“…ELF-EMF may be able to restore the equilibrium between free radicals and antioxidants, controlling the cascade of inflammatory progression. In fact, several studies have showed that the exposure of different cell types to a 50-Hz ELF-EMF induced an increase in intracellular ROS levels [ 11 , 18 ].…”
Section: Discussionmentioning
confidence: 99%
“…In SH-SY5Y cells, short ELF-EMF exposure increased the intracellular 5-hydroxyindoleacetic acid/5-hydroxytryptamine ratio [ 9 , 10 ]. Also, a rapid and sustained elevation in nitric oxide synthetase (NOS) activity, a time-dependent elevation in catalase (CAT) activity, and increased cytochrome (CYP) 450 activity and O 2 − production were observed [ 11 ]. A significant modulation of iNOS, CAT, and CYP 450 protein expression was recorded in cells exposed to ELF-EMF [ 11 , 12 ].…”
Extremely low frequency electromagnetic fields (ELF-EMFs) have been known to modulate inflammatory responses by targeting signal transduction pathways and influencing cellular redox balance through the generation of oxidants and antioxidants. Here, we studied the molecular mechanism underlying the anti-oxidative effect of ELF-EMF in THP-1 cells, particularly with respect to antioxidant enzymes, such as heme oxygenase-1 (HO-1), regulated transcriptionally through nuclear factor E2-related factor 2 (Nrf2) activation. Cells treated with lipopolysaccharides (LPS) were exposed to a 50 Hz, 1 mT extremely low frequency electromagnetic fields for 1 h, 6 h and, 24 h. Our results indicate that ELF-EMF induced HO-1 mRNA and protein expression in LPS-treated THP-1 cells, with peak expression at 6 h, accompanied with a concomitant migration to the nucleus of a truncated HO-1 protein form. The immunostaining analysis further verified a nuclear enrichment of HO-1. Moreover, ELF-EMF inhibited the protein expressions of the sirtuin1 (SIRT1) and nuclear factor kappa B (NF-kB) pathways, confirming their anti-inflammatory/antioxidative role. Pretreatment with LY294002 (Akt inhibitor) and PD980559 (ERK inhibitor) inhibited LPS-induced Nrf2 nuclear translocation and HO-1 protein expression in ELF-EMF-exposed cells. Taken together, our results suggest that short ELF-EMF exposure exerts a protective role in THP-1 cells treated with an inflammatory/oxidative insult such as LPS, via the regulation of Nrf-2/HO-1 and SIRT1 /NF-kB pathways associated with intracellular glutathione (GSH) accumulation.
“…ELF-EMF may be able to restore the equilibrium between free radicals and antioxidants, controlling the cascade of inflammatory progression. In fact, several studies have showed that the exposure of different cell types to a 50-Hz ELF-EMF induced an increase in intracellular ROS levels [ 11 , 18 ].…”
Section: Discussionmentioning
confidence: 99%
“…In SH-SY5Y cells, short ELF-EMF exposure increased the intracellular 5-hydroxyindoleacetic acid/5-hydroxytryptamine ratio [ 9 , 10 ]. Also, a rapid and sustained elevation in nitric oxide synthetase (NOS) activity, a time-dependent elevation in catalase (CAT) activity, and increased cytochrome (CYP) 450 activity and O 2 − production were observed [ 11 ]. A significant modulation of iNOS, CAT, and CYP 450 protein expression was recorded in cells exposed to ELF-EMF [ 11 , 12 ].…”
Extremely low frequency electromagnetic fields (ELF-EMFs) have been known to modulate inflammatory responses by targeting signal transduction pathways and influencing cellular redox balance through the generation of oxidants and antioxidants. Here, we studied the molecular mechanism underlying the anti-oxidative effect of ELF-EMF in THP-1 cells, particularly with respect to antioxidant enzymes, such as heme oxygenase-1 (HO-1), regulated transcriptionally through nuclear factor E2-related factor 2 (Nrf2) activation. Cells treated with lipopolysaccharides (LPS) were exposed to a 50 Hz, 1 mT extremely low frequency electromagnetic fields for 1 h, 6 h and, 24 h. Our results indicate that ELF-EMF induced HO-1 mRNA and protein expression in LPS-treated THP-1 cells, with peak expression at 6 h, accompanied with a concomitant migration to the nucleus of a truncated HO-1 protein form. The immunostaining analysis further verified a nuclear enrichment of HO-1. Moreover, ELF-EMF inhibited the protein expressions of the sirtuin1 (SIRT1) and nuclear factor kappa B (NF-kB) pathways, confirming their anti-inflammatory/antioxidative role. Pretreatment with LY294002 (Akt inhibitor) and PD980559 (ERK inhibitor) inhibited LPS-induced Nrf2 nuclear translocation and HO-1 protein expression in ELF-EMF-exposed cells. Taken together, our results suggest that short ELF-EMF exposure exerts a protective role in THP-1 cells treated with an inflammatory/oxidative insult such as LPS, via the regulation of Nrf-2/HO-1 and SIRT1 /NF-kB pathways associated with intracellular glutathione (GSH) accumulation.
“…Such changes can modify the BS [9]. Also, we use the experimental findings concerning the significant modulation of catalase, CYP450, and inducible nitric oxide synthase activity in myelogenous leukemia cells [86] to reaffirm our idea with respect to the effect of ELF-EMF on the enzymological system. A more critical step is the activation of xenobiotics whose interaction produces OS in the form of electrophiles and ROS [30,40].…”
Carcinogenesis induced chemically produces mutations affecting standard cells' behavior. An electrophilic attack on DNA result as the primary characteristic. Once xenobiotics are administrated to mammals they suffer a metabolic activation in the liver through cytochrome P450 (CYP450) enzymes, converting them to toxic compounds, generating oxidative stress (OS), and bursting electrophiles near the site of oxidation. CYP450 are electron carrier proteins that generate spin-correlated radical pair (RP) intermediaries. An extremely low-frequency electromagnetic field (ELF-EMF) can modulate the spin-flip conversion between singlet and triplet spin states of the RP populations, modifying the product formation during their metabolization. Experimentally, we induce hepatic cancer chemically; we found that ELF-EMF inhibits both the number and area of preneoplastic lesions by more than 50%. Furthermore, theoretically, we develop a quantum mechanical model based on the RP mechanism (RPM) in the Haberkorn approximation to explain the cytoprotective effects of ELF-EMF. Here, we review the status of the action's mechanism of ELF-EMF on our research on early hepatocarcinogenesis.
“…Similarly, several studies have also shown increased formation of ROS after exposure to ELF-MF (Ciejka et al, 2011;Patruno et al, 2015). This most likely occurs through the Fenton reaction (Lai & Singh, 2004), which is an iron-mediated catalytic process through which hydrogen peroxide is converted into more potent and toxic hydroxyl free radicals (Phillips et al, 2009) (Figure 3).…”
Section: Radical Pair Mechanismmentioning
confidence: 78%
“…An ELF-MF induced imbalance in intracellular ROS concentration, either through excessive production of ROS or deterioration in the cells' antioxidant defensive capabilities ultimately leads to cellular oxidative stress (Limon-Pacheco & Gonsebatt, 2009). This has been suggested by the studies indicating ELF-MF exposure inhibits melatonin production and the CAT antioxidant defence (Akdag et al, 2010), while also enhancing ROS concentrations (Patruno et al, 2015). However, a study by Hong and co-authors (2012) analysed whether ELF-MF exposure of cultured human breast epithelial MCF10A cells could elicit oxidative stress by measuring intracellular ROS levels as well as antioxidant enzyme activity within these exposed cells.…”
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