Can Melatonin Act as an Antioxidant in Hydrogen Peroxide-Induced Oxidative Stress Model in Human Peripheral Blood Mononuclear Cells?

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.

Response to oxidative stress of peripheral blood mononuclear cells from multiple sclerosis patients and healthy controls

“…We did not find any significant difference between the two groups, suggesting that both PBMCs from MS patients and healthy controls present an initial reduction in mitochondrial activity after an oxidative challenge, but they are able to restore the physiologic activity levels within a longer period of time (3 h). PBMCs are able to adapt to oxidative stress; our data are consistent with similar H 2 O 2 treatments at increasing concentrations (50 μM, 100 μM, and 250 μM for 2 h) with no cytotoxic effect (Emamgholipour et al 2016). In this study, performed on PBMCs from 14 healthy subjects, only 2 h of 500 μM H 2 O 2 were able to significantly reduce the mitochondrial activity (Emamgholipour et al 2016).…”

“…PBMCs are able to adapt to oxidative stress; our data are consistent with similar H 2 O 2 treatments at increasing concentrations (50 μM, 100 μM, and 250 μM for 2 h) with no cytotoxic effect (Emamgholipour et al 2016). In this study, performed on PBMCs from 14 healthy subjects, only 2 h of 500 μM H 2 O 2 were able to significantly reduce the mitochondrial activity (Emamgholipour et al 2016).…”

“…PBMCs from both MS patients and healthy controls show a significant variation in their mitochondrial function, measured with the MTT assay, considering different exposure times to oxidative stress. This assay is extensively used for estimating the mitochondrial activity of cells, thus providing a first snapshot of the cell metabolic activity (Osera et al 2011;Emamgholipour et al 2016). In particular, after 15 min of oxidative stress, the mitochondrial activity decreases, and it is restored after 3 h of exposure to H 2 O 2 .…”

Protective effect of 3-O-methyl quercetin and kaempferol from Semecarpus anacardium against H2O2 induced cytotoxicity in lung and liver cells

“…5g and h ). Recently, Emamgholipour et al (2016) [ 49 ] reported that peripheral blood mononuclear cells (PBMNCS) showed decreased expression of SOD levels with H 2 O 2 treatment compared to untreated cells both mRNA expression and activity. Pre-treatment of PBMCS with melatonin, a known antioxidant prior to exposure to H 2 O 2 caused a significant increase in SOD levels in comparison with PBMNCS treated only with H 2 O 2 [ 49 ].…”

“…Recently, Emamgholipour et al (2016) [ 49 ] reported that peripheral blood mononuclear cells (PBMNCS) showed decreased expression of SOD levels with H 2 O 2 treatment compared to untreated cells both mRNA expression and activity. Pre-treatment of PBMCS with melatonin, a known antioxidant prior to exposure to H 2 O 2 caused a significant increase in SOD levels in comparison with PBMNCS treated only with H 2 O 2 [ 49 ]. Interestingly, cells pretreated with 100 μg of isolated antioxidant compounds following exposure to H 2 O 2 (100 μM) showed a significant increase in levels of CAT and SOD2 compared to H 2 O 2 treated cells, suggesting cytoprotective nature of isolated antioxidant compounds, 3-O-methyl quercetin and kaempferol in mediating the cell survival.…”