Background: Past studies have demonstrated that D3T a potent enzyme inducer has a positive effect on upregulating the Nrf2 antioxidant system. (Kwak)
Title: Cruciferous nutraceutical 3h-1,2-dithiole-3-thione protects human primary astrocytes against neurocytotoxicity elicited by mptp, mpp(+), 6-ohda, hne and acrolein.
Summary: This is one of the first studies that in "human astrocytes cruciferous nutraceutical D3T potently induces the cellular GSH system and the phase 2 enzyme NQO1, which is accompanied by dramatically increased resistance of these cells to the damage induced by various neurotoxicants. The results of this study may have important implications for the development of novel neuroprotective strategies.
Citation: Jia, Z., Zhu, H., Li, Y., and Misra, H. P. (2009). Cruciferous nutraceutical 3h-1,2-dithiole-3-thione protects human primary astrocytes against neurocytotoxicity elicited by mptp, mpp(+), 6-ohda, hne and acrolein. Neurochemical research, 34(11):1924-1934. http://www.citeulike.org/user/HEIRS/article/4483340
Other References: Kwak, M.-K., Itoh, K., Yamamoto, M., and Kensler, T. W. (2002). Enhanced expression of the transcription factor nrf2 by cancer chemopreventive agents: Role of antioxidant response element-like sequences in the nrf2 promoter. Mol. Cell. Biol., 22(9):2883-2892. http://www.citeulike.org/user/HEIRS/article/883878
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 neurotoxins. Show all posts
Showing posts with label neurotoxins. Show all posts
Monday, October 12, 2009
Sunday, October 11, 2009
HIF-1 May Provide Protection in Parkinson's and Metal-Induced Oxidative Stress Disorders
Title: Inhibition of prolyl hydroxylase protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity.
Summary: "protection against MPTP neurotoxicity may be mediated by alterations in iron homeostasis and defense against oxidative stress and mitochondrial dysfunction brought about by cellular HIF-1α induction. This study provides novel data extending the possible therapeutic utility of HIF induction to a Parkinson disease model of neurodegeneration, which may prove beneficial not only in this disorder itself but also in other diseases associated with metal-induced oxidative stress."
Lee, D. W., Rajagopalan, S., Siddiq, A., Gwiazda, R., Yang, L., Beal, M. F., Ratan, R. R., and Andersen, J. K. (2009). Inhibition of prolyl hydroxylase protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity. Journal of Biological Chemistry, 284(42):29065-29076.
Summary: "protection against MPTP neurotoxicity may be mediated by alterations in iron homeostasis and defense against oxidative stress and mitochondrial dysfunction brought about by cellular HIF-1α induction. This study provides novel data extending the possible therapeutic utility of HIF induction to a Parkinson disease model of neurodegeneration, which may prove beneficial not only in this disorder itself but also in other diseases associated with metal-induced oxidative stress."
Lee, D. W., Rajagopalan, S., Siddiq, A., Gwiazda, R., Yang, L., Beal, M. F., Ratan, R. R., and Andersen, J. K. (2009). Inhibition of prolyl hydroxylase protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity. Journal of Biological Chemistry, 284(42):29065-29076.
Monday, September 21, 2009
Mitochondria in neurodegenerative disorders: regulation of the redox state and death signaling leading to neuronal death and survival. Journal of Neural Transmission
......"recent findings on new functions of mitochondria in regulation of their redox state and function through reversible “S-glutathionylation”, a mixed disulfide binding between sulfhydryl groups of GSH and protein cysteine in complex I subunits. Type A monoamine oxidase (MAO-A) localized at the mitochondrial outer membrane is a binding site of neurotoxins leading to apoptosis.
Naoi, M., Maruyama, W., Yi, H., Inaba, K., Akao, Y., and Shamoto-Nagai, M. Mitochondria in neurodegenerative disorders: regulation of the redox state and death signaling leading to neuronal death and survival. Journal of Neural Transmission.http://www.citeulike.org/user/HEIRS/article/5812429
Naoi, M., Maruyama, W., Yi, H., Inaba, K., Akao, Y., and Shamoto-Nagai, M. Mitochondria in neurodegenerative disorders: regulation of the redox state and death signaling leading to neuronal death and survival. Journal of Neural Transmission.http://www.citeulike.org/user/HEIRS/article/5812429
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