Doleski Pedro H, Leal Daniela B R, Machado Vanessa S, Bottari Nathieli B, Casali Emerson A, Moritz Cesar E J, Camillo Giovana, Vogel Fernanda F, Stefani Lenita M, da Silva Aleksandro Schafer
Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (USFM), Brazil; Department of Biochemistry and Molecular Biology, Universidade Federal de Santa Maria (UFSM), Brazil.
Department of Microbiology and Parasitology, Universidade Federal de Santa Maria (USFM), Brazil.
Microb Pathog. 2017 Mar;104:180-183. doi: 10.1016/j.micpath.2017.01.022. Epub 2017 Jan 12.
The aim of this study was to evaluate the levels of purine nucleosides and xanthine oxidase (XO) activity in the liver of mice chronically infected by Toxoplasma gondii and treated with diphenyl diselenide (PhSe). For this experiment, forty Swiss mice were used. Twenty animals were orally infected by approximately 50 bradizoites of a cystogenic ME-49 strain of T. gondii, and the same number of uninfected mice was used as a control group. Ten infected and ten uninfected mice were subcutaneously treated twice (days 1 and 20 post-infection (PI)) with 5 μmol kg of (PhSe). On day 30 PI, liver samples were collected to measure the levels of hypoxanthine (HYPO), xanthine (XAN), uric acid (UA), and XO activity. Infected animals showed increased (P < 0.05) levels of hepatic XAN and UA, as well as XO activity compared to uninfected animals. The use of (PhSe) in healthy mice increased the levels of all nucleosides, but decreased XO activity compared to healthy untreated animals. The group of infected and treated animals showed increased XAN and UA levels, and XO activity compared to the healthy control group, however infected and treated mice showed a decrease in the XO activity compared to the infected untreated group. We conclude that chronic infection caused by T. gondii can induce hepatic changes, such as increased UA levels and XO activity, that can increase the pro-oxidative profile. The (PhSe) treatment of healthy animals altered the levels of nucleosides, possibly due to low XO activity that decreased nucleoside degradation. Finally, (PhSe) treatment decreased XO activity in the infected group and increased nucleoside levels; however it was unable to reduce the UA levels found during the infection.
本研究的目的是评估慢性感染刚地弓形虫并用二苯基二硒醚（PhSe）处理的小鼠肝脏中嘌呤核苷水平和黄嘌呤氧化酶（XO）活性。本实验使用了40只瑞士小鼠。20只动物经口感染约50个刚地弓形虫产囊ME-49株的缓殖子，相同数量的未感染小鼠作为对照组。10只感染小鼠和10只未感染小鼠在感染后第1天和第20天皮下注射两次5 μmol/kg的（PhSe）。在感染后第30天，采集肝脏样本以测量次黄嘌呤（HYPO）、黄嘌呤（XAN）、尿酸（UA）水平和XO活性。与未感染动物相比，感染动物的肝脏XAN和UA水平以及XO活性升高（P < 0.05）。与未处理的健康动物相比，在健康小鼠中使用（PhSe）可提高所有核苷水平，但降低XO活性。与健康对照组相比，感染并处理的动物组XAN和UA水平以及XO活性升高，然而与未处理的感染组相比，感染并处理的小鼠XO活性降低。我们得出结论，刚地弓形虫引起的慢性感染可诱导肝脏变化，如UA水平和XO活性升高，这可增加促氧化状态。对健康动物进行（PhSe）处理会改变核苷水平，可能是由于XO活性降低导致核苷降解减少。最后，（PhSe）处理降低了感染组的XO活性并提高了核苷水平；然而，它无法降低感染期间发现的UA水平。
