As stated above, the mechanism of NAC-related organ protection is primarily attributed to scavenging oxygen free radicals, either directly, or through increasing intracellular glutathione concentration [3, 4]. Indeed, decreased malonaldehyde production indicates an attenuation of membrane damage from oxygen-free radicals [3], but other protective mechanisms may play a role as well [21]. Improved local microcirculation may be a major potential NAC-related organ-protective mechanism. NAC was reported to augment papillary flow [22] and was found to improve renal vasodilation in response to acetylcholine [15]. Thus, perhaps some of the protective effects of NAC can be attributed to improved glomerular hemodynamics or to the prevention of hypoxic tubular damage via restoration of altered renal microcirculation.