Chronic Exposure of Rats to 100-MHz (CW) Radiofrequency Radiation: Assessment of Biological Effects

1981 ◽  
Vol 86 (3) ◽  
pp. 488 ◽  
Author(s):  
Ralph J. Smialowicz ◽  
J. S. Ali ◽  
Ezra Berman ◽  
Steve J. Bursian ◽  
James B. Kinn ◽  
...  
2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Sophia Murat El Houdigui ◽  
Christelle Adam-Guillermin ◽  
Giovanna Loro ◽  
Caroline Arcanjo ◽  
Sandrine Frelon ◽  
...  

AbstractContamination of the environment after the Chernobyl and Fukushima Daiichi nuclear power plant (NPP) disasters led to the exposure of a large number of humans and wild animals to radioactive substances. However, the sub-lethal consequences induced by these absorbed radiological doses remain understudied and the long-term biological impacts largely unknown. We assessed the biological effects of chronic exposure to ionizing radiation (IR) on embryonic development by exposing zebrafish embryo from fertilization and up to 120 hours post-fertilization (hpf) at dose rates of 0.5 mGy/h, 5 mGy/h and 50 mGy/h, thereby encompassing the field of low dose rates defined at 6 mGy/h. Chronic exposure to IR altered larval behaviour in a light-dark locomotor test and affected cardiac activity at a dose rate as low as 0.5 mGy/h. The multi-omics analysis of transcriptome, proteome and transcription factor binding sites in the promoters of the deregulated genes, collectively points towards perturbations of neurogenesis, muscle development, and retinoic acid (RA) signaling after chronic exposure to IR. Whole-mount RNA in situ hybridization confirmed the impaired expression of the transcription factors her4.4 in the central nervous system and myogenin in the developing muscles of exposed embryos. At the organ level, the assessment of muscle histology by transmission electron microscopy (TEM) demonstrated myofibers disruption and altered neuromuscular junctions in exposed larvae at 5 mGy/h and 50 mGy/h. The integration of these multi-level data demonstrates that chronic exposure to low dose rates of IR has an impact on neuronal and muscle progenitor cells, that could lead to motility defects in free swimming larvae at 120 hpf. The mechanistic understanding of these effects allows us to propose a model where deregulation of RA signaling by chronic exposure to IR has pleiotropic effects on neurogenesis and muscle development.


Author(s):  
Beatrice Campanella ◽  
Laura Colombaioni ◽  
Edoardo Benedetti ◽  
Agostino Di Ciaula ◽  
Lisa Ghezzi ◽  
...  

A mini review of the toxicity of Thallium (Tl) at low doses is herein presented. Thallium has severe toxicity. Although its acute biological effects have been widely investigated and are well known, its biological effects on human health and in cell cultures at low doses (<100 μg/L) due, for example, to Tl chronic exposure via consumption of contaminated water or foods, have often been overlooked or underestimated. Relatively few papers have been published on this topic and are herein reviewed to provide a focused scientific opinion in the light of current worldwide regulatory issues.


1993 ◽  
Vol 5 (3) ◽  
pp. 244-247
Author(s):  
Kenichi Saito ◽  
◽  
Yukari Tsuchida ◽  
Kouichiro Yamada ◽  
Masahiro Sugiyamaand Nobuo Goto ◽  
...  

The present study consists of two experiments. The first experiment investigates the influence of chronic exposure of 428MHz radio frequency (RF) with an incident power density of 4mW/cm² on the development of chick embryos. Prolonged incubation was found in exposured eggs as compared to the non-exposured (22 vs 21 days). The average thymus weight in both sexes was smaller than that of the control. RF exposure also led to a significant decrease in the thymic cell density of female chicks. The second experiment was conducted in order to reveal the effects of chronic exposure of the immune system of mice exposed to 428MHz-RF with an incident power density of 1mW/cm² during pregnancy. It was found that RF exposure alters the immune system of mice. RF suppressed the cell-mediated immune-competence by local delayed hypersensitivity. These results suggest that chronic exposure of 428MHz-RF radiation induce biological effects on chick embryo and mice.


2003 ◽  
Vol 160 (2) ◽  
pp. 143-151 ◽  
Author(s):  
Marie La Regina ◽  
Eduardo G. Moros ◽  
William F. Pickard ◽  
William L. Straube ◽  
Jack Baty ◽  
...  

2019 ◽  
Vol 26 (8) ◽  
pp. 713-725 ◽  
Author(s):  
Fiorenza Gianì ◽  
Giuseppe Pandini ◽  
Nunzio Massimo Scalisi ◽  
Paolo Vigneri ◽  
Carmine Fazzari ◽  
...  

