Supplementation with vitamin E prevented alterations induced by static magnetic fields on rat glucose metabolism and liver glycogen content.

PMID: 

Environ Sci Pollut Res Int. 2014 Nov ;21(22):12731-8. Epub 2014 Jun 27. PMID: 24965009

Abstract Title: 

Vitamin E prevents glucose metabolism alterations induced by static magnetic field in rats.

Abstract: 

In the present study, we investigate the effects of a possible protective role of vitamin E (vit E) or selenium (Se) on glucose metabolism disruption induced by static magnetic field (SMF) in rats. Rats have been exposed to SMF (128 mT, 1 h/day during 5 days). Our results showed that SMF failed to alter body weight and relative liver weight. Our data demonstrated that exposure to SMF increased (+21 %) blood glucose level and caused a decrease (-15 %) in liver glycogen content. Moreover, the same treatment induced a reduction of pancreatic islet area. Interestingly, supplementation with vit E (DLα-tocopherol acetate, 150 mg/kg per os during 5 days) prevented alterations induced by SMF on glucose metabolism and liver glycogen content, whereas supplementation with Se (Na2SeO3, 0.20 mg/l, in drinking water for 4 weeks) restored only hepatic glycogen contents. By contrast, both vit E and Se failed to correct the area of pancreatic islets.

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Oxidative stress and hydrogen peroxide work synergistically to stimulate apoptosis.

PMID: 

Acta Biol Hung. 2010 Jun ;61(2):158-67. PMID: 20519170

Abstract Title: 

Effect of ELF-EMF on number of apoptotic cells; correlation with reactive oxygen species and HSP.

Abstract: 

It is by now accepted that extremely low frequency electromagnetic fields ELF-EMF (0-300 Hz) affect biological systems although the mechanism has not been elucidated yet. In this study the effect of ELFEMF on the number of apoptotic cells of K562 human leukemia cell line induced or not with oxidative stress and the correlation with heat-shock protein 70 (hsp70) levels was investigated. One sample was treated with H 2 O 2 while the other was left untreated. ELF-EMF (1 mT, 50 Hz) was applied for 3 hours. ELF-EMF alone caused a decrease in the number of apoptotic cells and a slight increase in viability. However, it increased the number of apoptotic cells. In cells treated with H 2 O 2 . hsp70 and reactive oxygen species (ROS) levels were increased by ELF-EMF. These results show that the effect of ELF-EMF on biological systems depends on the status of the cell: while in cells not exposed to oxidative stress it is able to decrease the number of apoptotic cells by inducing an increase in hsp levels, it increases the number of apoptotic cells in oxidative stress-induced cells.

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50-Hz electromagnetic fields increase free radical release and IL-1B production by mouse macrophages.

PMID: 

J Cell Biochem. 2006 Sep 1 ;99(1):168-77. PMID: 16598759

Abstract Title: 

Alteration in cellular functions in mouse macrophages after exposure to 50 Hz magnetic fields.

Abstract: 

The aim of the present study is to investigate whether extremely low frequency electromagnetic fields (ELF-EMF) affect certain cellular functions and immunologic parameters of mouse macrophages. In this study, the influence of 50 Hz magnetic fields (MF) at 1.0 mT was investigated on the phagocytic activity and on the interleukin-1beta (IL-1beta) production in differentiated macrophages. MF-exposure led to an increased phagocytic activity after 45 min, shown as a 1.6-fold increased uptake of latex beads in MF-exposed cells compared to controls. We also demonstrate an increased IL-1beta release in macrophages after 24 h exposure (1.0 mT MF). Time-dependent IL-1beta formation was significantly increased already after 4 h and reached a maximum of 12.3-fold increase after 24 h compared to controls. Another aspect of this study was to examine the genotoxic capacity of 1.0 mT MF by analyzing the micronucleus (MN) formation in long-term (12, 24, and 48 h) exposed macrophages. Our data show no significant differences in MN formation or irregular mitotic activities in exposed cells. Furthermore, the effects of different flux densities (ranging from 0.05 up to 1.0 mT for 45 min) of 50 Hz MF was tested on free radical formation as an endpoint of cell activation in mouse macrophage precursor cells. All tested flux densities significantly stimulated the formation of free radicals. Here, we demonstrate the capacity of ELF-EMF to stimulate physiological cell functions in mouse macrophages shown by the significantly elevated phagocytic activity, free radical release, and IL-1beta production suggesting the cell activation capacity of ELF-EMF in the absence of any genotoxic effects.

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Biochanin A induces S phase arrest and apoptosis in lung cancer cells.

n/a

PMID: 

Biomed Res Int. 2018 ;2018:3545376. Epub 2018 Oct 3. PMID: 30402472

Abstract Title: 

Biochanin A Induces S Phase Arrest and Apoptosis in Lung Cancer Cells.

