PMID: 

Environ Toxicol Pharmacol. 2011 Jan ;31(1):100-6. Epub 2010 Sep 29. PMID: 21787674

Abstract Title: 

Selenium supplementation ameliorates static magnetic field-induced disorders in antioxidant status in rat tissues.

Abstract: 

The aim of this study was to investigate the effect of selenium supplementation on the antioxidant enzymatic system (such as GPx, GR and SOD), GSH and selenium level in liver, kidney, muscle and brain of static magnetic field (SMF) exposed rats. Male adult rats were divided into control rats (n=6), SMF-exposed rats (128 mT; 1h/day for 5 days), selenium-treated rats (Na(2)SeO(3), 0.2mg/l, in drinking water for 4 weeks) and co-exposed rats (selenium for 4 weeks and SMF during the last 5 consecutive days). Sub-acute exposure to SMF induces a decrease of selenium levels in kidney, muscle and brain. Our results also revealed a decrease of GPx activities in kidney and muscle. By contrast, SMF exposure increased total GSH levels and total SOD activities in liver, while glutathione reductase activity is unaffected. Selenium supplementation in SMF-exposed rats restored selenium levels in kidney, muscle and brain and elevated the activities of GPx in kidney and muscle to those of control group. In the liver, selenium supplementation failed to bring down the elevated levels of total GSH and SOD activity. Our investigations suggested that sub-acute exposure to SMF altered the antioxidant response by decreasing the level of total selenium in kidney, muscle and brain. Interestingly, selenium supplementation ameliorates antioxidant capacity in rat tissues exposed to SMF.

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PMID: 

Toxicol Ind Health. 2011 Nov ;27(10):949-55. Epub 2011 Apr 19. PMID: 21505001

Abstract Title: 

Effect of selenium pre-treatment on plasma antioxidant vitamins A (retinol) and E (α-tocopherol) in static magnetic field-exposed rats.

Abstract: 

In the present study, we evaluate the effect of the co-exposure to static magnetic field (SMF) and selenium (Se) on the antioxidant vitamins A and E levels and some other parameters of oxidative stress in rat. Sub-acute exposure of male adult rats to a uniform SMF (128 mT, 1 h/day during 5 consecutive days) increased plasma activity of glutathione peroxidase (+35%) but decreasedα-tocopherol (-67%) and retinol levels (-41%). SMF exposure failed to alter the plasmatic thiobarbituric acid-reactive species (TBARs), total thiol groups and selenium concentrations. Sub-chronic administration of Se (Na(2)SeO(3), 0.2 mg/L, for 30 consecutive days, per os) ameliorated the antioxidant capacities in SMF-treated rats. Our investigation demonstrated that sub-acute exposure to SMF induced oxidative stress, which may be prevented by a pretreatment with selenium.

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PMID: 

Electromagn Biol Med. 2016 ;35(1):65-74. Epub 2014 Dec 11. PMID: 25496054

Abstract Title: 

The developmental effects of extremely low frequency electric fields on visual and somatosensory evoked potentials in adult rats.

Abstract: 

The purpose of our study was to investigate the developmental effects of extremely low frequency electric fields (ELF-EFs) on visual evoked potentials (VEPs) and somatosensory-evoked potentials (SEPs) and to examine the relationship between lipid peroxidation and changes of these potentials. In this context, thiobarbituric acid reactive substances (TBARS) levels were determined as an indicator of lipid peroxidation. Wistar albino female rats were divided into four groups; Control (C), gestational (prenatal) exposure (Pr), gestational+ postnatal exposure (PP) and postnatal exposure (Po) groups. Pregnant rats of Pr and PP groups were exposed to 50 Hz electric field (EF) (12 kV/m; 1 h/day), while those of C and Po groups were placed in an inactive system during pregnancy. Following parturition, rats of PP and Po groups were exposed to ELF-EFs whereas rats of C and Pr groups were kept under the same experimental conditions without beingexposed to any EF during 68 days. On postnatal day 90, rats were prepared for VEP and SEP recordings. The latencies of VEP components in all experimental groups were significantly prolonged versus C group. For SEPs, all components of PP group, P2, N2 components of Pr group and P1, P2, N2 componentsof Po group were delayed versus C group. As brain TBARS levels were significantly increased in Pr and Po groups, retina TBARS levels were significantly elevated in all experimental groups versus C group. In conclusion, alterations seen in evoked potentials, at least partly, could be explained by lipid peroxidation in the retina and brain.

