Schumacher Justin D, Guo Grace L
Department of Pharmacology and Toxicology, School of Pharmacy, Rutgers University, 160 Frelinghuysen Road, Piscataway, NJ, 08854, USA.
Department of Pharmacology and Toxicology, School of Pharmacy, Rutgers University, 160 Frelinghuysen Road, Piscataway, NJ, 08854, USA.
Toxicol Appl Pharmacol. 2015 Nov 15;289(1):40-7. doi: 10.1016/j.taap.2015.08.022. Epub 2015 Sep 5.
Drug-induced steatohepatitis is a rare form of liver injury known to be caused by only a handful of compounds. These compounds stimulate the development of steatohepatitis through their toxicity to hepatocyte mitochondria; inhibition of beta-oxidation, mitochondrial respiration, and/or oxidative phosphorylation. Other mechanisms discussed include the disruption of phospholipid metabolism in lysosomes, prevention of lipid egress from hepatocytes, targeting mitochondrial DNA and topoisomerase, decreasing intestinal barrier function, activation of the adenosine pathway, increasing fatty acid synthesis, and sequestration of coenzyme A. It has been found that the majority of compounds that induce steatohepatitis have cationic amphiphilic structures; a lipophilic ring structure with a side chain containing a cationic secondary or tertiary amine. Within the last decade, the ability of many chemotherapeutics to cause steatohepatitis has become more evident coining the term chemotherapy-associated steatohepatitis (CASH). The mechanisms behind drug-induced steatohepatitis are discussed with a focus on cationic amphiphilic drugs and chemotherapeutic agents.
药物性脂肪性肝炎是一种罕见的肝损伤形式,已知仅由少数几种化合物引起。这些化合物通过对肝细胞线粒体的毒性、抑制β-氧化、线粒体呼吸和/或氧化磷酸化来刺激脂肪性肝炎的发展。讨论的其他机制包括溶酶体中磷脂代谢的破坏、阻止脂质从肝细胞流出、靶向线粒体DNA和拓扑异构酶、降低肠道屏障功能、激活腺苷途径、增加脂肪酸合成以及辅酶A的螯合。已发现大多数诱导脂肪性肝炎的化合物具有阳离子两亲性结构;一种具有含阳离子仲胺或叔胺侧链的亲脂性环状结构。在过去十年中,许多化疗药物导致脂肪性肝炎的能力变得更加明显,从而产生了化疗相关性脂肪性肝炎(CASH)这一术语。本文将重点讨论阳离子两亲性药物和化疗药物引起药物性脂肪性肝炎的机制。