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This oxidative damage severely impairs the mitochondria's ability to produce adenosine triphosphate (ATP), the currency of cellular energy

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Brown PL et al

Proposed Mechanisms Preventing GABA receptor downregulation Counteracting compensatory NMDA glutamate receptor sensitization Stabilizing benzodiazepine receptor configuration (preventing shift to inverse agonist state) Upregulating GABAergic neurotransmission through pathways distinct from benzodiazepine action itself This tolerance prevention has profound clinical implications

Hydrogen donor system for Escherichia coli ribonucleoside-diphosphate reductase dependent upon glutathione