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10.1161/HC0902.104710 63 FedorovaO

3, May 2018, pp

A fourth factor must now be built into the equation, namely, gene mutations that might favour the cytoplasmic presence of trypsin (97): the enzyme, as also chymotrysin, is readily inhibited by GSH via SH-SS exchange (24) should it break loose of constraint by SPINK1 (serine protease inhibitor Kazal type 1) (118), but less GSH is then available for control of electrophilic / oxidative stress and other vital roles (24, 30, 162)

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