Subsequent oxidation yields the radical cation which is unstable in this case and is transformed into Rum(P)(CN')2. Such processes, which involve the transfer of an electron from the metal to the porphyrin ring, have been observed before, but no kinetic data were provided. We were able to measure the rate of the above process as k ~5 X 103 s"1 and to conclude that its rate-determining step is the removal of the carbonyl ligand. Radiolysis of the Ru11 porphyrin in dichloromethane saturated with KOH led to formation of the µ-dimer [(0H)RuIVP]20. Gradual exchange of the two OH groups by Cl' was also followed by radiolysis and the spectrum of the mixed µ-dimer (OH)RuIV-P-0-RuIVP(Cl") is reported.Acknowledgment. This research was supported by the Office of Basic Energy Sciences of the U.S. Department of Energy.Registry No. Run(OEP)(CO), 41636-35-5; Run(TPP)(CO), 32073-84-0; Run(OEP'+)(CO)(Cl), 118513-65-8; Run(TPP1+)(CO)(Cl), 118494-31-8; Run(OEP)(CO)(CN'), 77340-22-8; Rum(OEP)(CN)2, 77340-18-2; (HO)RuIV(OEP), 77089-60-2; Ru"(OEP)(CO)(OH'),

The reactions 2CH30, -+ 2CH30 + O2 (la), 2CH302 -CH30H + HCHO + 0, (lb), and 2CH302 -CH300CH3 + O2 (IC) have been studied at temperatures between 248 and 573 K. At temperatures above 373 K, the resulting decay traces were distorted away from pure second order at short wavelengths (around 210 nm), owing to the presence of the hydroperoxy radicals formed via the nonterminating pathway (la) and the subsequent rapid step CH30 + 0, -HCHO + H 0 2 (2). This distortion enabled the nonterminating/terminating branching ratio, 0, to be determined. Combining the present results with previously published work on the branching ratios gave In ( 3 = 3.80 -1470/T. Thus, although reaction 1 acts as a termination reaction under atmospheric conditions, it largely serves to convert CH302 into H 0 2 under combustion conditions.The temperature dependence of 0 enabled the real rate constant for the reaction, kl, to be. obtained over the entire experimental temperature range, giving k , = 1.3 X $E,R/K2 = 1712, and Absolute uncertainties, including contributions from both the experimental measurements and the dependence of kl on various analysis parameters, are estimated to be 22%, independent of temperature. No dependence of either the branching ratio or k , on the total pressure was found. The mechanism of the title reaction is discussed and the present results are compared with existing studies of alkylperoxy self-reactions. The implications for combustion and atmospheric modeling are also discussed. exp(365/n cm3 molecule-' s-I, with u2*/cm6 molecule-2 = 2.00 X molecule-' s-I = -5.61 X IntroductionThe self-reactions of peroxy radicals are of both practical and theoretical interest. Peroxy radicals are known to be key intermediates in both the combustion1 and atmospheric2 oxidation of hydrocarbons, and a detailed knowledge of the reactions between peroxy radicals would thus be an important contribution toward our understanding of these highly important and complicated processes. In general, such reactions display a negative temperature dependence and often several parallel reaction pathways, suggesting the intermediacy of an association complex, and a very complicated potential energy surface for the reaction. For ex-

Nitric oxide (NO) is an important effector molecule of the immune system in eliminating numerous pathogens. Peritoneal macrophages fromTrypanosoma brucei brucei-infected mice express type II NO synthase (NOS-II), produce NO, and kill parasites in the presence ofl-arginine in vitro. Nevertheless, parasites proliferate in the vicinity of these macrophages in vivo. The present study shows thatl-arginine availability modulates NO production. Trypanosomes use l-arginine for polyamine synthesis, required for DNA and trypanothione synthesis. Moreover, arginase activity is up-regulated in macrophages from infected mice from the first days of infection. Arginase competes with NOS-II for their common substrate, l-arginine. In vitro, arginase inhibitors decreased urea production, increased macrophage nitrite production, and restored trypanosome killing. In vivo, a dramatic decrease inl-arginine concentration was observed in plasma from infected mice. In situ restoration of NO production and trypanosome killing were observed when excess l-arginine, but notd-arginine or l-arginine plusN ω-nitro-l-arginine (a NOS inhibitor), was injected into the peritoneum of infected mice. These data indicate the role of l-arginine depletion, induced by arginase and parasites, in modulating the l-arginine–NO pathway under pathophysiological conditions.

This study was performed as part of the Sonderforschungsbereich 233, "Dynamics and Chemistry of Hydrometeores". It was also supported by the CNRS program "Phase Atmosphérique des Cycles Biogéochimiques".

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