Experimental protocols.

<p>Experimental protocols.</p

Activity of cytosolic aconitase.

<p>Activity of cytosolic aconitase.</p

The Methionine-Centered Redox Cycle.

<p>The formation of methionine sulfoxide (MetO) can result from the oxidation of free methionine, or a methionyl residue of a protein. Additional oxidation will generate methionine sulfone (MetO₂), a product that is almost irreversible in biological systems, and can cause protein denaturation. MetO can be reduced by methionine sulfoxide reductases (MsrA or MsrB isoform), through thioredoxin (Trx). Thioredoxin reductase (TrxR) regenerates the oxidized Trx (Trx_ox) via critical components of the cellular redox system, NADP/NADP(H) [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0159951#pone.0159951.ref032" target="_blank">32</a>].</p

Infarct sizes of the rat hearts after exposure to the different experimental protocols.

<p>Data are presented as Mean ± SEM.* p < 0.05 versus I/R.</p

Activities of methionine sulfoxide reductase.

<p>Activities of methionine sulfoxide reductase.</p

Hemodynamic parameters of the rat hearts after exposure to the different experimental protocols.

<p>Hemodynamic parameters of the rat hearts after exposure to the different experimental protocols.</p

Ferritin and iron content at various times of the perfusion protocol.

<p>Ferritin and iron content at various times of the perfusion protocol.</p

Thioredoxin and thioredoxin-reductase protein levels.

<p>Thioredoxin and thioredoxin-reductase protein levels.</p