It was well established that the hepatotoxicity of APAP begins with the metabolic conversion of APAP to its reactive metabolite (N/-acetyl-p-benzoquinone imine, or NAPQI) ( CYP2E1 catalyzes the oxidation of APAP to NAPQI, a highly reactive metabolite inducing severe massive hepatocellular necrosis ( CYP2E1 knockout mice showed resistance to the APAP high dose-associated hepatotoxicity, suggesting that CYP2E1 is the major cytochrome P450 enzyme participating in APAP metabolism and toxicity ( CYP2E1 in APAP toxicity, CYP enzymes, notably CYP2E1 , generate ROS and lipid peroxidation ( As CYP2E1 is the major source of NAPQI, an evaluation of the CYP2E1 expression level was done in this study
How it works : Direct delivery to the bloodstream for nearly 100% absorption
So, proinflammatory and procoagulant proteins, including HMGB1, TNF?, ICAM1 and NFkB, disrupt the BBB and tight junction proteins, including ZO-1, occludin and claudin-5, are critical for the formation and maintenance of BBB integrity
Navaneetharaja N, Griffiths V, Wileman T, Carding SR
