scholarly journals The effects of 50 Hz magnetic field exposure on DNA damage and cellular functions in various neurogenic cells

2017 ◽  
Vol 58 (4) ◽  
pp. 474-486 ◽  
Author(s):  
Liling Su ◽  
Aziguli Yimaer ◽  
Xiaoxia Wei ◽  
Zhengping Xu ◽  
Guangdi Chen
Keyword(s):  
Magnetic Field ◽  
Dna Damage ◽  
Cortical Neurons ◽  
Cell Cycle Progression ◽  
Low Frequency ◽  
Epidemiological Studies ◽  
Neurogenic Tumor ◽  
Dna Double Strand Breaks ◽  
Cellular Functions ◽  
Field Exposure

Abstract Epidemiological studies have indicated a possible association between extremely low–frequency magnetic field (ELF-MF) exposure and the risk of nervous system diseases. However, laboratory studies have not provided consistent results for clarifying this association, despite many years of studies. In this study, we have systematically investigated the effects of 50 Hz MF exposure on DNA damage and cellular functions in both neurogenic tumor cell lines (U251, A172, SH-SY5Y) and primary cultured neurogenic cells from rats (astrocytes, microglia, cortical neurons). The results showed that exposure to a 50 Hz MF at 2.0 mT for up to 24 h did not influence γH2AX foci formation (an early marker of DNA double-strand breaks) in any of six different neurogenic cells. Exposure to a 50 Hz MF did not affect cell cycle progression, cell proliferation or cell viability in neurogenic tumor U251, A172 or SH-SY5Y cells. Furthermore, the MF exposure for 24 h did not significantly affect the secretion of cytokines (TNF-α, IL-6 or IL-1β) in astrocytes or microglia, or the phagocytic activity of microglia. In addition, MF exposure for 1 h per day did not significantly influence expression levels of microtubule-associated protein tau, microtubule-associated protein 2, postsynaptic density 95 or gephyrin in cortical neurons, indicating an absence of effects of MF exposure on the development of cortical neurons. In conclusion, our data suggest that exposure to a 50 Hz MF at 2.0 mT did not elicit DNA damage effects or abnormal cellular functions in the neurogenic cells studied.

Fifty hertz extremely low-frequency magnetic field exposure elicits redox and trophic response in rat-cortical neurons

2009 ◽  
Vol 219 (2) ◽  
pp. 334-343 ◽  
Author(s):  
Silvia Di Loreto ◽  
Stefano Falone ◽  
Valentina Caracciolo ◽  
Pierluigi Sebastiani ◽  
Antonella D'Alessandro ◽  
...  
Keyword(s):  
Magnetic Field ◽  
Cortical Neurons ◽  
Low Frequency ◽  
Field Exposure ◽  
Magnetic Field Exposure ◽  
Extremely Low Frequency ◽  
Frequency Magnetic Field ◽  
Rat Cortical Neurons

Exposure of adults to extremely low frequency magnetic field in France: results of the EXPERS study

2019 ◽  
Vol 55 (1) ◽  
pp. 39-50 ◽  
Author(s):  
I. Magne ◽  
M. Souques ◽  
L. Courouve ◽  
A. Duburcq ◽  
E. Remy ◽  
...  
Keyword(s):  
Magnetic Field ◽  
Low Frequency ◽  
Personal Exposure ◽  
Epidemiological Studies ◽  
Field Exposure ◽  
Extremely Low Frequency ◽  
Measurement Protocol ◽  
Main Variable ◽  
Frequency Magnetic Field ◽  
The Magnetic Field

Assessing the exposure of adults to magnetic field is a central point in the context of epidemiological studies. The EXPERS study is the first study at national scale in Europe with measurements of personal exposure to extremely low frequency magnetic fields, involving 1046 French adults with 24 h personal measurements. The proportion of adults with a 24 h AM of ≥ 1 µT was 2.1% for all adults and 0.3% for adults for which no alarm clock was identified, as this requirement of the measurement protocol was sometimes not respected. The alarm clocks were the main variable linked to the adults’ exposure measurements. The vicinity of the home to a high voltage power line increased the magnetic field exposure. However, only 1.7% of the adults were living close to a 63 to 400 kV overhead line, and only one of them had a personal exposure ≥ 1 μT with an AM of 1.1 μT. The exposure of adults was also correlated with some characteristics of the home and its environment, and some durations of activities, such as the duration of work and the duration in rail transport. The distribution of adults’ personal exposure was significantly different from the distribution of exposure during sleep, and from the distribution of exposure assessed from measurements during sleep and work. This highlights the complexity of the exposure assessment in epidemiological studies.

