DNA damage response and apoptosis induced by hyperthermia in human umbilical cord blood lymphocytes

Zastko, Lucián; Petrovičová, Petra; Račková, Anna; Jakl, Lukas; Jakušová, Viera; Markovà, Eva; Belyaev, Igor

doi:10.1016/j.tiv.2021.105127

Cited by 6 publications

(4 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These neurological disorders include changes in sleep habits [29], headache [30], and changes in EEG [31,32]. However, there are several studies indicating more harmful nonthermal effects on human health [33][34][35][36][37][38].…”

Section: Discussionmentioning

confidence: 99%

The Biocompatibility of Wireless Power Charging System on Human Neural Cells

et al. 2021

View full text Add to dashboard Cite

The progress in technology and science leads to the invention and use of many electrical devices in the daily lives of humans. In addition to that, people have been easily exposed to increased newly generated artificial electromagnetic waves. Exponential use of modern electronic devices has automatically led to increase in electromagnetic wave exposure. Therefore, we constructed the prototype of wireless power charging system to study the biocompatibility of electromagnetic field (EMF) generated by this system on various human cell lines. There are many studies indicating the negative bio-effect of EMF on various types of cells, such as induction of apoptosis. From the other point of view, these effects could rather be beneficial in the way, that they could eliminate the progress of various diseases or disorders. For that reason, we compared the impact of EMF (87 kHz, 0.3–1.2 mT, 30 min) on human normal as well as cancer cell lines based on morphological and cellular level. Our results suggested that EMF generated by wireless power charging systems does not have any detrimental effect on cell morphology, viability and cytoskeletal structures of human neural cells.

show abstract

Section: Discussionmentioning

confidence: 99%

The Biocompatibility of Wireless Power Charging System on Human Neural Cells

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Apoptosis may alter the number of visualized foci due to limited access of DNA markers to the DSB site. This was why we decided to analyze apoptosis along with foci to assess the effects of cal A. Apoptosis is usually assessed by annexin V-FITC/PI assay, but γH2AX pan-staining has also been used to this aim [ 26 , 27 , 28 , 40 ]. In line with previous studies [ 30 , 31 ], which reported that human lymphocytes undergo apoptosis within 4–24 h after irradiation in a dose-dependent manner, we did not observe the effect of irradiation on apoptosis with any assay 2 h post-irradiation.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Calyculin A Effect on γH2AX/53BP1 Focus Formation and Apoptosis in Human Umbilical Cord Blood Lymphocytes

Zastko

Račková

Petrovičová

et al. 2021

IJMS

Self Cite

View full text Add to dashboard Cite

Dephosphorylation inhibitor calyculin A (cal A) has been reported to inhibit the disappearance of radiation-induced γH2AX DNA repair foci in human lymphocytes. However, other studies reported no change in the kinetics of γH2AX focus induction and loss in irradiated cells. While apoptosis might interplay with the kinetics of focus formation, it was not followed in irradiated cells along with DNA repair foci. Thus, to validate plausible explanations for significant variability in outputs of these studies, we evaluated the effect of cal A (1 and 10 nM) on γH2AX/53BP1 DNA repair foci and apoptosis in irradiated (1, 5, 10, and 100 cGy) human umbilical cord blood lymphocytes (UCBL) using automated fluorescence microscopy and annexin V-FITC/propidium iodide assay/γH2AX pan-staining, respectively. No effect of cal A on γH2AX and colocalized γH2AX/53BP1 foci induced by low doses (≤10 cGy) of γ-rays was observed. Moreover, 10 nM cal A treatment decreased the number of all types of DNA repair foci induced by 100 cGy irradiation. 10 nM cal A treatment induced apoptosis already at 2 h of treatment, independently from the delivered dose. Apoptosis was also detected in UCBL treated with lower cal A concentration, 1 nM, at longer cell incubation, 20 and 44 h. Our data suggest that apoptosis triggered by cal A in UCBL may underlie the failure of cal A to maintain radiation-induced γH2AX foci. All DSB molecular markers used in this study responded linearly to low-dose irradiation. Therefore, their combination may represent a strong biodosimetry tool for estimation of radiation response to low doses. Assessment of colocalized γH2AX/53BP1 improved the threshold of low dose detection.

show abstract

“…Hyperthermia has the potential to decrease cell growth and cause alterations in the nuclei of the cells that are exposed to it, which leads to apoptosis. ( Kang et al, 2020 ; Zastko et al, 2021 ). Melatonin could enhance the number of apoptotic cells when this hormone is added to hyperthermia treatment, which is used on both U937 and HL-60 AML cell lines.…”

Section: Synergistic Cytotoxicity Of Melatonin and Anticancer Drugs I...mentioning

confidence: 99%

Melatonin as a regulator of apoptosis in leukaemia: molecular mechanism and therapeutic perspectives

Mafi,

Rismanchi,

Gholinezhad

et al. 2023

Front. Pharmacol.

View full text Add to dashboard Cite

Leukaemia is a dangerous malignancy that causes thousands of deaths every year throughout the world. The rate of morbidity and mortality is significant despite many advancements in therapy strategies for affected individuals. Most antitumour medications used now in clinical oncology use apoptotic signalling pathways to induce cancer cell death. Accumulated data have shown a direct correlation between inducing apoptosis in cancer cells with higher tumour regression and survival. Until now, the efficacy of melatonin as a powerful antitumour agent has been firmly established. A change in melatonin concentrations has been reported in multiple tumours such as endometrial, hematopoietic, and breast cancers. Findings show that melatonin’s anticancer properties, such as its prooxidation function and ability to promote apoptosis, indicate the possibility of utilizing this natural substance as a promising agent in innovative cancer therapy approaches. Melatonin stimulates cell apoptosis via the regulation of many apoptosis facilitators, including mitochondria, cytochrome c, Bcl-2, production of reactive oxygen species, and apoptosis receptors. This paper aimed to further assess the anticancer effects of melatonin through the apoptotic pathway, considering the role that cellular apoptosis plays in the pathogenesis of cancer. The effect of melatonin may mean that it is appropriate for use as an adjuvant, along with other therapeutic approaches such as radiotherapy and chemotherapy.

show abstract

DNA damage response and apoptosis induced by hyperthermia in human umbilical cord blood lymphocytes

Cited by 6 publications

References 32 publications

The Biocompatibility of Wireless Power Charging System on Human Neural Cells

The Biocompatibility of Wireless Power Charging System on Human Neural Cells

Evaluation of Calyculin A Effect on γH2AX/53BP1 Focus Formation and Apoptosis in Human Umbilical Cord Blood Lymphocytes

Melatonin as a regulator of apoptosis in leukaemia: molecular mechanism and therapeutic perspectives

Contact Info

Product

Resources

About