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吗啡介导的氧化应激恶化导致SIV/SHIV感染猕猴的疾病快速进展。

Morphine-mediated deterioration of oxidative stress leads to rapid disease progression in SIV/SHIV-infected macaques.

作者信息

Pérez-Casanova Antonio, Noel Richard J, Rivera-Amill Vanessa, Husain Kazim, Kumar Anil

机构信息

AIDS Research Program, Ponce School of Medicine, Ponce, PR 00732.

出版信息

AIDS Res Hum Retroviruses. 2007 Aug;23(8):1004-7. doi: 10.1089/aid.2006.0286.

Abstract

Oxidative stress is well documented in HIV infection, but the effect of concomitant substance abuse is largely unknown. We studied oxidative stress in our macaque model of morphine abuse and AIDS. In plasma, we found an approximately 50% decrease in catalase activity with morphine dependence that was exacerbated by infection in rapid progressors. Superoxide dismutase was decreased by a similar degree, but only in the presence of both morphine and viral infection. The loss of these antioxidant systems was coincident with significantly increased plasma malondialdehyde upon viral infection that displayed a synergistic increase in conjunction with morphine and rapid disease.

摘要

氧化应激在HIV感染中已有充分记录,但同时存在药物滥用的影响在很大程度上尚不清楚。我们在猕猴吗啡滥用和艾滋病模型中研究了氧化应激。在血浆中,我们发现随着吗啡依赖,过氧化氢酶活性大约降低了50%,在快速进展型感染者中这种降低因感染而加剧。超氧化物歧化酶也有类似程度的降低,但仅在同时存在吗啡和病毒感染的情况下。这些抗氧化系统的丧失与病毒感染后血浆丙二醛显著增加同时出现,丙二醛在与吗啡和快速疾病共同作用时呈现协同增加。

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