This investigation was conducted to validate the use of dimethyl sulfoxide (DMSO) as a quantitative molecular probe for the generation of hydroxyl radicals (HO) in aqueous systems. Reaction of HO with DMSO produces methane sulfinic acid as a primary product, which can be detected by a simple calorimetric assay. To evaluate this method for estimating total HO production, we studied three model systems, including the Fenton reaction,  irradiation of water, and ultraviolet photolysis of hydrogen peroxide, for which the theoretical maximum yield of HO could be calculated and compared to measured DMSO oxidation. The results confirm that 0.05 to 1 M DMSO may be used to capture nearly all of the expected HO radicals formed. Thus, methane sulfinic acid production from DMSO holds promise as an easily measured marker for HO formation in aqueous systems pretreated with DMSO.

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Progressive loss of CD4 ؉ T lymphocytes, accompanied by opportunistic infections characteristic of the acquired immune deficiency syndrome, has been reported in the absence of any known etiology. The pathogenesis of this syndrome, a subset of idiopathic CD4 ؉ T lymphocytopenia (ICL), is uncertain. We report that CD4 ؉ T cells from seven of eight ICL patients underwent accelerated programmed cell death, a process facilitated by T cell receptor cross-linking. Apoptosis was associated with enhanced expression of Fas and Fas ligand in unstimulated cell populations, and partially inhibited by soluble anti-Fas mAb. In addition, apoptosis was suppressed by aurintricarboxylic acid, an inhibitor of calcium-dependent endonucleases and proteases, in cells from four of seven patients. The in vivo significance of these findings was supported by three factors: the absence of accelerated apoptosis in persons with stable, physiologic CD4 lymphopenia without clinical immune deficiency; detection of serum antihistone H2B autoantibodies, one consequence of DNA fragmentation, in some patients; and its selectivity, with apoptosis limited to the CD4 population in some, and occurring among CD8 ϩ T cells predominantly in those individuals with marked depletion of both CD4 ؉ and CD8 ؉ peripheral T lymphocyte subsets. These data suggest that patients with idiopathic loss of CD4 ؉ T lymphocytes linked to clinical immune suppression have evidence for accelerated T cell apoptosis in vitro that may be pathophysiologic and amenable to therapy with apoptosis inhibitors. ( J. Clin. Invest. 1996. 97:672-680.)