Model
Digital Document
Publisher
Florida Atlantic University
Description
The excess generation of Reactive oxygen species (ROS) can damage
cell components and disrupt cellular functions. Methionine in proteins is easily
oxidized by ROS and converted to methionine sulfoxide. The enzyme peptide
Methionine Sulfoxide Reductase reduces methionine sulfoxide back to methionine.
We report here that MsrA over expression in rat cardiac myocytes prevents damage
from ROS and increases cell viability after hypoxic/reoxygenation events. The nonsteroidal
anti-inflamatory drug (NSAID) sulindac contains a methyl sulfoxide moiety
that can scavenge ROS. Sulindac can be reduced by MsrA and contribute as an
antioxidant in the cell. Our results demonstrate that 1 OOuM sulindac can reduce cell
death in rat cardiac myocytes during hypoxia/reoxygenation, and
ischemia/reperfusion in Langendorf[ perfusions. The BNIP proteins are pro-apoptotic
members of the Bcl-2 family of apoptosis regulating proteins. Hypoxia/acidosis
stabilizes BNIP-3 and increases its association with the mitochondria, causing the
release of cytochrome C and cell death. We report the retrograde perfusion
Langendorffmodel is inconclusive in mouse hearts.
cell components and disrupt cellular functions. Methionine in proteins is easily
oxidized by ROS and converted to methionine sulfoxide. The enzyme peptide
Methionine Sulfoxide Reductase reduces methionine sulfoxide back to methionine.
We report here that MsrA over expression in rat cardiac myocytes prevents damage
from ROS and increases cell viability after hypoxic/reoxygenation events. The nonsteroidal
anti-inflamatory drug (NSAID) sulindac contains a methyl sulfoxide moiety
that can scavenge ROS. Sulindac can be reduced by MsrA and contribute as an
antioxidant in the cell. Our results demonstrate that 1 OOuM sulindac can reduce cell
death in rat cardiac myocytes during hypoxia/reoxygenation, and
ischemia/reperfusion in Langendorf[ perfusions. The BNIP proteins are pro-apoptotic
members of the Bcl-2 family of apoptosis regulating proteins. Hypoxia/acidosis
stabilizes BNIP-3 and increases its association with the mitochondria, causing the
release of cytochrome C and cell death. We report the retrograde perfusion
Langendorffmodel is inconclusive in mouse hearts.
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