Abstract: 

Lung cancer is among the most common malignancies with a poor 5-year survival rate reaching only 16%. Thus, new effective treatment modalities and drugs are urgently needed for the treatment of this malignancy. In this study, we conducted the first investigation of the effects of Biochanin A on lung cancer and revealed the mechanisms underlying its potential anticancer effects. Biochanin A decreased cell viability in a time-dependent and dose-dependent manner and suppressed colony formation in A549 and 95D cells. In addition, Biochanin A induced S phase arrest and apoptosis and decreased mitochondrial membrane potential (ΔΨm) in A549 and 95D cells in a dose-dependent manner. Our results of subcutaneous xenograft models showed that the growth of Biochanin A group was significantly inhibited compared with that of control groups. Finally, P21, Caspase-3, and Bcl-2 were activated in Biochanin A-treated cells and Biochanin A-treated xenografts which also demonstrated that Biochanin A induced cell cycle arrest and apoptosis in lung cancer cells by regulating expression of cell cycle-related proteins and apoptosis-related proteins. In conclusion, this study suggests that Biochanin A inhibits the proliferation of lung cancer cells and induces cell cycle arrest and apoptosis mainly by regulating cell cycle-related protein expression and activating the Bcl-2 and Caspase-3 pathways, thus suggesting that Biochanin A may be a promising drug to treat lung cancer.

50-Hz magnetic fields are able to potentiate cellular damage induced in vitro by oxidizing agents.

PMID: 

Bioelectromagnetics. 1997 ;18(2):125-31. PMID: 9084863

Abstract Title: 

In vitro effects of 50 Hz magnetic fields on oxidatively damaged rabbit red blood cells.

Abstract: 

The aim of this study was to investigate the effects of 50 Hz magnetic fields (0.2-0.5 mT) on rabbit red blood cells (RBCs) that were exposed simultaneously to the action of an oxygen radical-generating system, Fe(II)/ascorbate. Previous data obtained in our laboratory showed at the exposure of rabbit erythrocytes or reticulocytes to Fe(II)/ascorbate hexokinase inactivation, whereas the other glycolytic enzymes do not show any decay. We also observed depletion of reduced glutathione (GSH) content with a concomitant intracellular and extracellular increase in oxidized glutathione (GSSG) and a decrease in energy charge. In this work we investigated whether 50 Hz magnetic fields could influence the intracellular impairments that occur when erythrocytes or reticulocytes are exposed to this oxidant system, namely, inactivation of hexokinase activity, GSH depletion, a change in energy charge, and hemoglobin oxidation. The results obtained indicate the a 0.5 mT magnetic field had no effect on intact RBCs, whereas it increased the damage with Fe(II)/ascorbate to a 0.5 mT magnetic field induced a significant further decay in hexokinase activity (about 20%) as well as a twofold increase in methemoglobin production compared with RBCs that were exposed to the oxidant system alone. Although further studies will be needed to determine the physiological implications of these data, the results reported in this study demonstrate that the effects of the magnetic fields investigated are able to potentiate the cellular damage induced in vitro by oxidizing agents.

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Long-term EMF exposure may be linked to higher levels of oxidative stress.

PMID: 

Environ Res. 2001 Jun ;86(2):198-207. PMID: 11437466

Abstract Title: 

Evidence of oxidative stress in American kestrels exposed to electromagnetic fields.

Abstract: 

Exposure to electromagnetic fields (EMFs) alters melatonin, behavior, growth, and reproduction of captive American kestrels (Falco sparverius), particularly of males. EMF exposure is a"possible"human carcinogen and associated with some neurodegenerative diseases. Oxidative stress contributes to cancer, neurodegenerative diseases, and immune disorders. We tested whether EMF exposure elicits an avian immune response and alters oxidative stress levels. Captive male kestrels were bred under control or EMF conditions equivalent to those experienced by wild kestrels. Short-term EMF exposure (one breeding season) suppressed plasma total proteins, hematocrits, and carotenoids in the first half of the breeding season. It also suppressed erythrocyte cells and lymphocyte proportions, but elevated granulosa proportions at the end of the breeding season. Long-term EMF exposure (two breeding seasons) suppressed hematocrits in the first half of the reproductive period too. Results indicate that only short-term EMF birds experience an immune response, particularly during the early half of the breeding season. The elevation of granulocytes, and the suppression of carotenoids, total proteins, and previously melatonin in the same kestrels, signifies that the short-term EMF male kestrels had higher levels of oxidative stress, due to an immune response and/or EMF exposure. Long-term EMF exposure may be linked to higher levels of oxidative stress through EMF exposure only.

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Antiproliferative activity of combined biochanin A and ginsenoside Rh2 on MDA-MB-231 and MCF-7 human breast cancer cells.

PMID: 

Molecules. 2018 Nov 8 ;23(11). Epub 2018 Nov 8. PMID: 30413008

Abstract Title: 

Antiproliferative Activity of Combined Biochanin A and Ginsenoside Rh₂ on MDA-MB-231 and MCF-7 Human Breast Cancer Cells.

