Hormesis/Bibliography: Difference between revisions
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''' | ==Articles== | ||
*'''<u>Contents:</u>''' | |||
*Hopkin K. (2008) [http://www.the-scientist.com/article/display/55118/ The Science of Stress.] ''The Scientist'' 22:54. | |||
**”lt started with OxyR. Storz was recruited to the OxyR project in 1985, when her thesis advisor Bruce Ames got interested in studying how bacteria adapt to oxidative stress. "We knew that if you treated E. coli with low doses of oxidants, they became resistant to high doses of oxidants," says Storz. "And the question was: How did they induce these defenses?"” | |||
*Schmeisser S, Zarse K, Ristow M. (2011) [http://dx.doi.org/10.1055/s-0031-1286308 Lonidamine extends lifespan of adult Caenorhabditis elegans by increasing the formation of mitochondrial reactive oxygen species]. ''Horm Metab Res'' 43:687-92. | |||
**<font face="Gill Sans MT">"The aim of the study was to test whether pharmaceutical concentrations of the glycolytic inhibitor lonidamine are capable of extending lifespan in a nematodal model organism for aging processes, the roundworm Caenorhabditis elegans...Lonidamine significantly extends both median and maximum lifespan of C. elegans...Moreover, the compound increases paraquat stress resistance, and promotes mitochondrial respiration, culminating in increased formation of reactive oxygen species (ROS). Extension of lifespan requires activation of pmk-1, an orthologue of p38 MAP kinase, and is abolished by co-application of an antioxidant, indicating that increased ROS formation is required for the extension of lifespan by lonidamine. Consistent with the concept of mitohormesis, lonidamine is capable of promoting longevity in a pmk-1 sensitive manner by increasing formation of ROS."</font> | |||
*Ristow M, Schmeisser S. (2011) [http://dx.doi.org/10.1016/j.freeradbiomed.2011.05.010 Extending life span by increasing oxidative stress]. ''Free Radic Biol Med'' 51:327-36. | |||
**<font face="Gill Sans MT">"This review aims to summarize published evidence that several longevity-promoting interventions may converge by causing an activation of mitochondrial oxygen consumption to promote increased formation of reactive oxygen species (ROS). These serve as molecular signals to exert downstream effects to ultimately induce endogenous defense mechanisms culminating in increased stress resistance and longevity, an adaptive response more specifically named mitochondrial hormesis or mitohormesis. Consistently, we here summarize findings that antioxidant supplements that prevent these ROS signals interfere with the health-promoting and life-span-extending capabilities of calorie restriction and physical exercise. Taken together and consistent with ample published evidence, the findings summarized here question Harman's Free Radical Theory of Aging and rather suggest that ROS act as essential signaling molecules to promote metabolic health and longevity."</font> | |||
==Books== | |||
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*[http://www.nationmaster.com/encyclopedia/Hormesis Hormesis.] NationMaster Encyclopedia. | |||
**'''<u>Contents:</u>''' | |||
:* Possible explanation | :* Possible explanation | ||
:*Policy consequences | :*Policy consequences | ||
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:*Non-acceptance | :*Non-acceptance | ||
:*See also | :*See also | ||
:*References | :*References | ||
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Latest revision as of 17:30, 7 December 2011
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Articles
- Hopkin K. (2008) The Science of Stress. The Scientist 22:54.
- ”lt started with OxyR. Storz was recruited to the OxyR project in 1985, when her thesis advisor Bruce Ames got interested in studying how bacteria adapt to oxidative stress. "We knew that if you treated E. coli with low doses of oxidants, they became resistant to high doses of oxidants," says Storz. "And the question was: How did they induce these defenses?"”
- Schmeisser S, Zarse K, Ristow M. (2011) Lonidamine extends lifespan of adult Caenorhabditis elegans by increasing the formation of mitochondrial reactive oxygen species. Horm Metab Res 43:687-92.
- "The aim of the study was to test whether pharmaceutical concentrations of the glycolytic inhibitor lonidamine are capable of extending lifespan in a nematodal model organism for aging processes, the roundworm Caenorhabditis elegans...Lonidamine significantly extends both median and maximum lifespan of C. elegans...Moreover, the compound increases paraquat stress resistance, and promotes mitochondrial respiration, culminating in increased formation of reactive oxygen species (ROS). Extension of lifespan requires activation of pmk-1, an orthologue of p38 MAP kinase, and is abolished by co-application of an antioxidant, indicating that increased ROS formation is required for the extension of lifespan by lonidamine. Consistent with the concept of mitohormesis, lonidamine is capable of promoting longevity in a pmk-1 sensitive manner by increasing formation of ROS."
- Ristow M, Schmeisser S. (2011) Extending life span by increasing oxidative stress. Free Radic Biol Med 51:327-36.
- "This review aims to summarize published evidence that several longevity-promoting interventions may converge by causing an activation of mitochondrial oxygen consumption to promote increased formation of reactive oxygen species (ROS). These serve as molecular signals to exert downstream effects to ultimately induce endogenous defense mechanisms culminating in increased stress resistance and longevity, an adaptive response more specifically named mitochondrial hormesis or mitohormesis. Consistently, we here summarize findings that antioxidant supplements that prevent these ROS signals interfere with the health-promoting and life-span-extending capabilities of calorie restriction and physical exercise. Taken together and consistent with ample published evidence, the findings summarized here question Harman's Free Radical Theory of Aging and rather suggest that ROS act as essential signaling molecules to promote metabolic health and longevity."