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Among the proposed mechanisms for these effects, the reduction of toxic metabolites from fatty acids, especially LCAC under ischemic conditions, increased glucose oxidation during reperfusion, and consequently the reduction of lactate and H+ ion accumulation, resulting in the inhibition of acidosis in myocardial cells during ischemia, as well as the inhibition of harmful effects of free radicals released during reperfusion, are more prominently noted

R., Pelegrini P

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23 Similar to other hepatotoxicants, APAP-induced liver injury is followed by compensatory liver regeneration, where the hepatocytes in closest proximity to the necrotic zones divide and replace dead cells

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Persistent increase in plasma and urinary leukotrienes after acute asthma