Wen Jian-Jun, Nagajyothi Fnu, Machado Fabiana S, Weiss Louis M, Scherer Philipp E, Tanowitz Herbert B, Garg Nisha Jain
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX, USA.
Parasitol Res. 2014 Sep;113(9):3159-65. doi: 10.1007/s00436-014-3977-7. Epub 2014 Jun 20.
The protozoan parasite Trypanosoma cruzi causes Chagas disease. Cardiac and adipose tissues are among the early targets of infection and are sites of persistent infection. In the heart and adipose tissue, T. cruzi infection results in an upregulation of pro-inflammatory mediators. In the heart, infection is associated with an increase in the markers of oxidative stress. To date, markers of oxidative stress have not been evaluated in adipose tissue in this infection. Brown and white adipose tissues were obtained from CD-1 mice infected with the Brazil strain of T. cruzi for 15, 30, and 130 days post infection. Protein carbonylation and lipid peroxidation assays were performed on these samples. There was an upregulation of these markers of oxidative stress at all time-points in both white and brown adipose tissue. Determinants of anti-oxidative stress were downregulated at similar time-points. This increase in oxidative stress during T. cruzi infection most likely has a deleterious effect on host metabolism and on the heart.
原生动物寄生虫克氏锥虫会引发恰加斯病。心脏组织和脂肪组织是早期感染靶点，也是持续性感染的部位。在心脏和脂肪组织中，克氏锥虫感染会导致促炎介质上调。在心脏中，感染与氧化应激标志物增加有关。迄今为止，尚未对这种感染情况下脂肪组织中的氧化应激标志物进行评估。从感染巴西株克氏锥虫15天、30天和130天的CD-1小鼠身上获取棕色和白色脂肪组织。对这些样本进行蛋白质羰基化和脂质过氧化检测。在白色和棕色脂肪组织的所有时间点，这些氧化应激标志物均上调。抗氧化应激的决定因素在相似时间点下调。克氏锥虫感染期间氧化应激的增加很可能对宿主代谢和心脏产生有害影响。
