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Abstract
Objective: Plasma acts as a good indicator of oxidative stress in blood. L-Carnitine is an antioxidant that reduces metabolic stress in cells, thereby providing a protective effect against oxidative stress (OS). L-Carnitine as an additive in storage has not been explored. Thus, this study attempts to analyze the role of L-carnitine in blood storage solution, citrate phosphate dextrose adenine (CPDA)-1, through OS markers including antioxidant enzymes, lipid peroxidation, and protein oxidation.Materials and Methods:Blood was collected from male Wistar rats and stored in CPDA-1 solution with L-carnitine (10 mM, 30 mM, and 60 mM: groups LC 10, LC 30, and LC 60, respectively) and without L-carnitine (control group). Plasma was isolated every 5th day and the OS markers were analyzed.Results:Superoxide dismutase (SOD) and sulfhydryl (SH) increased over storage in controls, LC 30, and LC 60. Catalase increased in LC 30 and LC 60 during storage. Thiobarbituric acid reactive substances (TBARS) and protein carbonyl (PrC) levels in all groups increased initially and reduced towards the end of storage. SOD and SH levels were maintained while TBARS and PrC levels increased in LC 10.Conclusion:L-Carnitine was beneficial in terms of increased antioxidant capacity and SH and decreased lipid peroxidation. This forms the basis for further studies on L-carnitine as a constituent in storage solutions.
Highlights
L-Carnitine (L-3 hydroxy-4-N-N-N-trimethylaminobutyrate) is an essential nutrient that the body uses to convert fat into energy
L-Carnitine was beneficial in terms of increased antioxidant capacity and SH and decreased lipid peroxidation
Changes between the groups are represented in upper case
Summary
L-Carnitine (L-3 hydroxy-4-N-N-N-trimethylaminobutyrate) is an essential nutrient that the body uses to convert fat into energy. It is required for the transport of fatty acids from the cytosol into the mitochondria during breakdown of lipids via β-oxidation. It acts as an antioxidant that reduces metabolic stress in cells, thereby providing a protective effect against lipid peroxidation and oxidative stress (OS) in the phospholipid membrane and the myocardial and endothelial cells [1]. Disturbances in the redox state can cause OS, which is an imbalance between the production of reactive oxygen species (ROS) and the biological system’s natural ability to detoxify these intermediates or repair the resulting damage caused by them [2].
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