期刊文献+

Blood F_2-isoprostanes are significantly associated with abnormalities of lipid status in rats with steatosis

Blood F_2-isoprostanes are significantly associated with abnormalities of lipid status in rats with steatosis
下载PDF
导出
摘要 AIM: To investigate oxidative stress and lipid peroxi-dation in hepatic steatosis and the underlying implica-tions in pathological mechanisms of non-alcoholic fatty liver disease (NAFLD). METHODS: F_2-isoprostanes (iPF2α-) in blood and liver samples from steatotic (n = 9) and control (n = 7) rats were measured as in vivo marker of lipid peroxida-tion by a mass spectrometric approach. The lipid pro-fi le and endogenous antioxidant status (SOD and CAT) in the rats were also analyzed. RESULTS: Signifi cantly higher levels of iPF2α-(mean 3.47 vs 2.40 pmol/mg tissue, P = 0.004) and lower activities of SOD (mean 1.26 U vs 1.40 U, P < 0.001) and CAT (mean 1026.36 U/mg vs 1149.68 U/mg pro-tein, without signifi cance) were observed in the livers of steatotic rats. Plasma total iPF2α-was signifi cantly correlated with the abnormalities of blood lipids as well as alanine aminotransferase (ALT) levels in the rats with simple steatosis, whereas no similar tendencies were observed in the control rats. CONCLUSION: Enhancement of hepatic oxidative imbalance occurring at the steatotic stage of NAFLD suggests a possibility that manifestation of the local ⅢⅢⅢoxidative damage precedes that of systemic oxidative imbalance. Predominant metabolic features of the in-creased lipid peroxidation further suggest a close asso-ciation of the oxidative imbalance and the dyslipidemia with functional deterioration of the steatotic liver. The fi ndings need to be further evaluated, especially in hu-man studies. AIM: To investigate oxidative stress and lipid peroxi-dation in hepatic steatosis and the underlying implica-tions in pathological mechanisms of non-alcoholic fatty liver disease (NAFLD). METHODS: F2-isoprostanes (iPF2α-) in blood and liver samples from steatotic (n = 9) and control (n = 7) rats were measured as in vivo marker of lipid peroxida-tion by a mass spectrometric approach. The lipid pro-fi le and endogenous antioxidant status (SOD and CAT) in the rats were also analyzed. RESULTS: Signifi cantly higher levels of iPF2α-(mean 3.47 vs 2.40 pmol/mg tissue, P = 0.004) and lower activities of SOD (mean 1.26 U vs 1.40 U, P 〈 0.001) and CAT (mean 1026.36 U/mg vs 1149.68 U/mg pro-tein, without signifi cance) were observed in the livers of steatotic rats. Plasma total iPF2α-was signifi cantly correlated with the abnormalities of blood lipids as well as alanine aminotransferase (ALT) levels in the rats with simple steatosis, whereas no similar tendencies were observed in the control rats. CONCLUSION: Enhancement of hepatic oxidative imbalance occurring at the steatotic stage of NAFLD suggests a possibility that manifestation of the local ⅢⅢⅢoxidative damage precedes that of systemic oxidative imbalance. Predominant metabolic features of the in-creased lipid peroxidation further suggest a close asso-ciation of the oxidative imbalance and the dyslipidemia with functional deterioration of the steatotic liver. The fi ndings need to be further evaluated, especially in hu-man studies.
出处 《World Journal of Gastroenterology》 SCIE CAS CSCD 2008年第29期4677-4683,共7页 世界胃肠病学杂志(英文版)
基金 the Science and Technology Commission of Shanghai Municipality, No. 05PJ14044 No. 06DZ19002
关键词 ISOPROSTANES Oxidative stress Lipid per-oxidation STEATOSIS Non-alcoholic fatty liver disease 氧化压 脂肪变性 非酒精性脂肪肝 治疗方法
  • 相关文献

参考文献31

  • 1[1]Angulo P.Nonalcoholic fatty liver disease.N Engl J Ivied 2002; 346:1221-1231
  • 2[2]Day CP,James OF.Steatohepatitis:a tale of two "hits"? Gastroenterology 1998; 114:842-845
  • 3[3]Berson A,De Beco V,Letteron P,Robin MA,Moreau C,El Kahwaji J,Verthier N,Feldmann G,Fromenty B,Pessayre D.Steatohepatitis-inducing drugs cause mitochondrial dysfunction and lipid peroxidation in rat hepatocytes.Gastroenterology 1998; 114:764-774
  • 4[4]Kaplowitz N.Mechanisms of liver cell injury.J Hepatol 2000; 32:39-47
  • 5[5]Ramadori G,Armbrust T.Cytokines in the liver.Eur J Gastroenterol Hepatol 2001; 13:777-784
  • 6[6]McClain CJ,Mokshagundam SP,Barve SS,Song Z,Hill DB,Chen T,Deaciuc I.Mechanisms of non-alcoholic steatohepatitis.Alcohol 2004; 34:67-79
  • 7[7]Bugianesi E,McCullough AJ,Marchesini G.Insulin resistance:a metabolic pathway to chronic liver disease.Hepatology 2005; 42:987-1000
  • 8[8]Cortez-Pinto H,de Moura MC,Day CP.Non-alcoholic steatohepatitis:from cell biology to clinical practice.J Hepatol 2006; 44:197-208
  • 9[9]Letteron P,Fromenty B,Terris B,Degott C,Pessayre D.Acute and chronic hepatic steatosis lead to in vivo lipid peroxidation in mice.J Hepatol 1996; 24:200-208
  • 10[10]Oliveira CP,da Costa Gayotto LC,Tatai C,Della Bina BI,Janiszewski M,Lima ES,Abdalla DS,Lopasso FP,Laurindo FR,Laudanna AA.Oxidative stress in the pathogenesis of nonalcoholic fatty liver disease,in rats fed with a choline-deficient diet.J Cell Mol Med 2002; 6:399-406

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部