Abstract: 

Breast cancer is the most frequently diagnosed cancer in women worldwide. The antiproliferative activities of biochanin A (BA) and ginsenoside Rh₂ were determined by evaluating their inhibitory effect on MDA-MB-231 human breast cancer cell proliferation. The combination of BA with Rh₂ was also assessed. In MDA cells, combination treatment led to a decrease in the ECvalues of BA and Rh₂ to 25.20 μM and 22.75 μM, respectively. In MCF-7 cells, the ECvalues of combined BA and Rh₂ decreased to 27.68 μM and 25.41 μM, respectively. BA combined with Rh₂ also improved the inhibition of MDA-MB-231 and MCF-7 cell migration and invasion compared to the individual compounds. Western blot analysis demonstrated upregulation in p-p53, p-p38, and p-ASK1 proteins while levels of TRAF2 were downregulated. These results suggest that BA combined with Rh₂ exhibits synergistic effects against MDA-MB-231 and MCF-7 cell proliferation.

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Exposure to ELF-MFs may act as a risk factor for the occurrence of oxidative stress-based nervous system pathologies associated with ageing.

PMID: 

Int J Biochem Cell Biol. 2008 ;40(12):2762-70. Epub 2008 Jun 10. PMID: 18585472

Abstract Title: 

Chronic exposure to 50Hz magnetic fields causes a significant weakening of antioxidant defence systems in aged rat brain.

Abstract: 

Several studies suggest that extremely low-frequency magnetic fields (ELF-MFs) may enhance the free radical endogenous production. It is also well known that one of the unavoidable consequences of ageing is an overall oxidative stress-based decline in several physiological functions and in the general resistance to stressors. On the basis of these assumptions, the aim of this study was to establish whether the ageing process can increase susceptibility towards widely present ELF-MF-mediated pro-oxidative challenges. To this end, female Sprague-Dawley rats were continuously exposed to a sinusoidal 50 Hz, 0.1 mT magnetic field for 10 days. Treatment-induced changes in the major antioxidant protection systems and in the neurotrophic support were investigated, as a function of the age of the subjects. All analyses were performed in brain cortices, due to the high susceptibility of neuronal cells to oxidative injury. Our results indicated that ELF-MF exposure significantly affects anti-oxidative capability, both in young and aged animals, although in opposite ways. Indeed, exposed young individuals enhanced their neurotrophic signalling and anti-oxidative enzymatic defence against a possible ELF-MF-mediated increase in oxygen radical species. In contrast, aged subjects were not capable of increasing their defences in response to ELF-MF treatment but, on the contrary, they underwent a significant decrease in the major antioxidant enzymatic activities. In conclusion, our data seem to suggest that the exposure to ELF-MFs may act as a risk factor for the occurrence of oxidative stress-based nervous system pathologies associated with ageing.

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Long-term ELF-MF exposure may enhance the oxidative/nitrosative stress in liver tissue of the female rats.

PMID: 

J Radiat Res. 2008 Mar ;49(2):181-7. PMID: 18367817

Abstract Title: 

Effects of long-term exposure of extremely low frequency magnetic field on oxidative/nitrosative stress in rat liver.

Abstract: 

Thirty-two adult Wistar-Albino female and male rats were used to investigate the long-term (45 days) effects of extremely low frequency magnetic field (ELF-MF; 50Hz, 1mT, 4h/day) exposure on oxidative/nitrosative stress in liver tissues of rats. The rats were divided randomly into four groups: female control (FC; n = 8) and MF-exposed female rats (F-MF; n = 8); male control (MC; n = 8) and MF-exposed male rats (M-MF; n = 8). Liver tissue from each animal was harvested and utilized for malondialdehyde (MDA) and 3-nitrotyrosine (3-NT) detection. MDA levels were measured by MDA-TBA method, while the 3-NT levels were determined by the HPLC-UV system. There were no significant differences between the MDA levels of the control (FC; MC) and MF-exposed (F-MF; M-MF) rats (P>0.05). In the F-MF rats, 3-NT levels were significantly increased when compared to those of the FC rats (P

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Biochanin A significantly enhanced the anticancer efficacy of temozolomide in glioblastoma multiforme cells.

PMID: 

Anticancer Res. 2019 Jan ;39(1):57-66. PMID: 30591440

Abstract Title: 

Combination of Biochanin A and Temozolomide Impairs Tumor Growth by Modulating Cell Metabolism in Glioblastoma Multiforme.

Abstract: 

BACKGROUND/AIM: Several epidemiological studies have reported the chemopreventive potential of biochanin A, in cancer development and progression. We investigated the anticancer potential of combination of biochanin A and temozolomide against U-87 MG and T98 G [glioblastoma multiforme (GBM)] cells.MATERIALS AND METHODS: We evaluated the effect of biochanin A and temozolomide treatment on cell viability, expression of survival proteins, cell cycle, cell metabolism and mitochondrial function.RESULTS: Enhanced inhibitory effects of the combination treatment were observed on cell viability, expression of cell survival proteins EGFR, p-ERK, p-AKT, c-myc and MT-MMP1, and increased expression of the tumor suppressor, p-p53. Combination treatment also induced arrest in the Gphase of the cell cycle. A shift in the metabolic phenotype of cells from glycolytic to oxidative phosphorylation was observed on combination treatment and the permeabilized cells showed a significant impairment in complex IV activity.CONCLUSION: Biochanin A significantly enhanced the anticancer efficacy of temozolomide in GBM cells.

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