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An intronic variation in SLC52A1 causes exon skipping and transient riboflavin-responsive multiple acyl-CoA dehydrogenation deficiency

IL-10 deficiency exacerbates the brain inflammatory response to permanent ischemia without preventing resolution of the lesion

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J Pregnancy 2012:586578

8 The mechanisms of APAP-induced cell death, which apply to both animals and humans, include the formation of the reactive metabolite N-acetyl-p-benzoquinone imine (NAPQI) by cytochrome P450 2E1 (Cyp2E1), depletion of hepatic GSH, and protein adduct formation, primarily in mitochondria