scholarly journals Bromodomain proteins: repairing DNA damage within chromatin

2017 ◽  
Vol 372 (1731) ◽  
pp. 20160286 ◽  
Author(s):  
Li-Ya Chiu ◽  
Fade Gong ◽  
Kyle M. Miller
Keyword(s):  
Dna Damage ◽  
Chromatin Modification ◽  
Chromatin Remodelling ◽  
Dna Double Strand Breaks ◽  
Dna Breaks ◽  
Cellular Functions ◽  
Strand Breaks ◽  
Bromodomain Proteins ◽  
Molecular Signals ◽  
Key Participants

Genome surveillance and repair, termed the DNA damage response (DDR), functions within chromatin. Chromatin-based DDR mechanisms sustain genome and epigenome integrity, defects that can disrupt cellular homeostasis and contribute to human diseases. An important chromatin DDR pathway is acetylation signalling which is controlled by histone acetyltransferase (HAT) and histone deacetylase (HDAC) enzymes, which regulate acetylated lysines within proteins. Acetylated proteins, including histones, can modulate chromatin structure and provide molecular signals that are bound by acetyl-lysine binders, including bromodomain (BRD) proteins. Acetylation signalling regulates several DDR pathways, as exemplified by the preponderance of HATs, HDACs and BRD proteins that localize at DNA breaks to modify chromatin for lesion repair. Here, we explore the involvement of acetylation signalling in the DDR, focusing on the involvement of BRD proteins in promoting chromatin remodelling to repair DNA double-strand breaks. BRD proteins have widespread DDR functions including chromatin remodelling, chromatin modification and transcriptional regulation. We discuss mechanistically how BRD proteins read acetylation signals within chromatin to trigger DDR and chromatin activities to facilitate genome–epigenome maintenance. Thus, DDR pathways involving BRD proteins represent key participants in pathways that preserve genome–epigenome integrity to safeguard normal genome and cellular functions. This article is part of the themed issue ‘Chromatin modifiers and remodellers in DNA repair and signalling’.

scholarly journals Sustained CHK2 activity, but not ATM activity, is critical to maintain a G1 arrest after DNA damage in untransformed cells

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Iraia García-Santisteban ◽  
Alba Llopis ◽  
Lenno Krenning ◽  
Jon Vallejo-Rodríguez ◽  
Bram van den Broek ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Cycle Progression ◽  
Double Strand Breaks ◽  
G1 Arrest ◽  
Dna Double Strand Breaks ◽  
Independent Manner ◽  
Cycle Progression ◽  
Strand Breaks ◽  
G1 Checkpoint ◽  
The Impact

Abstract Background The G1 checkpoint is a critical regulator of genomic stability in untransformed cells, preventing cell cycle progression after DNA damage. DNA double-strand breaks (DSBs) recruit and activate ATM, a kinase which in turn activates the CHK2 kinase to establish G1 arrest. While the onset of G1 arrest is well understood, the specific role that ATM and CHK2 play in regulating G1 checkpoint maintenance remains poorly characterized. Results Here we examine the impact of ATM and CHK2 activities on G1 checkpoint maintenance in untransformed cells after DNA damage caused by DSBs. We show that ATM becomes dispensable for G1 checkpoint maintenance as early as 1 h after DSB induction. In contrast, CHK2 kinase activity is necessary to maintain the G1 arrest, independently of ATM, ATR, and DNA-PKcs, implying that the G1 arrest is maintained in a lesion-independent manner. Sustained CHK2 activity is achieved through auto-activation and its acute inhibition enables cells to abrogate the G1-checkpoint and enter into S-phase. Accordingly, we show that CHK2 activity is lost in cells that recover from the G1 arrest, pointing to the involvement of a phosphatase with fast turnover. Conclusion Our data indicate that G1 checkpoint maintenance relies on CHK2 and that its negative regulation is crucial for G1 checkpoint recovery after DSB induction.

