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Ivanova, S. et al.

Ivanova, Batliwalla, Mocco, Kiss, Huang, Mack, Coon, Eaton, Al-Abed, Gregersen, Shohami, Connolly, Tracey,

Neuroprotection in cerebral ischemia by neutralization of 3-aminopropanal.

Cerebral ischemia stimulates increased activity of polyamine oxidase, a ubiquitous enzyme that catabolizes polyamines to produce 3-aminopropanal. 3-Aminopropanal is a reactive aldehyde that mediates progressive neuronal necrosis and glial apoptosis. Here we report that increased levels of 3-aminopropanal-modified protein levels in humans after aneurysmal subarachnoid hemorrhage correlate with the degree of cerebral injury as measured by admission Hunt/Hess grade. In vitro screening of clinically approved drugs reveals that N-2-mercaptopropionyl glycine (N-2-MPG), an agent clinically approved for prevention of renal stones in patients with cysteinuria, significantly inhibits the cytotoxicity of 3-aminopropanal. N-2-MPG reacts with 3-aminopropanal to yield a nontoxic thioacetal adduct, as confirmed by electrospray ionization mass spectroscopy. Administration of N-2-MPG in clinically relevant doses to rats significantly reduces cerebral 3-aminopropanal-modified protein immunoreactivity and infarct volume in a standardized model of middle cerebral artery occlusion, even when the agent is administered after the onset of ischemia. These results implicate 3-aminopropanal as a therapeutic target for cerebral ischemia.[1]

References

Neuroprotection in cerebral ischemia by neutralization of 3-aminopropanal. Ivanova, S., Batliwalla, F., Mocco, J., Kiss, S., Huang, J., Mack, W., Coon, A., Eaton, J.W., Al-Abed, Y., Gregersen, P.K., Shohami, E., Connolly, E.S., Tracey, K.J. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]

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