"Considerable evidence indicates a role for methionine sulfoxide reductase A (MsrA) in lens cell resistance to oxidative
stress through its maintenance of mitochondrial function.
Correspondingly, increased protein methionine sulfoxide (PMSO) is
associated with lens aging and human cataract formation, suggesting
that loss of MsrA activity is associated with this disease. Here we
tested the hypothesis that loss of MsrA protein repair is associated
with cataract formation. To test this hypothesis we examined the effect
of MsrA deletion on lens opacity in mice treated with hyperbaric oxygen, identified lens mitochondrial proteins oxidized upon deletion
of MsrA and determined the ability of MsrA to repair the identified
proteins."
They conclude that
"These results establish that MsrA deletion causes
increased light scattering in mice exposed to HBO [hyperbaric oxygen] and they identify cyt
c [cytochrome c] as oxidized in the knockout lenses. They also establish that MsrA can
restore the in vitro activity of cyt c through its repair of PMSO.
These results support the hypothesis that MsrA is important for the
maintenance of lens transparency and provide evidence that repair of
mitochondrial cyt c by MsrA could play an important role in defense of
the lens against cataract formation."
CBR member Frank Giblin collaborates with a team of researchers from the Florida Atlantic University to study cataract formation in the lens of the eye.
Created by Brad Roth (roth@oakland.edu) on Friday, July 3, 2009 Modified by Brad Roth (roth@oakland.edu) on Friday, July 3, 2009 Article Start Date: Friday, July 3, 2009