Assessment of extremely low frequency magnetic field exposure from GSM mobile phones

2013 ◽  
Vol 35 (3) ◽  
pp. 210-221 ◽  
Author(s):  
Carolina Calderón ◽  
Darren Addison ◽  
Terry Mee ◽  
Richard Findlay ◽  
Myron Maslanyj ◽  
...  
Keyword(s):  
Magnetic Field ◽  
Mobile Phones ◽  
Low Frequency ◽  
Field Exposure ◽  
Magnetic Field Exposure ◽  
Extremely Low Frequency ◽  
Frequency Magnetic Field

scholarly journals The chromatin-remodeling factor CHD4 coordinates signaling and repair after DNA damage

2010 ◽  
Vol 190 (5) ◽  
pp. 731-740 ◽  
Author(s):  
Dorthe Helena Larsen ◽  
Catherine Poinsignon ◽  
Thorkell Gudjonsson ◽  
Christoffel Dinant ◽  
Mark R. Payne ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Repair ◽  
Chromatin Remodeling ◽  
Cell Cycle Progression ◽  
Clonogenic Survival ◽  
Dna Double Strand Breaks ◽  
Checkpoint Signaling ◽  
Strand Breaks ◽  
Delay Cell

In response to ionizing radiation (IR), cells delay cell cycle progression and activate DNA repair. Both processes are vital for genome integrity, but the mechanisms involved in their coordination are not fully understood. In a mass spectrometry screen, we identified the adenosine triphosphate–dependent chromatin-remodeling protein CHD4 (chromodomain helicase DNA-binding protein 4) as a factor that becomes transiently immobilized on chromatin after IR. Knockdown of CHD4 triggers enhanced Cdc25A degradation and p21Cip1 accumulation, which lead to more pronounced cyclin-dependent kinase inhibition and extended cell cycle delay. At DNA double-strand breaks, depletion of CHD4 disrupts the chromatin response at the level of the RNF168 ubiquitin ligase, which in turn impairs local ubiquitylation and BRCA1 assembly. These cell cycle and chromatin defects are accompanied by elevated spontaneous and IR-induced DNA breakage, reduced efficiency of DNA repair, and decreased clonogenic survival. Thus, CHD4 emerges as a novel genome caretaker and a factor that facilitates both checkpoint signaling and repair events after DNA damage.

scholarly journals Cluster Analysis of Residential Personal Exposure to ELF Magnetic Field in Children: Effect of Environmental Variables

2019 ◽  
Vol 16 (22) ◽  
pp. 4363 ◽  
Author(s):  
Gabriella Tognola ◽  
Emma Chiaramello ◽  
Marta Bonato ◽  
Isabelle Magne ◽  
Martine Souques ◽  
...  
Keyword(s):  
Magnetic Field ◽  
Cluster Analysis ◽  
Harmonic Component ◽  
Low Frequency ◽  
Electric Heating ◽  
Personal Exposure ◽  
Electric Networks ◽  
Field Exposure ◽  
Indoor Exposure ◽  
Exposure Patterns

Personal exposure to Extremely Low Frequency Magnetic Fields (ELF MF) in children is a very timely topic. We applied cluster analysis to 24 h indoor personal exposures of 884 children in France to identify possible common patterns of exposures. We investigated how electric networks near child home and other variables potentially affecting residential exposure, such as indoor sources of ELF MF, the age and type of the residence and family size, characterized the magnetic field exposure patterns. We identified three indoor personal exposure patterns: children living near overhead lines of high (63–150 kV), extra-high (225 kV) and ultra-high voltage (400 kV) were characterized by the highest exposures; children living near underground networks of low (400 V) and mid voltage (20 kV) and substations (20 kV/400 V) were characterized by mid exposures; children living far from electric networks had the lowest level of exposure. The harmonic component was not relevant in discriminating the exposure patterns, unlike the 50 Hz or broadband (40–800 Hz) component. Children using electric heating appliances, or living in big buildings or in larger families had generally a higher level of personal indoor exposure. Instead, the age of the residence was not relevant in differentiating the exposure patterns.

Sign in / Sign up

Export Citation Format

Share Document