Vascular endothelial toxicity induced by HIV protease inhibitor View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2004-06

AUTHORS

Reshma S. Baliga, Cynthia Liu, Dale G. Hoyt, Alysia A. Chaves, John A. Bauer

ABSTRACT

HIV-protease inhibitor (HIV-PI) drugs are critical for highly active antiretroviral therapy (HAART) efficacy, but several recent reports have suggested that metabolic and/or cardiovascular toxicities are associated with these drugs. Given the importance of the HIV-PI drug class and the widespread and chronic use of these agents in an expanding patient population, further understanding of this potential drug toxicity is imperative. Here, we investigated a role for direct endothelial toxicity induced by saquinavir (SAQ), the first HIV-PI drug marketed in the United States and still an important component of HAART therapies. In initial studies using isolated vascular tissues, we observed selective impairment of endothelium-dependent vasodilation with no effect on contractile responses. Subsequent studies using human endothelial cells in culture at clinically relevant concentrations (5 and 10 μM, 2–48 h), demonstrated concentration-dependent increases in cell death, mainly via apoptosis rather than necrosis (determined via Annexin-V positive membrane labeling). Live cell imaging also demonstrated increased intracellular oxidant production (as measured by DCF fluorescence), which could be abrogated by incubation with the antioxidant N-acetylcysteine (NAC). NAC also prevented SAQ-induced apoptotic cell death. These data demonstrate, that SAQ has direct toxicological effects on endothelial cells, and that the toxicity apparently involves apoptotic pathway activation via reactive oxygen and/or nitrogen species. More... »

PAGES

199-206

References to SciGraph publications

  • 2003-06. Saquinavir in DRUGS
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1385/ct:4:2:199

    DOI

    http://dx.doi.org/10.1385/ct:4:2:199

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1000109223

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/15371635


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