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HIV Protease Inhibitor Ritonavir Induces Cytotoxicity of Human Endothelial Cells
Zhong et al., Arteriosclerosis, Thrombosis, and Vascular Biology, doi:10.1161/01.atv.0000034707.40046.02 (In Vitro)
Zhong et al., HIV Protease Inhibitor Ritonavir Induces Cytotoxicity of Human Endothelial Cells, Arteriosclerosis, Thrombosis, and Vascular Biology, doi:10.1161/01.atv.0000034707.40046.02 (In Vitro)
Aug 2002   Source   PDF  
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In Vitro study showing that ritonavir (part of paxlovid) can cause endothelial mitochondrial DNA damage and cell death at concentrations near clinical plasma levels.
Zhong et al., 22 Aug 2002, peer-reviewed, 7 authors.
In Vitro studies are an important part of preclinical research, however results may be very different in vivo.
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Abstract: Vascular Biology HIV Protease Inhibitor Ritonavir Induces Cytotoxicity of Human Endothelial Cells Dian-sheng Zhong, Xiang-huai Lu, Brian S. Conklin, Peter H. Lin, Alan B. Lumsden, Qizhi Yao, Changyi Chen Objective—Although HIV protease inhibitors have been successfully used against HIV infection, many metabolic side effects and premature cardiovascular diseases are often associated with this therapy. The mechanisms of these complications are not clear. In this study, we investigated the effect of the HIV protease inhibitor ritonavir on human endothelial cell cultures. Methods and Results—By using nonradioactive cell proliferation and cytotoxicity assays, human endothelial cells treated with ritonavir showed a significant decrease in cell viability and an increase in cytotoxicity in a time- and dose-dependent fashion. Mitochondrial DNA was also substantially damaged with ritonavir treatment by long polymerase chain reaction analysis. In contrast, ritonavir had a very limited effect on endothelial apoptosis, as assessed by analyses of DNA fragmentation and cellular caspase-3 activity. Conclusions—These data demonstrate, for the first time, that the HIV protease inhibitor ritonavir at concentrations near clinical plasma levels is able to directly cause endothelial mitochondrial DNA damage and cell death mainly through necrosis pathways but not through apoptosis. This study suggests that HIV protease inhibitor–mediated endothelial injury may contribute to its cardiovascular complications. (Arterioscler Thromb Vasc Biol. 2002;22:1560-1566.) Key Words: HIV protease inhibitor 䡲 ritonavir 䡲 cytotoxicity 䡲 endothelial cells 䡲 cardiovascular disease H hypothesized that HIV protease inhibitors could cause endothelial injury or dysfunction by either direct cytotoxic effect or indirect effect of protease inhibitor–related metabolic changes on endothelial cell growth and function. In the present study, we investigated the effects of ritonavir, one of the HIV protease inhibitors, on cell viability, cytotoxicity, mitochondrial DNA damage, and apoptosis in human endothelial cell cultures. The present study may provide insight into the understanding of cardiovascular complications associated with the use of HIV protease inhibitors. uman immunodeficiency virus protease is an important virally encoded enzyme that cleaves the gag and gagpol protein precursors to produce mature and infectious virus particles. Thus, HIV protease has been the target of antiviral therapy. HIV protease inhibitors were introduced in 1995 for the treatment of HIV-infected patients. HIV protease inhibitors, including saquinavir, ritonavir, indinavir, nelfinavir, and amprenavir, rapidly and profoundly reduce the viral load, as indicated by a decline in plasma HIV RNA concentrations within a few days after the start of treatment.1,2 Reductions in the viral load are paralleled by mean increases in the CD4⫹ count of 100 to 150 cells/mm3.3,4 However, HIV protease inhibitors are often associated with a number of metabolic side effects and cardiovascular complications. The major concern raised by protease inhibitor–associated elevation in plasma levels of cholesterol and triglycerides relates to the risk of premature development of atherosclerosis.5–7 Indeed, rapidly evolving plaques may be particularly unstable and thus prone to rupture, generating an acute coronary event in HIV protease inhibitor–treated patients.8..
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