndrome and type 2 diabetes mellitus(T2DM) and this appears to underlie the development of cardiovascular disease,T2 DM and diabetic complications.Increased oxidative stress...Oxidative stress is increased in metabolic syndrome and type 2 diabetes mellitus(T2DM) and this appears to underlie the development of cardiovascular disease,T2 DM and diabetic complications.Increased oxidative stress appears to be a deleterious factor leading toinsulin resistance,dyslipidemia,β-cell dysfunction,impaired glucose tolerance and ultimately leading to T2 DM.Chronic oxidative stress,hyperglycemia and dyslipidemia are particularly dangerous for β-cells from lowest levels of antioxidant,have high oxidative energy requirements,decrease the gene expression of key β-cell genes and induce cell death.If β-cell functioning is impaired,it results in an under production of insulin,impairs glucose stimulated insulin secretion,fasting hyperglycemia and eventually the development of T2 DM.展开更多
Cancer cells often upregulate nutrient transporters to fulfill their increased biosynthetic and bioenergetic needs,and to maintain redox homeostasis.One nutrient transporter frequently overexpressed in human cancers i...Cancer cells often upregulate nutrient transporters to fulfill their increased biosynthetic and bioenergetic needs,and to maintain redox homeostasis.One nutrient transporter frequently overexpressed in human cancers is the cystine/glutamate antiporter solute carrier family 7 member 11(SLC7A11;also known as xCT).SLC7A11 promotes cystine uptake and glutathione biosynthesis,resulting in protection from oxidative stress and ferroptotic cell death.Recent studies have unexpectedly revealed that SLC7A11 also plays critical roles in glutamine metabolism and regulates the glucose and glutamine dependency of cancer cells.This review discusses the roles of SLC7A11 in regulating the anti-oxidant response and nutrient dependency of cancer cells,explores our current understanding of SLC7A11 regulation in cancer metabolism,and highlights key open questions for future studies in this emerging research area.A deeper understanding of SLC7A11 in cancer metabolism may identify new therapeutic opportunities to target this important amino acid transporter for cancer treatment.展开更多
Redox state constitutes an important background of numerous liver disorders. The redox state participates in the course of inflammatory, metabolic and proliferative liver diseases. Reactive oxygen species(ROS) are pri...Redox state constitutes an important background of numerous liver disorders. The redox state participates in the course of inflammatory, metabolic and proliferative liver diseases. Reactive oxygen species(ROS) are primarily produced in the mitochondria and in the endoplasmic reticulum of hepatocytes via the cytochrome P450 enzymes. Under the proper conditions, cells are equipped with special molecular strategies that control the level of oxidative stress and maintain a balance between oxidant and antioxidant particles. Oxidative stress represents an imbalance between oxidant and antioxidant agents. Hepatocytic proteins, lipids and DNA are among the cellular structures that are primarily affected by ROS and reactive nitrogen species. The process results in structural and functional abnormalities in the liver. Thus, the phenomenon of oxidative stress should be investigated for several reasons. First, it may explain the pathogenesis of various liver disorders. Moreover, monitoring oxidative markers among hepatocytes offers the potential to diagnose the degree of liver damage and ultimately to observe the response to pharmacological therapies. The present report focuses on the role of oxidative stress in selected liver diseases.展开更多
文摘The homeostasis of free radicals is vital to the evolution and life of oxygen-requiring organisms. Under normal physiological conditions, rates of the production of free radicals are virtually equal to rates of their removal. The cytotoxic effect of free radicals is deleterious to cells and mediates the pathogenesis of a wide array of diseases. Therefore, antioxidants (e.g. vitamin C, vitamin E, β-carotene, and glutathione) are essential to the survival, health, and reproduction of animals, including humans. Antioxidants may be classified as nutritionally essential (e.g. vitamin antioxidants), indirectly essential (e.g., dietary fibre), conditionally essential (e.g. flavonoids and other effective phytochemicals) or non-essential. In the body, appropriate nutrition should not only prevent diseases, but also promote free radical