Thyroid cancer incidence is increased in volcanic areas where environment pollution biocontaminates residents. Tungsten (W) is the most increased heavy metal in drinking water of Mount Etna volcanic area where it exceeds the normal range in the urine of 27% inhabitants. The possible connection between increased tungsten and thyroid cancer has never been studied. We investigated in vitro the effect tungsten on both human thyrocytes in primary culture, thyrospheres (aggregates of stem/precursor thyroid cells) and thyrocytes differentiated from tungsten-exposed thyrospheres. Chronic exposure to low-dose (nanomolar range, as in the urines of volcanic area residents) soluble tungsten had major biological effects on thyroid stem/precursor cells, promoting growth with a biphasic (hormetic) dose-response and reducing apoptosis. No such effects were observed in mature thyrocytes. In addition, tungsten-exposed thyrospheres had abnormal expression of genes commonly altered also in thyroid cancer and increased activation of the DNA-repair proteins H2AX and 53BP1. Moreover, exposure to tungsten decreased thyrosphere differentiation, as indicated by the reduced expression of thyroid-specific genes in derived thyrocytes that also showed preneoplastic changes such as increased anchorage-independent growth, clonogenic growth and migration capacity. The mechanism of action of tungsten on thyroid stem/precursor cells is unclear but involves membrane G-proteins and activation of the ERK signaling pathway. These data indicate that chronic exposure to slightly increased tungsten, harmless for mature thyrocytes, importantly affects the biology of stem/precursor thyroid cells and of their progeny, inducing characteristics of preneoplastic transformation.


2021 ◽  
Vol 93 (2) ◽  
Author(s):  
LARISA ILIJIN ◽  
MARIJA MRDAKOVIĆ ◽  
DAJANA TODOROVIĆ ◽  
MILENA VLAHOVIĆ ◽  
ANJA GRČIĆ ◽  
...  

1988 ◽  
Vol 6 (6) ◽  
pp. 655-660 ◽  
Author(s):  
James Peeling ◽  
John S. Lewis ◽  
Martin Samoiloff ◽  
Ernst Bock ◽  
Edward Tomchuk

2019 ◽  
Author(s):  
Samia Ruby ◽  
Jesús Marín-Sáez ◽  
Aurélie Fildier ◽  
Audrey Buleté ◽  
Myriam Abdallah ◽  
...  

BackgroundAryl phosphate esters (APEs), a main class of organophosphorus ester molecules, are widely used and commonly present in the environment. Health hazards associated with these compounds remain largely unknown and the effects of diphenyl phosphate (DPhP), one of their most frequent derivatives in human samples, are poorly characterised.ObjectiveOur aim was to investigate whether DPhP per se may represent a more relevant marker of exposure to APEs and determine its potential deleterious biological effects in chronically exposed mice.MethodsConventional animals (FVB mice) were acutely (intravenous or oral gavage) or chronically (0.1 mg.mL-1, 1 mg.mL-1, 10 mg.mL-1 in drink water) exposed to relevant doses of DPhP or triphenyl phosphate (TPhP), one of its main precursors in the environment. Both molecules were measured in blood and other relevant tissues by liquid chromatography-mass spectrometry (LC-MS). Biological effects of chronic DPhP exposure were addressed through liver multi-omics analysis combining mRNA extraction and sequencing to high resolution LC-MS to determine the corresponding metabolic profile. Deep statistical exploration was performed to extract correlated information, guiding further physiological analyses (immunohistochemistry (IHC) and animal growth measurement).ResultsAcute and chronic exposure to DPhP led to significant levels of this molecule in blood and other tissues, an effect missing with TPhP. Multi-omics analysis confirmed the existence of biological effects of DPhP, even at a very low dose of 0.1 mg.mL-1 in drinking water. Chemical structural homology and pathway mapping demonstrated a clear reduction of the fatty-acid catabolic processes centred on acylcarnitine and mitochondrial β-oxidation. Interestingly, mRNA expression confirmed and extended these observations by demonstrating at all tested doses the overall repression of genes involved in lipid catabolic processes and regulated by PPARα, a master regulator of β-oxidation and its associated ketogenesis. IHC analysis confirmed the alteration of these pathways by showing a specific downregulation of Hmgcs2, a kernel target gene of PPARα, at all doses tested, and surprisingly, a strong reduction of the lipid droplet content only at the highest dose. Overall, DPhP absorption led to weight loss, which was significant using the highest dose.ConclusionsOur results suggest that in mice, the effects of chronic exposure to DPhP, even at a low dose, are not negligible. Fatty acid metabolism in the liver in particular is essential for controlling fast and feast periods with adverse consequences on the overall physiology. Therefore, the impact of DPhP on circulating fat, cardiovascular and metabolic disease incidence deserves, in light of our results, further investigations.


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