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PMID: 

Biomed Res Int. 2013 ;2013:602987. Epub 2013 Aug 6. PMID: 24027759

Abstract Title: 

Bioeffects of static magnetic fields: oxidative stress, genotoxic effects, and cancer studies.

Abstract: 

The interaction of static magnetic fields (SMFs) with living organisms is a rapidly growing field of investigation. The magnetic fields (MFs) effect observed with radical pair recombination is one of the well-known mechanisms by which MFs interact with biological systems. Exposure to SMF can increase the activity, concentration, and life time of paramagnetic free radicals, which might cause oxidative stress, genetic mutation, and/or apoptosis. Current evidence suggests that cell proliferation can be influenced by a treatment with both SMFs and anticancer drugs. It has been recently found that SMFs can enhance the anticancer effect of chemotherapeutic drugs; this may provide a new strategy for cancer therapy. This review focuses on our own data and other data from the literature of SMFs bioeffects. Three main areas of investigation have been covered: free radical generation and oxidative stress, apoptosis and genotoxicity, and cancer. After an introduction on SMF classification and medical applications, the basic phenomena to understand the bioeffects are described. The scientific literature is summarized, integrated, and critically analyzed with the help of authoritative reviews by recognized experts; international safety guidelines are also cited.

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PMID: 

Radiat Environ Biophys. 2017 05 ;56(2):193-200. Epub 2017 Mar 3. PMID: 28258386

Abstract Title: 

Assessing the combined effect of extremely low-frequency magnetic field exposure and oxidative stress on LINE-1 promoter methylation in human neural cells.

Abstract: 

Extremely low frequency magnetic fields (ELF-MF) have been classified as"possibly carcinogenic", but their genotoxic effects are still unclear. Recent findings indicate that epigenetic mechanisms contribute to the genome dysfunction and it is well known that they are affected by environmental factors. To our knowledge, to date the question of whether exposure to ELF-MF can influence epigenetic modifications has been poorly addressed. In this paper, we investigated whether exposure to ELF-MF alone and in combination with oxidative stress (OS) can affect DNA methylation, which is one of the most often studied epigenetic modification. To this end, we analyzed the DNA methylation levels of the 5'untranslated region (5'UTR) of long interspersed nuclear element-1s (LINE-1 or L1), which are commonly used to evaluate the global genome methylation level. Human neural cells (BE(2)C) were exposed for 24 and 48 h to extremely low frequency pulsed magnetic field (PMF; 50 Hz, 1 mT) in combination with OS. The methylation levels of CpGs located in L1 5'UTR region were measured by MassARRAY EpiTYPER. The results indicate that exposures to the single agents PMF and OS induced weak decreases and increases ofDNA methylation levels at different CpGs. However, the combined exposure to PMF and OS lead to significant decrease of DNA methylation levels at different CpG sites. Most of the changes were transient, suggesting that cells can restore homeostatic DNA methylation patterns. The results are discussedand future research directions outlined.

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PMID: 

Gen Physiol Biophys. 2015 Jan ;34(1):23-32. Epub 2014 Nov 14. PMID: 25395602

Abstract Title: 

Does static magnetic field-exposure induced oxidative stress and apoptosis in rat kidney and muscle? Effect of vitamin E and selenium supplementations.

