Treatment of platelet concentrates with the L-carnitine modulates platelets oxidative stress and platelet apoptosis due to mitochondrial reactive oxygen species reduction and reducing cytochrome C release during storage.

Abstract

Platelet concentrate (PC) transfusion is administrated to reduce the hemostatic complications in patients with thrombocytopenia. Strength platelet against oxidative stress conditions lead to decrease in platelet storage lesion (PSL). This study was aimed to evaluate L-carnitine (LC) effects on platelet oxidative stress and platelet apoptosis during storage time. PC bags were randomly selected and each bag was divided into two equal parts. L-carnitine was added to test groups. Normal saline was added to control groups. Platelets count, mean platelet volume (MPV), pH, Platelet aggregation, nitric oxide metabolism (nitric/nitrate), total antioxidant capacity (TAC), malondealdehyde concentration (MDA), lactate dehydrogenase (LDH) enzyme activity, mitochondrial reactive oxygen species (ROS) and cytochrome C releasing were assayed by standard methods in 1, 3, 5 and 7days of platelet storage. LDH enzyme activity was increased during storage but it had lower level in L-carnitine-treated platelets. LC treatment led to reduction in MDA concentration (3.35 ± 0.98 vs 5.3 ± 1.32, p = 0.003 and 6.52 ± 1.88 vs 5.67 ± 1.25, p = 0.005 for day 5 and day 7 respectively). Increased level of TAC was detected in LC-treated platelets in comparison to control (0.29 ± 0.06 vs 0.21 ± 0.05, p = 0.008 and 0.22 ± 0.03 vs 0.16 ± 0.03, p = 0.003 for day 5 and day 7 respectively). Interestingly, mitochondrial ROS and cytochrome C releasing was significantly lower in LC-treated versus control group during platelet storage. L-carnitine not only decreases mitochondrial ROS but also reduces cytochrome C releasing in PCs during storage. It might be considered as safe additive to decrease PSL in the future.