A laboratory study on N-acetyl cysteine in SSP+ modulating oxidative stress and delaying the progression of storage lesion in platelets

Introduction: Oxidative stress (OS) contributes to platelet storage lesion (PSL) and can be attenuated by using antioxidant additives in the storage solution. N-acetyl cysteine (NAC), a thiolcontaining antioxidant, scavenges reactive oxygen species (ROS) directly, upregulates antioxidant defenses, and has anti-apoptotic properties. This study explores the effect of the antioxidant additive NAC on platelets during storage. Methods: Platelets obtained from the blood of male Wistar rats (n = 5) were resuspended in SSP+ and divided into i) Controls, ii) 0.5-NAC, and iii) 1-NAC; stored at 22◦C for 11 days. The markers of platelet function (aggregation, ATP secretion, P-selectin), viability (caspase-3, MTT), OS (superoxides, nitrites), lipid peroxidation (thiobarbituric reactive substances), protein oxidation (protein sulfhydryls, advanced oxidation protein products), antioxidant defenses (superoxide dismutase, catalase, glutathione, total antioxidant capacity), and metabolism (pH, glucose, lactate dehydrogenase) were analyzed on storage days 1, 4, 7, and 11. Results: 1- NAC augmented antioxidant defenses, improved viability, and decreased protein oxidation, lipid peroxidation, and platelet activation. Aggregation without collagen decreased in 0.5-NAC and 1- NAC compared to controls. Both 0.5-NAC and 1-NAC were effective in maintaining platelet functions during storage. However, 1-NAC protected platelets from oxidation, enhanced antioxidant defenses, and maintained viability until day 7 of storage. 1-NAC could effectively scavenge ROS and enhance GSH and antioxidant enzymes in comparison to 0.5-NAC. Conclusion: N-acetyl cysteine at 1 mM concentration in SSP+ could maintain the efficacy of platelets as these cells could endure OS until day 7 of storage. This study emphasizes the potential of NAC as an effective component of platelet storage solutions to prolong the shelf-life of platelets.