Abstract: 

Static magnetic fields (SMFs) effect observed with radical pair recombination is one of the well-known mechanisms by which SMFs interact with biological systems. Our aim was to study whether SMF induces oxidative stress and apoptosis in rat tissues and to evaluate the possible protector effect of selenium (Se) and vitamin E (vit E) supplementations. Rats were randomly divided into control, SMF-exposed, Se-treated, vit E-treated, SMF exposed rats and co-treated with Se, and SMF exposed rats and co-treated with vit E. After animal sacrifice, catalase (CAT) activity and malondialdehyde (MDA) concentration were measured and apoptosis inducing factor (AIF) immunohistochemical labeling was performed in kidney and muscle. Exposure of rats to SMF (128 mT, 1 h/day for 5 days) increased the MDA concentrations (+25%) and CAT activities (+34%) in kidney but not in muscle. By contrast, the same treatment failed to induce a caspase-independent pathway apoptosis in both tissues. Interestingly, Se pre-treatment inhibited the increase of MDA concentrations and CAT activities in kidney in SMF-exposed rats. However, vit E administration corrected only MDA levels in rat kidney. In conclusion, exposure to SMF induced oxidative stress in kidney that can be prevented by treatment with Se or vit E.

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PMID: 

Environ Sci Pollut Res Int. 2015 Oct ;22(20):16060-6. Epub 2015 Jun 12. PMID: 26062464

Abstract Title: 

Static magnetic field exposure-induced oxidative response and caspase-independent apoptosis in rat liver: effect of selenium and vitamin E supplementations.

Abstract: 

In the present study, we investigated the implication of oxidative stress and apoptosis under static magnetic field (SMF) in the brain and liver. Moreover, we estimated the protective role of selenium and vitamin E in rat tissues against disorders induced by SMF. Exposure of rats to SMF (128 mT, 1 h/day during five consecutive days) increased the activity of catalase (CAT) (+24 %) in the liver but not in the brain. By contrast, the same treatment failed to alter malondialdehyde (MDA) concentration in the brain and liver. Exposure to SMF also induced hepatocyte apoptosis through a caspase-independent pathway involving mitochondrial apoptosis-inducing factor (AIF) but not in the brain. Selenium and vitamin E supplementations to SMF-exposed rats restored liver CAT activity but failed to minimize liver apoptosis.

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PMID: 

J Food Biochem. 2019 Sep ;43(9):e12963. Epub 2019 Jul 2. PMID: 31489655

Abstract Title: 

Effects of phenolic compounds from aqueous extract of Trifolium repens against acetaminophen-induced hepatotoxicity in mice.

Abstract: 

The aqueous extract of Trifolium repens (TR) leaves was analyzed for the phenolic profile using reversed phase HPLC-DAD and administered to mice against acetaminophen-induced hepatoxicity. Twenty-four phenolic compounds were identified and quantified. The highest amounts present were of kaempferol-3-(caffeoyldiglucoside)-7-glucoside (983.7 µg/ml), followed by p-coumaroyl-4-glucoside (905.6 µg/ml) and daidzein-O-sulfate (808.3 µg/ml). The aqueous extract was administered to mice along with acetaminophen at different doses. Acetaminophen was found to significantly alter body weight, serum biochemistry, and hematological indices of mice, which were ameliorated by the co-administration of aqueous extract. Liver histopathological studies revealed that acetaminophen significantly induced toxicity, while TR aqueous extract provides curative functions. Lipid peroxidation and total reduced glutathione in the liver were also normalized by the aqueous extract of TR. The aqueous extract of TR was rich in important phenolic compounds, which can be used as a source of beneficial bioactive compounds with hepato-protective function. PRACTICAL APPLICATIONS: Acetaminophen has been widely used as antipyretic and analgesic. However, the major complication reported is hepatotoxicity. Synthetic or conventional drugs used for hepatic diseases or against hepatotoxicity are insufficient and causes severe side effects. For this purpose, traditional medicinal plants or nutraceuticals are used to decrease in the side effects of differenthepatotoxic medicine are demanding. Food and neutraceuticals are rich in important polyphenolic compounds which are the best antioxidants. This study was aimed to evaluate the phenolic composition of aqueous extract of Trifolium repens and its potential protective action against the acetaminophen-induced toxicity in mice. This study showed for the first time that the aqueous extract of TR was protective against the hepatotoxicity induced by acetaminophen.

