High fat diets may caugment environmental illness by disrupting processes in a variety of pathways such as the Nrf2 and contributes to a variety of patholgies including non-alcoholic liver disease. GSK-3b is a protein that can serve as an "on-off switch" for the antioxidant system. A new study shows that knock-down of this protein may provide cells with more resistance to some of the damaging effects of saturated fats in the diet.
Ibrahim, S. H. et al. Glycogen synthase kinase-3 (GSK-3) inhibition attenuates hepatocyte lipoapoptosis. Journal of hepatology (2010). URL http://dx.doi.org/10.1016/j.jhep.2010.09.039. http://www.citeulike.org/user/HEIRS/article/8365324
Explores the mental, physical, cellular and biochemical aspects of environmental illnesses such as obesity, diabetes, chronic fatigue syndrome, PTSD, fibromyalgia, chemical sensitivities, neurological disorders and numerous others. We advocate for better access to medical care, healthier lifestyles, resource conservation and the use of assistance animals for the disabled to promote a better quality of life.
Showing posts with label mitochondrial. Show all posts
Showing posts with label mitochondrial. Show all posts
Friday, December 17, 2010
Sunday, August 8, 2010
AKT/GSK-3beta/beta-catenin signalling within hippocampus and amygdala reflects genetically determined differences in posttraumatic stress disorder like symptoms.
"Taken together our study identifies lasting changes in the AKT/GSK-3beta/beta-catenin cascade within the hippocampus and amygdala as molecular correlates of genetically determined differences in the severity of PTSD-like symptoms."
CiteULike: AKT/GSK-3beta/beta-catenin signalling within hippocampus and amygdala reflects genetically determined differences in posttraumatic stress disorder like symptoms.:
Supplemental: Resveratrols, a compound found in wine and grapes exert their protective effects against neuronal damage and death are mediated throught this same pathway.
Fukui, M., Choi, H. J. J., and Zhu, B. T. T. (2010). Mechanism for the protective effect of resveratrol against oxidative stress-induced neuronal death. Free radical biology & medicine, 49(5):800-813. http://www.citeulike.org/user/HEIRS/article/7301406
Xi, J., Wang, H., Mueller, R. A., Norfleet, E. A., and Xu, Z. (2009). Mechanism for resveratrol-induced cardioprotection against reperfusion injury involves glycogen synthase kinase 3beta and mitochondrial permeability transition pore. European journal of pharmacology, 604(1-3):111-116. http://www.citeulike.org/user/HEIRS/article/7588469
CiteULike: AKT/GSK-3beta/beta-catenin signalling within hippocampus and amygdala reflects genetically determined differences in posttraumatic stress disorder like symptoms.:
Supplemental: Resveratrols, a compound found in wine and grapes exert their protective effects against neuronal damage and death are mediated throught this same pathway.
Fukui, M., Choi, H. J. J., and Zhu, B. T. T. (2010). Mechanism for the protective effect of resveratrol against oxidative stress-induced neuronal death. Free radical biology & medicine, 49(5):800-813. http://www.citeulike.org/user/HEIRS/article/7301406
Xi, J., Wang, H., Mueller, R. A., Norfleet, E. A., and Xu, Z. (2009). Mechanism for resveratrol-induced cardioprotection against reperfusion injury involves glycogen synthase kinase 3beta and mitochondrial permeability transition pore. European journal of pharmacology, 604(1-3):111-116. http://www.citeulike.org/user/HEIRS/article/7588469
Sunday, July 4, 2010
Thursday, June 10, 2010
Impaired redox signaling and antioxidant gene expression in endothelial cells in diabetes: a role for mitochondria and the Nrf2-Keap1 defense pathway.
"We hypothesize that diminished Nrf2/ARE activity contributes to increased oxidative stress and mitochondrial dysfunction in the vasculature leading to endothelial dysfunction, insulin resistance and abnormal angiogenesis observed in diabetes"
CiteULike: Impaired redox signaling and antioxidant gene expression in endothelial cells in diabetes: a role for mitochondria and the Nrf2-Keap1 defense pathway.:
Tuesday, December 29, 2009
CiteULike: Resveratrol Protects Mitochondria against Oxidative Stress through AMP-Activated Protein Kinase-Mediated Glycogen Synthase Kinase-3β Inhibition Downstream of Poly(ADP-ribose)polymerase-LKB1 Pathway
CiteULike: Resveratrol Protects Mitochondria against Oxidative Stress through AMP-Activated Protein Kinase-Mediated Glycogen Synthase Kinase-3β Inhibition Downstream of Poly(ADP-ribose)polymerase-LKB1 Pathway: "Shin, S. M., Cho, I. J., and Kim, S. G. (2009). Resveratrol protects mitochondria against oxidative stress through amp-activated protein kinase-mediated glycogen synthase kinase-3β inhibition downstream of poly(adp-ribose)polymerase-lkb1 pathway. Molecular Pharmacology, 76(4):884-895."