homeostasis. Thus, it is crucial to develop useful indicators of oxidative stress, such as the cellular ratio of /, lipid peroxidation, oxidative modification of protein and DNA damage. On the basis of the recent report that the improper therapy of iron deficiency results in free radical-mediated dysfunction of the gastrointestinal tract, it is important to verify whether the formulated requirement of nutrients meet the need of maintaining the homeostasis of free radicals. The recommended intake of vitamin E, vitamin C and other antioxidants may need to be revised so as to protect the body against oxidative stress brought about by endogenous and exogenous factors. In order to delay aging and promote health in humans of all ages, and eliminate oxidative damage in response to the treatment of certain diseases, special nutritional measures should be taken. These measures may include the control of caloric intake, reduction in the absorption of free radicals and electrophilic substances, and adequate provision of antioxidant nutrients as well as effective phytochemicals and nutraceuticals. We predict that the concept of free radical biology will continue to greatly advance life sciences, inclu
文摘Oxidative stress is increased in metabolic syndrome and type 2 diabetes mellitus(T2DM) and this appears to underlie the development of cardiovascular disease,T2 DM and diabetic complications.Increased oxidative stress appears to be a deleterious factor leading toinsulin resistance,dyslipidemia,β-cell dysfunction,impaired glucose tolerance and ultimately leading to T2 DM.Chronic oxidative stress,hyperglycemia and dyslipidemia are particularly dangerous for β-cells from lowest levels of antioxidant,have high oxidative energy requirements,decrease the gene expression of key β-cell genes and induce cell death.If β-cell functioning is impaired,it results in an under production of insulin,impairs glucose stimulated insulin secretion,fasting hyperglycemia and eventually the development of T2 DM.
基金supported by the Andrew Sabin Family Fellow Award and Institutional Research Grant from the University of Texas MD Anderson Cancer Center,Grants from National Institutes of Health(CA181196 and CA190370)Anna Fuller Fund,and Ellison Medical Foundation(AG-NS-0973-13).
文摘Cancer cells often upregulate nutrient transporters to fulfill their increased biosynthetic and bioenergetic needs,and to maintain redox homeostasis.One nutrient transporter frequently overexpressed in human cancers is the cystine/glutamate antiporter solute carrier family 7 member 11(SLC7A11;also known as xCT).SLC7A11 promotes cystine uptake and glutathione biosynthesis,resulting in protection from oxidative stress and ferroptotic cell death.Recent studies have unexpectedly revealed that SLC7A11 also plays critical roles in glutamine metabolism and regulates the glucose and glutamine dependency of cancer cells.This review discusses the roles of SLC7A11 in regulating the anti-oxidant response and nutrient dependency of cancer cells,explores our current understanding of SLC7A11 regulation in cancer metabolism,and highlights key open questions for future studies in this emerging research area.A deeper understanding of SLC7A11 in cancer metabolism may identify new therapeutic opportunities to target this important amino acid transporter for cancer treatment.
文摘Redox state constitutes an important background of numerous liver disorders. The redox state participates in the course of inflammatory, metabolic and proliferative liver diseases. Reactive oxygen species(ROS) are primarily produced in the mitochondria and in the endoplasmic reticulum of hepatocytes via the cytochrome P450 enzymes. Under the proper conditions, cells are equipped with special molecular strategies that control the level of oxidative stress and maintain a balance between oxidant and antioxidant particles. Oxidative stress represents an imbalance between oxidant and antioxidant agents. Hepatocytic proteins, lipids and DNA are among the cellular structures that are primarily affected by ROS and reactive nitrogen species. The process results in structural and functional abnormalities in the liver. Thus, the phenomenon of oxidative stress should be investigated for several reasons. First, it may explain the pathogenesis of various liver disorders. Moreover, monitoring oxidative markers among hepatocytes offers the potential to diagnose the degree of liver damage and ultimately to observe the response to pharmacological therapies. The present report focuses on the role of oxidative stress in selected liver diseases.