PMID: 

J Sci Food Agric. 2019 Sep 12. Epub 2019 Sep 12. PMID: 31512247

Abstract Title: 

Selenium affects the activity of black tea in preventing metabolic syndrome in high fat diet-fed Sprague-Dawley rats.

Abstract: 

BACKGROUND: Metabolic syndrome, a group of factors that increase the risk of health problems, is becoming increasingly common. Strategies to prevent metabolic syndrome have received substantial attention. Black tea consumption and selenium (Se) intake have been reported to be negatively associated with the prevalence of metabolic syndrome. Therefore, we sought to investigate whether Se-rich black tea might have a stronger effect than Se-deficient black tea in the prevention of metabolic syndrome.RESULTS: Sprague-Dawley rats were divided into four groups and fed a normal rodent diet, high fat diet, high fat diet containing 3% Se-rich black tea or high fat diet containing 3% Se-deficient black tea for 4 weeks. Blood and tissue samples were tested at the end of the experiment. The results suggested that both types of black tea ameliorated high fat diet-induced body weight gain, lowered serum triglycerides and attenuated intestinal barrier dysfunction. Se-rich black tea showed stronger activity indecreasing fasting serum glucose and increasing insulin sensitivity, as well as stronger hepatoprotection, owing to higher total antioxidant capacity and activated hepatic antioxidant enzymes. However, it did not exhibit better effects in preventing fat accumulation. The different effects of Se-rich and Se-deficient black tea on the gut microbiota might have been partially responsible for the results.CONCLUSION: Compared with Se-deficient black tea, Se-rich black tea displayed stronger activity in preventing high fat diet-induced hyperglycemia and liver damage but was not better at preventing fat accumulation and attenuating dysbiosis. More experiments are needed to further understand the underlying mechanisms. This article is protected by copyright. All rights reserved.

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PMID: 

Food Funct. 2019 Oct 16 ;10(10):6543-6555. PMID: 31545328

Abstract Title: 

Selenium influences mmu-miR-155 to inhibit inflammation in Staphylococcus aureus-induced mastitis in mice.

Abstract: 

Mastitis, a major disease affecting dairy cows, is most commonly caused by Staphylococcus aureus (S. aureus). Selenium (Se) can activate pivotal proteins in immune responses and regulate the immune system, and microRNA-155 (miR-155) is a key transcriptional regulator for inflammation-related diseases. We constructed the model of mouse mastitis in vivo and primary mouse mammary epithelial cells (MMECs) in vitro, which were induced by S. aureus. Se content of the mammary was estimated using an atomic fluorescence spectrophotometer. Histopathological analysis was performed via hematoxylin and eosin (H&E) staining. The mmu-miR-155-5p mimic was transfected in MMECs, and viability was determined through the MTT assay. Transfected efficiency was evaluated by qPCR and fluorescence staining. Cytokines including TNF-α, IL-1β, IL-10 and TLRs were detected with qPCR. In addition, western blotting was used to evaluate the expression of the NF-κB and MAPKs signaling pathways. The results demonstrated that a Se-supplemented diet improved the content of Se in mammary tissues. Histopathological studies indicated that the mammary glands were protected in the Se-supplemented group after S. aureus infection. Se-supplementation suppressed the production of MPO, mmu-miR-155, TNF-α, IL-1β, and TLR2 and significantly inhibited the phosphorylation of NF-κB and MAPKs in vivo and in vitro. All the data indicated that mmu-miR-155 played a pro-inflammatory role in our study, and Se-supplementation could suppress the expression of mmu-miR-155 to inhibit inflammation in S. aureus-induced mastitis in mice.

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