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Syringic Acid Attenuates Oxidative Stress in Plasma and Peripheral Blood Mononuclear Cells of Patients With Acute Myeloid Leukemia Publisher Pubmed



Haddadi N1 ; Mirzania M2 ; Ansarihadipour H1
Authors
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Authors Affiliations
  1. 1. Department of Biochemistry and Genetics, School of Medicine, Arak University of Medical Sciences, Arak, Iran
  2. 2. Department of Internal Medicine, Cancer Research Center Cancer Institute, Imam Khomeini Science, Tehran, Iran

Source: Nutrition and Cancer Published:2023


Abstract

Syringic acid (SA) is a natural phenolic acid that possesses antioxidant properties. The current study aimed to assess the possible ameliorative effects of SA on oxidative stress in patients with acute myeloid leukemia (AML). Twenty-two healthy donors as well as 22 sex- and age-matched AML patients participated in the study. AML patients were at the time of diagnosis and before remission. The peripheral blood mononuclear cells (PBMCs) and plasma samples were obtained and divided into four groups. The groups include: 1) buffer (B), containing isotonic phosphate buffer saline (100 mM, pH 7.4, 1 hr); 2) OX, containing solution subjected to iron-mediated oxidation (2.7 µM, 1 hr); 3) SA, containing SA solution (10 µM, 1 h) as ROS quencher and 4) SA + OX in which samples were pretreated with 10 µM of SA for 1 h, and then exposed to OX solution (2.7 µM) for 1 h. The results indicated that SA caused a significant increase in the activity of glutathione peroxidase (GPX) in PBMCs. Of note, the treatment of PBMCs and plasma samples of AML patients with SA was able to normalize the altered levels of GPX, superoxide dismutase (SOD), and catalase (CAT). The antioxidant effect of SA was further confirmed by analyzing the total oxidant status, lipid peroxidation, and protein carbonylation in both plasma samples and PBMCs of AML patients. According to the results, it seems that SA has strong protective effects on oxidative stress by elevating the total antioxidant status (TAS) of PBMCs and plasma specimens from AML patients. © 2023 Taylor & Francis Group, LLC.