The heat shock‐induced cell cycle arrest is attenuated by weak electromagnetic fields

Tokalov, Sergey V.; Gutzeit, Herwig O.

doi:10.1046/j.1365-2184.2003.00261.x

Cited by 17 publications

(21 citation statements)

References 45 publications

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“…HL-60 cells showed a significant increase of HSP72 mRNA levels for 4 h post incubation time, H9c2 cells for 1 and 6 h post incubation time, and Girardi Heart cells for 6 h, respectively. These mRNA-findings are in agreement with data of other groups, who have found increased mRNA levels of actin, histon H2B and MYC [Goodman et al, 1989], of c-myc and HSP70 [Goodman et al, 1994], and for HSP27, HSP70A, HSP70B and HSP70C in a dose dependent manner after exposure to electromagnetic fields in HL-60 cells [Tokalov and Gutzeit, 2003]. In contrast, some groups were unable to find any influence of EM fields on MYC and b-actin mRNA [Lacy-Hulbert et al, 1995], on HSP70 mRNA levels, HSP and HSE binding in HL-60 cells [Morehouse and Owen, 2000].…”

Section: Discussionsupporting

confidence: 95%

“…When the cells were exposed to both stressors (41 8C plus EM field) a much smaller fraction of the cells showed cell cycle arrest. The authors proposed that the effect was due to the induction of heat shock proteins by the EM field [Tokalov and Gutzeit, 2003]. In this work we investigate the effect of different electromagnetic field exposure applications on various cell lines looking not only at the expression of heat shock mRNA but also on heat shock protein levels.…”

Section: Introductionmentioning

confidence: 99%

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Expression of HSP72 after ELF‐EMF exposure in three cell lines

Gottwald

Sontag

Lahni

et al. 2007

Bioelectromagnetics

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It has been reported that magnetic fields with flux densities ranging from microT to mT are able to induce heat shock factor, HSP72 mRNA or heat shock proteins in various cells. In this study we investigated changes in the HSP72 mRNA transcription level in three cell lines (HL-60, H9c2, and Girardi heart cells) and in the intracellular HSP72 protein content in two cell lines (HL-60 and Girardi heart cells) after treatment schemes using electromagnetic fields with a flux density of 2 microT to 4 mT, a frequency of 50 Hz and exposure times from 15 to 30 min. None of the treatments or modalities showed any significant effect on the HSP72 protein level, although HSP72 mRNA could be induced, at least to some extent, with one of the parameter combinations in all cell lines tested. Obviously, HSP72 mRNA transcription and translation are not necessarily coupled in certain cells. This leads to the conclusion that electromagnetic field effects on HSP72 mRNA levels are not indicative for downstream effects unless increased mRNA levels can be correlated with increased HSP72 protein levels as well.

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Section: Discussionsupporting

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Expression of HSP72 after ELF‐EMF exposure in three cell lines

Gottwald

Sontag

Lahni

et al. 2007

Bioelectromagnetics

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“…Hsp70 can be activated by a number of factors, including non-physiological temperatures, oxidative stress, heavy metals, certain toxic chemicals, and also changes in radical homeostasis [169]. After EMF-exposure, changes in the activity or on the expression level of heat shock proteins has been detected in several laboratories suggesting that Hsp70 induction can be a consequence of EMF-exposure [162,[170][171][172][173][174][175][176][177][178]. It is likely, that Hsp-expression is dependent of the stimulus, the redox capacity, and of the cell type.…”

Section: Ros -Direct Dna-damage -Cancer Development 5 Biological Effmentioning

confidence: 98%

Cell Type Specific Redox Status is Responsible for Diverse Electromagnetic Field Effects

