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Keywords:
Womens Health, Vitamins, simulated ischemia-reperfusion, Sports, Sports Medicine, Sports Nutrition, USANA, Utah, Sierra Foothills Karate Health Advise, Self Defense, oxidants, Fitness, Health, Jason Kilgore, martial arts, Mens Health, Minerals, nutrition, cardiac cells, antioxidants, 2-dithiole-3-thione, MMA and Jason Kilgore, USANA HEALTH Sciences, 3-H1 minerals
Showing posts with label oxidants. Show all posts
Showing posts with label oxidants. Show all posts
Monday, December 3, 2007
Saturday, November 10, 2007
CoQuinone® 30
The energy that every cell needs to function is produced through a complex process in the mitochondria, an organelle within the cell often called the cellular powerhouse. Cells store energy in a molecule called adenosine-5-triphosphate or ATP. CoQ10 is an essential part of the electron transport chain used to make ATP which is synthesized and used by every cell in the body. CoQuinone 30 contains advanced levels of CoQ10. Cells with the highest energy demands, such as in the heart, contain the highest levels of CoQ10. CoQ10 has been studied for years in the U.S., Europe, and Japan for its role in producing cellular energy and re-energizing the heart and other muscles.*
Promotes a strong and healthy cardiovascular system*
Supports energy metabolism in muscles
Patent Priority Protected formula
*These statements have not been evaluated by the Food and Drug Administration.
*These statements have not been evaluated by the Food and Drug Administration.
This product is not intended to diagnose, treat, cure, or prevent any disease.
Saturday, November 3, 2007
Antioxidants and Phase 2 Enzymes in Cardiomyocytes
Antioxidants and Phase 2 Enzymes in Cardiomyocytes:
Chemical Inducibility and Chemoprotection Against Oxidant and Simulated Ischemia-Reperfusion Injury Zhuoxiao Cao*,1, Hong Zhu*, Li Zhang*, Xue Zhao, Jay L. Zweier* and Yunbo Li*,2
* Davis Heart and Lung Research Institute, Department of Internal Medicine and Division of Cardiovascular Medicine, The Ohio State University Medical Center, Columbus, Ohio 43210; and Department of Cardiology, Changzheng Hospital, The Second Military Medical University, 415 Fengyang Road, Shanghai 200003, China
The increasing recognition of the role for oxidative stress in cardiac disorders has led to extensive investigation on the protection by exogenous antioxidants against oxidative cardiac injury. On the other hand, another strategy for protecting against oxidative cardiac injury may be through upregulation of the endogenous antioxidants and phase 2 enzymes in the myocardium by chemical inducers. However, our current understanding of the chemical inducibility of cardiac cellular antioxidants and phase 2 enzymes is very limited.
In this study, using rat cardiac H9c2 cells we have characterized the concentration- and time-dependent induction of cellular antioxidants and phase 2 enzymes by 3H-1,2-dithiole-3-thione (D3T), and the resultant chemoprotective effects on oxidative cardiac cell injury. Incubation of H9c2 cells with D3T resulted in a marked concentration- and time-dependent induction of a number of cellular antioxidants and phase 2 enzymes, including catalase, reduced glutathione (GSH), GSH peroxidase, glutathione reductase (GR), GSH S-transferase (GST), and NAD(P)H:quinone oxidoreductase-1 (NQO1). D3T treatment of H9c2 cells also caused an increase in mRNA expression of catalase, -glutamylcysteine ligase catalytic subunit, GR, GSTA1, M1 and P1, and NQO1.
Moreover, both mRNA and protein expression of Nrf2 were induced in D3T-treated cells. D3T pretreatment led to a marked protection against H9c2 cell injury elicited by various oxidants and simulated ischemia-reperfusion. D3T pretreatment also resulted in decreased intracellular accumulation of reactive oxygen in H9c2 cells after exposure to the oxidants as well as simulated ischemia-reperfusion. This study demonstrates that a series of endogenous antioxidants and phase 2 enzymes in H9c2 cells can be induced by D3T in a concentration- and time-dependent fashion, and that the D3T-upregulated cellular defenses are accompanied by a markedly increased resistance to oxidative cardiac cell injury.
Key Words: cardiac cells • 3H-1,2-dithiole-3-thione • antioxidants • oxidants • simulated ischemia-reperfusion • cytotoxicity
Chemical Inducibility and Chemoprotection Against Oxidant and Simulated Ischemia-Reperfusion Injury Zhuoxiao Cao*,1, Hong Zhu*, Li Zhang*, Xue Zhao, Jay L. Zweier* and Yunbo Li*,2
* Davis Heart and Lung Research Institute, Department of Internal Medicine and Division of Cardiovascular Medicine, The Ohio State University Medical Center, Columbus, Ohio 43210; and Department of Cardiology, Changzheng Hospital, The Second Military Medical University, 415 Fengyang Road, Shanghai 200003, China
The increasing recognition of the role for oxidative stress in cardiac disorders has led to extensive investigation on the protection by exogenous antioxidants against oxidative cardiac injury. On the other hand, another strategy for protecting against oxidative cardiac injury may be through upregulation of the endogenous antioxidants and phase 2 enzymes in the myocardium by chemical inducers. However, our current understanding of the chemical inducibility of cardiac cellular antioxidants and phase 2 enzymes is very limited.
In this study, using rat cardiac H9c2 cells we have characterized the concentration- and time-dependent induction of cellular antioxidants and phase 2 enzymes by 3H-1,2-dithiole-3-thione (D3T), and the resultant chemoprotective effects on oxidative cardiac cell injury. Incubation of H9c2 cells with D3T resulted in a marked concentration- and time-dependent induction of a number of cellular antioxidants and phase 2 enzymes, including catalase, reduced glutathione (GSH), GSH peroxidase, glutathione reductase (GR), GSH S-transferase (GST), and NAD(P)H:quinone oxidoreductase-1 (NQO1). D3T treatment of H9c2 cells also caused an increase in mRNA expression of catalase, -glutamylcysteine ligase catalytic subunit, GR, GSTA1, M1 and P1, and NQO1.
Moreover, both mRNA and protein expression of Nrf2 were induced in D3T-treated cells. D3T pretreatment led to a marked protection against H9c2 cell injury elicited by various oxidants and simulated ischemia-reperfusion. D3T pretreatment also resulted in decreased intracellular accumulation of reactive oxygen in H9c2 cells after exposure to the oxidants as well as simulated ischemia-reperfusion. This study demonstrates that a series of endogenous antioxidants and phase 2 enzymes in H9c2 cells can be induced by D3T in a concentration- and time-dependent fashion, and that the D3T-upregulated cellular defenses are accompanied by a markedly increased resistance to oxidative cardiac cell injury.
Key Words: cardiac cells • 3H-1,2-dithiole-3-thione • antioxidants • oxidants • simulated ischemia-reperfusion • cytotoxicity
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