Previous Presentations
| arnox.scc.2.25.09.pdf |
Dale Kern
Dale's Presentation abstract:
arNOX: An Anti-aging Target
The ECTO-NOX (external NADH oxidase) or ENOX proteins are cell-surface located, terminal oxidases involved in the plasma membrane redox(PMRS) system. Aging leads to the accumulation of mitochondrial DNA lesions and a shift toward energy production via glycolysis resulting in a hyperactive PMRS system. ENOX 1 and ENOX 2 carry out four electron transfers to molecular oxygen to form water. arNOX (ENOX3) is unique in that it generates superoxide at the cell surface and its activity is elevated in individuals 50 – 70 years of age compared to those 20-40 years of age. The superoxide generated can then form H2O2 and other reactive oxygen species (ROS) capable of damaging adjacent cells, circulating lipoprotein and components of the skin’s extracellular matrix (ECM). Anti-oxidants, arNOX enzyme inhibitors and regulation of the ENOX3 gene promise to be viable interventions in aging.
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arNOX: An Anti-aging Target
The ECTO-NOX (external NADH oxidase) or ENOX proteins are cell-surface located, terminal oxidases involved in the plasma membrane redox(PMRS) system. Aging leads to the accumulation of mitochondrial DNA lesions and a shift toward energy production via glycolysis resulting in a hyperactive PMRS system. ENOX 1 and ENOX 2 carry out four electron transfers to molecular oxygen to form water. arNOX (ENOX3) is unique in that it generates superoxide at the cell surface and its activity is elevated in individuals 50 – 70 years of age compared to those 20-40 years of age. The superoxide generated can then form H2O2 and other reactive oxygen species (ROS) capable of damaging adjacent cells, circulating lipoprotein and components of the skin’s extracellular matrix (ECM). Anti-oxidants, arNOX enzyme inhibitors and regulation of the ENOX3 gene promise to be viable interventions in aging.
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| revolutionary_uvb_protection_-_imwscc_2010.pdf |
Kristen Presti
Kristen's Presentation Abstract:
New findings in the causes and prevention of UVB-induced photodamage of human skin.
Long term skin damage has traditionally been linked to either direct interaction of UV radiation with DNA or to the generation of reactive oxygen species which interact with the structural proteins of the skin. Recent research has shown that another mechanism may account for up to 50% of UVB radiation-induced long term skin damage. This involves a UV photoproduct of the amino acid tryptophan binding to the Arylhydrocarbon Receptor (AhR) in the cytoplasm, which triggers the downstream release of Cytochrome-P1A1, Cyclooxygenase-2, MMP-1, enzymes, etc., which are responsible for long term skin damage ranging from skin cancer to photoaging.
This paper presents a strategy for the use of materials which reversibly block the AhR from interacting with the tryptophan photoproduct, thereby preventing long term photodamage to the skin. Both in-vitro and in-vivo data on the efficacy of such a strategy will be presented.
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New findings in the causes and prevention of UVB-induced photodamage of human skin.
Long term skin damage has traditionally been linked to either direct interaction of UV radiation with DNA or to the generation of reactive oxygen species which interact with the structural proteins of the skin. Recent research has shown that another mechanism may account for up to 50% of UVB radiation-induced long term skin damage. This involves a UV photoproduct of the amino acid tryptophan binding to the Arylhydrocarbon Receptor (AhR) in the cytoplasm, which triggers the downstream release of Cytochrome-P1A1, Cyclooxygenase-2, MMP-1, enzymes, etc., which are responsible for long term skin damage ranging from skin cancer to photoaging.
This paper presents a strategy for the use of materials which reversibly block the AhR from interacting with the tryptophan photoproduct, thereby preventing long term photodamage to the skin. Both in-vitro and in-vivo data on the efficacy of such a strategy will be presented.
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