Simkó

2007

CMC

176

118

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Epidemiologic and experimental research on the potential carcinogenic effects of extremely low frequency electromagnetic fields (ELF-EMF) has been performed for a long time. Epidemiologic studies regarding ELF-EMF-exposure have focused primarily on leukaemia development due to residential sources in children and adults, and from occupational exposure in adults, but also on other kinds of cancer. Genotoxic investigations of EMF have shown contradictory results, a biological mechanism is still lacking that can explain the link between cancer development and ELF-EMF-exposure. Recent laboratory research has attempted to show general biological effects, and such that could be related to cancer development and/or promotion. Metabolic processes which generate oxidants and antioxidants can be influenced by environmental factors, such as ELF-EMF. Increased ELF-EMF exposure can modify the activity of the organism by reactive oxygen species leading to oxidative stress. It is well established that free radicals can interact with DNA resulting in single strand breaks. DNA damage could become a site of mutation, a key step to carcinogenesis. Furthermore, different cell types react differently to the same stimulus, because of their cell type specific redox status. The modulation of cellular redox balance by the enhancement of oxidative intermediates, or the inhibition or reduction of antioxidants, is discussed in this review. An additional aspect of free radicals is their function to influence other illnesses such as Parkinson's and Alzheimer's diseases. On the other hand, modulation of antioxidants by ELF-EMF can lower the intracellular defence activity promoting the development of DNA damage. It has also been demonstrated that low levels of reactive oxygen species trigger intracellular signals that involve the transcription of genes and leading to responses including cell proliferation and apoptosis. In this review, a general overview is given about oxidative stress, as well as experimental studies are reviewed as they are related to changes in oxidant and antioxidant content after ELF-EMF exposure inducing different biological effects. Finally, we conclude from our review that modulations on the oxidant and antioxidant level through ELF-EMF exposure can play a causal role in cancer development.

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“…The reason for the different behavior is not clear. Concentration differences in the cells may account for the differences, but alternative explanations must be considered when asynchronously cycling HL-60 cells are stressed by a physical stressor (heat shock) and hence are exposed to exactly the same stress, also cycling and cell cycle-arrested cell populations can be distinguished [40]. Further experiments using synchronized cell cultures are required to test if sensitive phases of the cell cycle may account for the observed effects.…”

Section: Discussionmentioning

confidence: 99%

Toxicity and Cell Cycle Effects of Synthetic 8-Prenylnaringenin and Derivatives in Human Cells

Tokalov¹,

Henker²,

Schwab

et al. 2004

Pharmacology

Self Cite

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The estrogenic flavanone rac-8-prenylnaringenin (8-PN) and 3 derivatives (rac-7-(O-prenyl)naringenin-4′-acetate (7-O-PN), rac-5-(O-prenyl)naringenin-4′,7-diacetate (5-O-PN), and rac-6-(1,1-dimethylallyl)naringenin (6-DMAN) were prepared by chemical synthesis and analyzed with respect to their toxicity and possible cell cycle effects in human acute myeloid leukemia (HL-60) cells. With the exception of 5-O-PN, all the other naringenins showed only weak toxic effects at concentrations below 50 µmol/l. A cell cycle analysis over several cell generations up to 4 days was carried out using the fluorescent dye carboxyfluorescein diacetate N-succinimidyl ester (CFSE) followed by propidium iodide (PI) staining at the end of the experiment. The well-studied flavonol quercetin was included in the analysis as a reference substance. All flavonoids affected cell proliferation, but the extent and the resulting changes in the proliferation pattern were specific for each substance. In contrast to the radical scavenging activity of quercetin, the tested flavanones showed no anti-oxidative properties using several different test systems. Similarly, the mitochondrial membrane potential (ΔΨm) was hardly effected by these compounds, while both menadione and quercetin strongly reduced the potential after 1 h of treatment. The reported chemical modification of interesting lead substances (like the strongly estrogenic 8-PN) presents a promising approach to modulate the properties of a relevant substance in a pharmacologically desirable way. The low toxicity and weak cytostatic properties of the tested naringenin derivatives is encouraging for further studies on known naringenin target molecules.

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The heat shock‐induced cell cycle arrest is attenuated by weak electromagnetic fields

Cited by 17 publications

References 45 publications

Expression of HSP72 after ELF‐EMF exposure in three cell lines

Expression of HSP72 after ELF‐EMF exposure in three cell lines

Cell Type Specific Redox Status is Responsible for Diverse Electromagnetic Field Effects

Toxicity and Cell Cycle Effects of Synthetic 8-Prenylnaringenin and Derivatives in Human Cells

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