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Many factors are presumably involved (Boogard et al., 1989), including relative distribution of N -acetyltransferase and aminoacylases, cellular and mitochondrial uptake mechanisms, susceptibility to inactivation of cysteine S -conjugate β-lyases and nearby enzymes/macromolecules, relative K m values, competition from natural amino acid substrates, absolute level of the enzyme, the presence of the enzyme in mitochondria, and the presence of α-keto substrate to keep the enzyme enzymatically active (if the lyase in question is an aminotransferase)

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3) restoration of mtNOS activity and H 2 S level that contributes to the regulation of CsA-sensitive mPTP opening and mitochondrial Ca 2+ homeostasis