Efficacy of preconditioning with N-acetylcysteine against reperfusion injury after prolonged cold ischaemia in rats liver in which glutathione had been reduced by buthionine sulphoximine

Abstract

In a glutathione-depleted liver NAC prevented hepatic injury and improved liver integrity after a cold ischaemic-reperfusion injury, by acting not as a substrate for glutathione synthesis but as a direct free radical scavenger.

Pretreatment with Pentoxifylline andN-Acetylcysteine in Liver Ischemia Reperfusion-Induced Renal Injury

“…22 Previous studies have shown that NAC, PTX, and/or multi-drug administration prevented hepatic reperfusion injury. 23,24 PTX is a hemorheologic agent used for patients with vascular disease and other conditions caused by defects in regional microcirculation. 25 PTX prevents increases of microvascular permeability and formation of edema.…”

Cryopreservation

“…An analysis of these stresses and the cryopreservation literature demonstrates the well documented involvement of apoptosis in cryopreservation failure and the benefits of cell stress response modulation to improve outcome. 51,[69][70][71][72][73][74][75][76] Although apoptosis was described in association with these reports, it was not until 1998 that apoptosis and cryopreservation failure were directly linked. 8 Over the last decade, there has been the emergence of numerous studies focused on understanding the role apoptosis plays in cryopreservation failure.…”

Bucillamine, a thiol antioxidant, prevents transplantation-associated reperfusion injury

“…The antioxidant enzyme superoxide dismutase had variable effectiveness in previous studies and has been most impressive when administered by gene therapy with viral vectors, an as-yet-unproven technology (12). N-acetylcysteine, especially at high doses, has been successful in preserving microcirculatory function in some studies but has been ineffective in others (28,(34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45). In a pilot clinical study, it also seemed to improve outcomes in patients (46).…”

“…In addition to its direct effect on oxidative stress, as a result of its capacity to scavenge oxygen radicals (21), bucillamine likely indirectly counters oxidative stress by supplying excess thiol groups that promote the rapid conversion of GSSG to GSH. N-acetylcysteine, a less potent thiol donor, also has been found to counter the effects of I͞R injury on GSH and GSSG levels in hepatic tissue (34)(35)(36)(37)(38). Thus, thiol donors that can be transported into cells such as bucillamine and other cysteine derivatives may be particularly attractive for preventing adverse oxidative processes during reperfusion.…”