To: keokalani'nui who wrote (684 ) 2/21/2002 12:04:30 PM From: tnsaf Read Replies (1) | Respond to of 717 Here is the abstract from the PNAS article. The text of the article indicates that the infected cells have a level of intracellular oxidative stress caused by the infection and that Gd-Tex increases this, causing infected cells to die. JasonProc. Natl. Acad. Sci. USA, Vol. 99, Issue 4, 2270-2274, February 19, 2002 Motexafin gadolinium (Gd-Tex) selectively induces apoptosis in HIV-1 infected CD4+ T helper cells (glutathione|redox modulation) Omar D. Perez*,,, Garry P. Nolan*,,, Darren Magda§, Richard A. Miller§, Leonard A. Herzenberg¶, and Leonore A. Herzenberg¶, * Department of Microbiology and Immunology, The Baxter Laboratories of Genetic Pharmacology, and Department of Molecular Pharmacology, Stanford University, Stanford, CA 94305-5175; § Pharmacyclics, Sunnyvale, CA 94085; and ¶ Department of Genetics, Stanford University, Stanford, CA 94305-5318 Contributed by Leonard A. Herzenberg, December 29, 2001 Here, we show that motexafin gadolinium (Gd-Tex), a compound that promotes intracellular oxidative stress, selectively induces apoptosis in HIV-1-infected CD4+ T cells in IL-2-stimulated cultures of peripheral blood mononuclear cells infected in vitro with HIV-1. This selective induction of apoptosis, which we detect by FACS analysis of intracellular HIV/p24 and concomitant surface and apoptosis marker expression, is abrogated by the glutathione precursor, N-acetyl-L-cysteine. Importantly, it occurs at Gd-Tex concentrations that are not cytotoxic to uninfected cells in the culture. These findings suggest that Gd-Tex may have therapeutic utility as an anti-HIV agent capable of selectively targeting and removing HIV-infected cells in an infected host. ------------------------------------------------------------ To whom reprint requests should be addressed. E-mail: lenherz@darwin.stanford.edu.