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首页> 外文期刊>Microbial Pathogenesis >Changes in cardiac and hepatic energetic metabolism in gerbils infected by Listeria monocytogenes
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Changes in cardiac and hepatic energetic metabolism in gerbils infected by Listeria monocytogenes

机译：李斯巴尼尔李斯特里亚单核细胞增生感染的红霉和肝脏能量代谢的变化

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摘要

Energy metabolism is a sensitive indicator of cellular disorders. Therefore, the objective of this study was to investigate changes in cardiac and hepatic energy metabolism during listeriosis using an experimental model. We divided gerbils into two groups: Control (n = 11) and orally Infected (n = 12) with 5 x 10(9) CFU/mL of Listeria monocytogenes. Euthanasia and sampling were performed on days 6 and 12 post-infection (PI). Histopathological lesions were not found in the heart; however, the liver showed pyogranuloma. In the hearts of infected animals, cytosolic creatine kinase activity was lower on day 6 and 12 PI; mitochondrial creatine kinase/pyruvate kinase (PK), and sodium potassium pump (Na+/K+-ATPase) activities were lower on day 12 PI. Hepatic PK and Na+/K+-ATPase activities were lower in the infected group on day 12 PI. Lipoperoxidation was higher in the livers and hearts of infected animals on day 12 PI, and antioxidant capacity against peroxyl radicals (ACAP) was also higher in this group. These data suggest that subclinical listeriosis alters hepatic and cardiac energy metabolism, possibly related to decreased activity of phosphotransferases and ATPase. Subsequent antioxidant responses are not sufficient to correct alterations in lipid peroxidation and bioenergetics, possibly leading to important cellular pathological mechanisms.
机译：能量代谢是细胞障碍的敏感指标。因此，本研究的目的是使用实验模型在休闲症期间研究心肌和肝能代谢的变化。我们将Gerbils分为两组：控制（n = 11）和口服感染（n = 12），其中5×10（9）cfu / ml histeria单核细胞增生。 Euthanasia和抽样在感染后的第6天和第12天进行（PI）进行。心脏未发现组织病理病变;然而，肝脏显示出脓肾炎。在感染动物的心中，在第6天和第12天的胞质肌酸激酶活性较低;线粒体肌酸激酶/丙酮酸激酶（PK）和钾泵（Na + / K + -AtPase）活性在第12天PI较低。在第12天PI时，感染的组肝脏PK和Na + / K + -AtPase活性较低。在第12天PI时感染动物的肝脏和心脏的肝脏和心脏较高，并且在该组中对抗氧化剂（ACAP）的抗氧化能力也更高。这些数据表明，亚临床局部病变改变了肝癌和心脏能量代谢，可能与磷酸转移酶和ATP酶的活性降低。随后的抗氧化反应不足以校正脂质过氧化和生物能器的改变，可能导致重要的细胞病理机制。

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