The cross-talk between Bax, Bcl2, caspases, and DNA damage in bystander HepG2 cells is regulated by γ-radiation dose and time of conditioned media transfer

ROS production in response to high-power microwave pulses induces p53 activation and DNA damage in brain cells: Radiosensitivity and biological dosimetry evaluation

“…Since microwave exposure can also directly cause DNA damage, which will help enhance p53 activation (Shahin et al, 2015;Mukherjee et al, 2022). We hypothesize that ROS generation and DNA damage may work in concert to control 3.5 GHz HPMinduced p53 activation and cell death.…”

“…Additionally, p53 generally exists in an essentially inactive state that is not very effective at binding to DNA and activating transcription. The ability of p53 to bind DNA and drive transcriptional activation is boosted, and its levels rise quickly, in response to DNA damage (Mukherjee et al, 2022).…”

“…HPM Induces the expression of p53/Caspase-3 dependent apoptosis (Figure 9). Numerous other cues besides ROS can also activate p53 (Mukherjee et al, 2022). Since 3.5 GHz HPM irradiation-induced p53 activation was partially inhibited by NAC in the current study, it is reasonable to hypothesize that ROS burst and DNA damage together may be responsible for upregulating p53 expression during 3.5 GHz HPM irradiationinduced apoptosis in astrocytes at the harmful dosage and may promoting DNA repair after 25 pulses in U87-MG directly by upregulating the expression of DNA repair genes which needs further exploration in future.…”

Radiation-induced Bystander Effect and Its Possible Countermeasures

“…In addition to the bystander signaling mechanisms, investigation of the dependence of signal strength on various irradiation parameters such as dose and post-irradiation aging of targeted cells is also necessary. Mukherjee et al studied the effect of dose-varied ICCM, collected at different post-irradiation times, on DNA damage and apoptosis of bystander cells [16]. In their study, different sets of culture media of human hepatocellular carcinoma HepG2 cells had undergone irradiation by γ-rays with doses of 2, 5, and 8 Gy; the respective ICCM was collected in the early and late postirradiated stages (1, 2, and 24 h) to transfer to unirradiated cells.…”

“…This study showed that compared to control (the directly irradiated cells), bystander cells had an increased level of H2AX phosphorylation, mitochondrial membrane depolarization, and elevation of intrinsic apoptotic pathway mediators such as p53, Bax, cas9, cas3, and PARP cleavage. These intrinsic apoptotic pathways in a nearby unirradiated cell (bystander cell), mediated by the bystander signals released from irradiated cell, is shown by the sketch in the scenario (1) in Figure 1 following reference [16]. The highest expression of the apoptosis markers was observed in 8 Gy irradiationinduced bystander cells, and the ICCM collected at the early time (1 or 2 h), though the 24 h ICCM induced the highest increase of H2AX and p53 phosphorylation and Bax levels.…”