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Thus, the presence of the basic residue seems to be a necessary but not a sufficient condition for GSH activation
While the above studies demonstrate that elevated intracellular zinc levels during ischemia serve as a critical mediator of neuronal death, zinc inhibition achieved through either early or late chelation paradigms may be effective in combating zinc neurotoxicity
LC-MS/MS data showed significant changes in ceramide profiles in NASH and HCC
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