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| 1 | Pyrrolizidine alkaloids-induced hepatic sinusoidal obstruction syndrome: Pathogenesis, clinical manifestations, diagnosis,treatment, and outcomes显示文摘Hepatic sinusoidal obstruction syndrome (HSOS) can be caused by the intake of pyrrolizidine alkaloids (PAs). To date, PAs-induced HSOS has not been extensively studied. In view of the difference in etiology of HSOS between the West and China, clinical profiles, imaging findings, treatment, and outcomes of HSOS associated with hematopoietic stem cell transplantation or oxaliplatin might be hardly extrapolated to PAs-induced HSOS. Reactive metabolites derived from PAs form pyrrole-protein adducts that result in toxic destruction of hepatic sinusoidal endothelial cells. PAs-induced HSOS typically manifests as painful hepatomegaly, ascites, and jaundice. Laboratory tests revealed abnormal liver function tests were observed in most of the patients with PAs-induced HSOS. In addition, contrast computed tomography and magnetic resonance imaging scan show that patients with PAs-induced HSOS have distinct imaging features, which reveal that radiological imaging provides an effective noninvasive method for the diagnosis of PAs-induced HSOS. Liver biopsy and histological examination showed that PAs-induced HSOS displayed distinct features in acute and chronic stages. Therapeutic strategies for PAs-induced HSOS include rigorous fluid management, anticoagulant therapy, glucocorticoids, transjugular intrahepatic portosystemic shunt, liver transplantation, etc. The aim of this review is to describe the pathogenesis, clinical profiles, diagnostic criteria, treatment, and outcomes of PAs-induced HSOS. | Xiao-Qian Yang Jin Ye Xin Li Qian Li Yu-Hu Song | 2019 | World Journal of Gastroenterology2019，25，28： | 29 |
| 2 | Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology显示文摘Acetaminophen(APAP)overdose is the most common cause of acute liver failure in the United States and mechanisms of liver injury induced by APAP overdose have been the focus of extensive investigation.Studies in the mouse model,which closely reproduces the human condition,have shown that hepatotoxicity is initiated by formation of a reactive metabolite N-acetyl-p-benzoquinone imine(NAPQI),which depletes cellular glutathione and forms protein adducts on mitochondrial proteins.This leads to mitochondrial oxidative and nitrosative stress,accompanied by activation of c-jun N-terminal kinase(JNK)and its translocation to the mitochondria.This then amplifies the mitochondrial oxidant stress,resulting in translocation of Bax and dynamin related protein 1(Drp1)to the mitochondria,which induces mitochondrial fission,and ultimately induction of the mitochondrial membrane permeability transition(MPT).The induction of MPT triggers release of intermembrane proteins such as apoptosis inducing factor(AIF)and endonuclease G into the cytosol and their translocation to the nucleus,causing nuclear DNA fragmentation and activation of regulated necrosis.Though these cascades of events were primarily identified in the mouse model,studies on human hepatocytes and analysis of circulating biomarkers from patients after APAP overdose,indicate that a number of mechanistic events are identical in mice and humans.Circulating biomarkers also seem to be useful in predicting the course of liver injury after APAP overdose in humans and hold promise for significant clinical use in the near future.Relevance for patients:This review focuses on the mechanisms behind APAP-induced hepatotoxicity and the relevance of these to the human pathophysiology.Current investigations on various biomarkers which may be useful in clinical management of APAP overdose patients are also discussed. | Anup Ramachandran Hartmut Jaeschke | 2017 | Journal of Clinical & Translational Research2017，3，1： | 6 |
| 3 | Recent progress in quantitative analysis of DNA adducts of nephrotoxin aristolochic acid显示文摘Aristolochic acid (AA), a mixture of structure-related nitrophenanthrene carboxylic acid derivatives derived from Aristolochia spp, is associated with nephrotoxin and carcinogen. AA-DNA adducts induced by reductive metabolic activation of AA were detected in tissues of animals and in patients exposed to AA. The DNA adducts were generally used as biomarkers in toxicological study of AA. In this short review, quantitative analysis of AA-DNA adducts in various in vitro and in vivo systems by using 32P-postlabelling assay, HPLC-UV, HPLC-radiation monitor, HPLC-FLD, HPLC-ESI/MS and UPLC-MS/MS methods is discussed. The distribution of AA-DNA adducts in various tissues is also summarized. | YUE Hao CHAN Wan YU KongJie GUO Lin LIU Ning LIU HuWei CAI ZongWei | 2009 | Science China Chemistry2009，52，10： | 2 |
| 4 | Active Oxygen Radical Scavenging Ability of Water-Soluble β-Alanine C_(60) Adducts显示文摘Water-soluble b-alanine C60 adducts were synthesized, and the scavenging ability to superoxygen anion radical O2- and hydroxyl radical.OH were studied by autoxidation of pyrogallol and chemiluminescence, respectively. It was found thatβ-alanine C60 adducts showed an excellent efficiency in eliminating superoxygen anion radical and hydroxyl radical. The 50% inhibition concentration (IC50) for superoxygen anion radical and hydroxyl radical were 0.15 mg/mL and 0.048 mg/mL, respectively. The difference should be mainly attributed to the different scavenging mechanisms. | Tao SUN, Zhi Shen JIA, Wei Xiang CHEN, Ya Xu JIN, Zhu De XU* Department of Chemistry, Zhejiang University, Hangzhou 310027 | 2001 | Chinese Chemical Letters2001，12，11： | 1 |
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