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The H-subunit has ferroxidase activity, converting Fe 2+ to Fe 3+ , while the L-subunit stabilizes the complex of subunits to remain in iron storage form

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Treatment with a thiol ester compound (gamma-glutamylcysteinyl ethyl esther) or exogenous GSH while examining cellular models of diminished GSH levels in concert with Complex I inhibitors MPP + , MPTP, or DHBT-1, restores mitochondrial Complex I activity, inhibits cell loss and protects against cell and striatal DA loss [73, 75, 82]