Radical forms of sulfur dioxide (SO2), sulfite (SO32−), sulfate (SO42−), and their conjugate acids are known to be generated in vivo through various chemical and biochemical pathways. Oxides of sulfur are environmentally pervasive compounds and are associated with a number of health problems. There is growing evidence that their toxicity may be mediated by their radical forms. Electron paramagnetic resonance (EPR) spin trapping using the commonly used spin trap, 5,5-dimethyl-1-pyrroline N-oxide (DMPO), has been employed in the detection of SO3•− and SO4•−. The thermochemistries of SO2•−, SO3•−, SO4•−, and their respective conjugate acids addition to DMPO were predicted using density functional theory (DFT) at the PCM/B3LYP/6-31+G**//B3LYP/6-31G* level. No spin adduct was observed for SO2•− by EPR but an S-centered adduct was observed for SO3•− and an O-centered adduct for SO4•−. Determination of adducts as S- or O-centered was made via comparison based on qualitative trends of experimental hfcc’s with theoretically calculated ones. The thermodynamics of the non-radical addition of SO32− and HSO3− to DMPO followed by conversion to the corresponding radical adduct via the Forrester-Hepburn mechanism was also calculated. Adduct acidities and decomposition pathways were investigated as well, including an EPR experiment using H217O to determine the site of hydrolysis of O-centered adducts. The mode of radical addition to DMPO is predicted to be governed by several factors, including spin population density, and geometries stabilized by hydrogen bonds. The thermodynamic data supports evidence for the radical addition pathway over the nucleophilic addition mechanism.

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Adding IFN alfa-2b to induction CVP in low-grade NHL did not induce a higher response rate, but it significantly increased the duration of the responses. We found significant differences in PFS that favored the patients who received CVP + IFN, but not in OS. To date, no additional benefit has been seen from the administration of IFN for maintenance.

Abstract Correspondence to: Frederick. Villamena@osumc.edu , Arsenic is one of the most environmentally significant toxins and a great global health concern. Long known for its acute toxicity, arsenic has also been discovered to be a potent carcinogen. Evidence links arsenic toxicity and carcinogenic actions to reactive oxygen species (ROS). In most animal including humans, arsenic undergoes a biomethylation to yield organic arsenic species, long assumed to be a process of detoxification. However, a growing body of evidence suggests that these organic arsenic species, particularly the reduced trivalent intermediates, may be just as if not more toxic than the inorganic analogs. Furthermore, current food safety regulations often monitor only inorganic arsenic levels. There is, therefore, a clear need for more literature and empirical data concerning the toxic mechanisms of arsenic.In this study, we examined organic and inorganic arsenites capacity to generate ROS when exposed to common oxidizing agents via EPR spectroscopy and spin-trapping with the cyclic nitrone 5,5-dimethyl-1-pyrroline-N-oxide (DMPO). Experimental observations were theoretically rationalized using density functional theory approach.