P53 Archives - EMFSA https://www.emfsa.co.za/tag/p53/ Electromagnetic fields South Africa Thu, 28 Oct 2021 18:53:45 +0000 en-US hourly 1 https://wordpress.org/?v=7.1.3 https://www.emfsa.co.za/wp-content/uploads/2021/02/cropped-EMFSA_logo-fv-32x32.png P53 Archives - EMFSA https://www.emfsa.co.za/tag/p53/ 32 32 Apoptotic Effect of 1800 MHz Electromagnetic Radiation on NIH/3T3 Cells https://www.emfsa.co.za/research-and-studies/apoptotic-effect-of-1800-mhz-electromagnetic-radiation-on-nih-3t3-cells/ Wed, 29 Jan 2020 15:57:13 +0000 https://www.emfsa.co.za/?p=12048 Li, D.-Y.; Song, J.-D.; Liang, Z.-Y.; Oskouei, K.; Xiao, X.-Q.; Hou, W.-Z.; Li, J.-T.; Yang, Y.-S.; Wang, M.-L.; Murbach, M. Apoptotic Effect of 1800 MHz Electromagnetic Radiation on NIH/3T3 Cells. Int. J. Environ. Res. Public Health 2020, 17, 819. Abstract To investigate the effect of 1800 MHz electromagnetic radiation (EMR) on apoptosis, we exposed NIH/3T3 cells at 1800 […]

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]]> Li, D.-Y.; Song, J.-D.; Liang, Z.-Y.; Oskouei, K.; Xiao, X.-Q.; Hou, W.-Z.; Li, J.-T.; Yang, Y.-S.; Wang, M.-L.; Murbach, M. Apoptotic Effect of 1800 MHz Electromagnetic Radiation on NIH/3T3 Cells. Int. J. Environ. Res. Public Health 2020, 17, 819.

Abstract

To investigate the effect of 1800 MHz electromagnetic radiation (EMR) on apoptosis, we exposed NIH/3T3 cells at 1800 MHz with a specific absorption rate (SAR) of 2 W/kg intermittently for 12, 24, 36, and 48 h. After exposure, Cell Counting Kit-8 (CCK-8) and flow cytometry were used to detect cell viability and apoptosis; the expression of p53, a molecule with the key role in apoptosis, was measured by real-time qPCR, western blot, and immunofluorescence; and images of the structure of the mitochondria, directly reflecting apoptosis, were captured by electron microscopy. The results showed that the viability of cells in the 12, 36, and 48 h exposure groups significantly decreased compared with the sham groups; after 48 h of exposure, the percentage of late apoptotic cells in the exposure group was significantly higher. Real-time qPCR results showed that p53 mRNA in the 48 h exposure group was 1.4-fold of that in the sham group; significant differences of p53 protein fluorescence expression were observed between the exposure groups and the sham groups after 24 h and 48 h. The mitochondrial swelling and vesicular morphology were found in the electron microscopy images after 48 h exposure. These findings demonstrated 1800 MHz, SAR 2 W/kg EMR for 48 h may cause apoptosis in NIH/3T3 cells and that this apoptosis might be attributed to mitochondrial damage and upregulation of p53 expression.

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ijerph-17-00819

The authors note that: “The potential biological effects of EMR have not been proved and current research data are insufficient to provide strong evidence of the possible health risks. The above findings indicate that there is a need for more scientific research support on the bioeffects of EMR“.

“In conclusion, this study reveals an increase in the apoptosis rate, upregulation of p53, and mitochondrial damage in NIH/3T3 cells are all caused by 1800 MHz, 2 W/kg EMR. We provide new experimental evidence for the biological effects of EMR on cells and also provide a reference for studying the health effects of long-term EMR exposure.

Figure 6: The sham groups and 0 h group cells showed normal mitochondrial structure, while NIH/3T3 cells treated by EMR appeared to be swollen and had vesicular morphology. The longer the irradiation time, the more frequent the appearance of altered mitochondria morphology (e.g., vesicular morphology and swelling). This means that EMR may cause damage to the mitochondrial structure.

See Figure 6. EMR at 1800 MHz may cause damage to mitochondria in NIH/3T3 cells. Electron microscopy was used to detect mitochondrial structure.

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]]> The role of radiation induced oxidative stress as a regulator of radio-adaptive responses https://www.emfsa.co.za/research-and-studies/the-role-of-radiation-induced-oxidative-stress-as-a-regulator-of-radio-adaptive-responses/ Sun, 26 Jan 2020 20:52:05 +0000 https://www.emfsa.co.za/?p=12003 Mohsen Sisakht, Maryam Darabian, Amir Mahmoodzadeh, Ali Bazi, Sayed Mohammad Shafiee, Pooneh Mokarram & Zahra Khoshdel (2020) The role of radiation induced oxidative stress as a regulator of radio-adaptive responses, International Journal of Radiation Biology, 96:5, 561-576, DOI: 10.1080/09553002.2020.1721597 Abstract Purpose Various sources of radiation including radiofrequency, electromagnetic radiation (EMR), low- dose X-radiation, low-level microwave radiation and ionizing radiation (IR) are indispensable […]

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  • Mohsen Sisakht, Maryam Darabian, Amir Mahmoodzadeh, Ali Bazi, Sayed Mohammad Shafiee, Pooneh Mokarram & Zahra Khoshdel (2020) The role of radiation induced oxidative stress as a regulator of radio-adaptive responses, International Journal of Radiation Biology, 96:5, 561-576, DOI: 10.1080/09553002.2020.1721597

    • Abstract

    Purpose

    Various sources of radiation including radiofrequency, electromagnetic radiation (EMR), low- dose X-radiation, low-level microwave radiation and ionizing radiation (IR) are indispensable parts of modern life. In the current review, we discussed the adaptive responses of biological systems to radiation with a focus on the impacts of radiation-induced oxidative stress (RIOS) and its molecular downstream signaling pathways.

    Materials and Methods

    A comprehensive search was conducted in Web of Sciences, PubMed, Scopus, Google Scholar, Embase, and Cochrane Library. Keywords included Mesh terms of “radiation”, “electromagnetic radiation”, “adaptive immunity”, “oxidative stress”, and “immune checkpoints”. Manuscript published up until December 2019 were included.

    Results

    RIOS induces various molecular adaptors connected with adaptive responses in radiation exposed cells. One of these adaptors includes p53 which promotes various cellular signaling pathways. RIOS also activates the intrinsic apoptotic pathway by depolarization of the mitochondrial membrane potential and activating the caspase apoptotic cascade. RIOS is also involved in radiation-induced proliferative responses through interaction with mitogen-activated protein kinases (MAPks) including p38 MAPK, ERK, and c-Jun N-terminal kinase (JNK). Protein kinase B (Akt)/phosphoinositide 3-kinase (PI3K) signaling pathway has also been reported to be involved in RIOS-induced proliferative responses. Furthermore, RIOS promotes genetic instability by introducing DNA structural and epigenetic alterations, as well as attenuating DNA repair mechanisms. Inflammatory transcription factors including macrophage migration inhibitory factor (MIF), nuclear factor κB (NF-κB), and signal transducer and activator of transcription-3 (STAT-3) paly major role in RIOS-induced inflammation.

    Results

    In conclusion, RIOS considerably contributes to radiation induced adaptive responses. Other possible molecular adaptors modulating RIOS-induced responses are yet to be divulged in future studies.

    https://www.tandfonline.com/doi/full/10.1080/09553002.2020.1721597

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