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Neuroinflammation plays a potential role in the medulla oblongata after moderate traumatic brain injury in mice as revealed by nontargeted metabonomics analysis

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BSO might deplete cysteine in vivo even though the mechanism of BSO action (i.e., inhibition of -GCS) might lead one to predict that BSO would cause a transient accumulation of cysteine (Standeven and Wetterhahn, 1991)

This polymorphism is responsible for a rise in SOD enzymatic activity used for detoxifying superoxide anion radicals, thus the resultant phenotypes produce a greater number of toxic intermediates as well as hydrogen peroxide