Adenosine inhibits superoxide production in rat peritoneal macrophages via elevation of cAMP level

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As a part of host-defense immune system, macrophages can response to a variety of stimulants and produce superoxide. We examined the effect of adenosine as a modulator on superoxide production induced by phorbol ester in rat peritoneal macrophages, using an acetyl-cytochrome c reduction method for its detection. 2-Cl-adenosine, a least metabolizable analog of adenosine, inhibited the superoxide production in a dose-dependent manner, and also showed the increasing effect on intracellular cAMP level. Superoxide production was also inhibited by the several reagents which increased intracellular cAMP level, including dibutyryl-cAMP. 8-bromo-cAMP (cell permeable cAMP analogs), forskolin (an adenyl-cyclase activator). Ro 20-1724 (an phosphodiesterase inhibitor), and propentofylline (a xanthine derivative), but not 8-bromo-cGMP (cell permeable cGMP analog). These results suggest that a high level of extracellular adenosine may attenuate immunity through regulating macrophage functions. On the other hand, the tissue damage which is resulted from an over-production of superoxide can be protected by adenosine and its related drugs via an elevation of intracellular cAMP level.

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