Abstract
Purpose. We aimed to investigate the possible effects of melatonin on gene expressions and activities of MnSOD and catalase under conditions of oxidative stress induced by hydrogen peroxide (H2O2) in peripheral blood mononuclear cells (PBMCs). Materials and Methods. PBMCs were isolated from healthy subjects and treated as follows: (1) control (only with 0.1% DMSO for 12 h); (2) melatonin (1 mM) for 12 h; (3) H2O2 (250 μM) for 2 h; (4) H2O2 (250 μM) for 2 h following 10 h pretreatment with melatonin (1 mM). The gene expression was evaluated by real-time PCR. MnSOD and catalase activities in PBMCs were determined by colorimetric assays. Results. Pretreatment of PBMCs with melatonin significantly augmented expression and activity of MnSOD which were diminished by H2O2. Melatonin treatment of PBMCs caused a significant upregulation of catalase by almost 2-fold in comparison with untreated cells. However, activity and expression of catalase increased by 1.5-fold in PBMCs under H2O2-induced oxidative stress compared with untreated cell. Moreover, pretreatment of PBMCs with melatonin resulted in a significant 1.8-fold increase in catalase expression compared to PBMCs treated only with H2O2. Conclusion. It seems that melatonin could prevent from undesirable impacts of H2O2-induced oxidative stress on MnSOD downregulation. Moreover, melatonin could promote inductive effect of H2O2 on catalase mRNA expression.
Highlights
Oxidative stress resulting from an imbalance between reactive oxygen species (ROS) production and neutralization plays an important role in the development of multiple pathophysiological states such as diabetes, atherosclerosis, cancers, neurodegenerative diseases, aging, and autoimmunity
peripheral blood mononuclear cells (PBMCs) were treated with the increasing concentration of melatonin (1 mM, 1 μM, and 1 nM) for 12 h and cell viability was assessed by MTT assay
We observed no significant change in cell viability after exposure to 10 h pretreatment with melatonin (1 mM) (98.9 ± 4.1%), 1 μM (94.6 ± 2.8%), and 1 nM (97.7 ± 4.5%) melatonin in comparison with untreated PBMCs and the cell viability was more than 90% under treatment with these concentrations (Figure 1)
Summary
Oxidative stress resulting from an imbalance between reactive oxygen species (ROS) production and neutralization plays an important role in the development of multiple pathophysiological states such as diabetes, atherosclerosis, cancers, neurodegenerative diseases, aging, and autoimmunity. In these conditions, antioxidant defense system is impaired and subsequently increases oxidative burden [1,2,3,4]. If excess ROS are not effectively eliminated by antioxidant defense system, it causes cellular damage by influencing gene expression and by oxidating DNA, proteins, and lipids. There is evidence that activation of antioxidant enzymes improves these conditions [9,10,11]
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