Saturday, December 26, 2009
Mitochondrial peroxiredoxin involvement in antioxidant defence and redox signalling
Summary: Prxs function as redox sensors that transmit signals as part of the cellular response to oxidative stress. In mammals, Prx 3 and Prx 5 are targeted to the mitochondrial matrix. Mitochondria are a major source of hydrogen peroxide, and this oxidant is implicated in the damage associated with aging and a number of pathologies
Cox, A. G., Winterbourn, C. C., and Hampton, M. B. (2010). Mitochondrial peroxiredoxin involvement in antioxidant defence and redox signalling. The Biochemical journal, 425(2):313-325. http://www.citeulike.org/user/HEIRS/article/6440040
Mitochondria and Free Radicals in Neurodegenerative Diseases
Cox, A. G., Winterbourn, C. C., and Hampton, M. B. (2010). Mitochondrial peroxiredoxin involvement in antioxidant defence and redox signalling. The Biochemical journal, 425(2):313-325. http://www.citeulike.org/user/HEIRS/article/6440040
Mitochondria and Free Radicals in Neurodegenerative Diseases
Friday, November 6, 2009
A key role for mitochondria in endothelial signaling by plasma cysteine/cystine redox potential.
Go, Y.-M. M., Park, H., Koval, M., Orr, M., Reed, M., Liang, Y., Smith, D., Pohl, J., and Jones, D. P. (2009). A key role for mitochondria in endothelial signaling by plasma cysteine/cystine redox potential. Free radical biology & medicine. http://www.citeulike.org/user/HEIRS/article/6076359
Tuesday, October 27, 2009
Hydrogen Sulfide Increases Glutathione Production and Suppresses Oxidative Stress in Mitochondria
Title: Hydrogen sulfide increases glutathione production and suppresses oxidative stress in mitochondria.
Summary: "H2S enhances GSH by enhancing cystine/cysteine transporters and redistributes GSH to mitochondria. H2S produced in mitochondria also may directly suppress oxidative stress. It provides a new mechanism of neuroprotection from oxidative stress by H2S."
Kimura, Y., Goto, Y.-I., and Kimura, H. (2009). Hydrogen sulfide increases glutathione production and suppresses oxidative stress in mitochondria. Antioxidants & Redox Signaling, pages 091026040507095+. http://www.citeulike.org/user/HEIRS/article/6015103
Summary: "H2S enhances GSH by enhancing cystine/cysteine transporters and redistributes GSH to mitochondria. H2S produced in mitochondria also may directly suppress oxidative stress. It provides a new mechanism of neuroprotection from oxidative stress by H2S."
Kimura, Y., Goto, Y.-I., and Kimura, H. (2009). Hydrogen sulfide increases glutathione production and suppresses oxidative stress in mitochondria. Antioxidants & Redox Signaling, pages 091026040507095+. http://www.citeulike.org/user/HEIRS/article/6015103
Thursday, October 15, 2009
Mitochondria has Role in Vitamin E Metabolism
Title: alpha-tocopherol beta-oxidation localized to rat liver mitochondria
Summary: "unexpected finding was that alpha-CEHC, the end product of alpha-tocopherol metabolism, was found almost exclusively in mitochondria. These data are the first to indicate a mitochondrial role in alpha-tocopherol metabolism."
Mustacich, D. J., Leonard, S. W., Patel, N. K., and Traber, M. G. (2009). alpha-tocopherol beta-oxidation localized to rat liver mitochondria. Free radical biology & medicine.http://www.citeulike.org/user/HEIRS/article/5931429
Summary: "unexpected finding was that alpha-CEHC, the end product of alpha-tocopherol metabolism, was found almost exclusively in mitochondria. These data are the first to indicate a mitochondrial role in alpha-tocopherol metabolism."
Mustacich, D. J., Leonard, S. W., Patel, N. K., and Traber, M. G. (2009). alpha-tocopherol beta-oxidation localized to rat liver mitochondria. Free radical biology & medicine.http://www.citeulike.org/user/HEIRS/article/5931429
Friday, October 9, 2009
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