The HL-60 human promyelocytic cell line constitutes an effective in vitro model for evaluating toxicity, oxidative stress and necrosis/apoptosis after exposure to black carbon particles and 2.45 GHz radio frequency

Abstract

The HL-60 human promyelocytic cell line constitutes an effective in vitro model for evaluating toxicity, oxidative stress and necrosis/apoptosis after exposure to black carbon particles and 2.45 GHz radio frequency Benavides RAS, Leiro-Vidal JM, Rodriguez-Gonzalez JA, Ares-Pena FJ, López-Martín E. The HL-60 human promyelocytic cell line constitutes an effective in vitro model for evaluating toxicity, oxidative stress and necrosis/apoptosis after exposure to black carbon particles and 2.45 GHz radio frequency. Sci Total Environ. 2023 Jan 9;867:161475. doi: 10.1016/j.scitotenv.2023.161475. Highlights • RF+ BC increase ROS production and have an oxidant-antioxidant effect on HL-60 cells. • RF or BC exposure activates expression of the anti-apoptotic gene BCL2a in HL-60 cells. • Cell necrosis due to BC was manifested at 24 h, while cell death (necrosis and/or apoptosis) due to irradiation and/or BC lasted up to 48 h. • Interaction between RF and BC enhanced cell toxicity in the promyelocytic cell line Abstract The cellular and molecular mechanisms by which atmospheric pollution from particulate matter and/or electromagnetic fields (EMFs) may prove harmful to human health have not been extensively researched. We analyzed whether the combined action of EMFs and black carbon (BC) particles induced cell damage and a pro- apoptotic response in the HL-60 promyelocytic cell line when exposed to 2.45 GHz radio frequency (RF) radiation in a gigahertz transverse electromagnetic (GTEM) chamber at sub-thermal specific absorption rate (SAR) levels. RF and BC induced moderately significant levels of cell damage in the first 8 or 24 h for all exposure times/doses and much greater damage after 48 h irradiation and the higher dose of BC. We observed a clear antiproliferative effect that increased with RF exposure time and BC dose. Oxidative stress or ROS production increased with time (24 or 48 h of radiation), BC dose and the combination of both. Significant differences between the proportion of damaged and healthy cells were observed in all groups. Both radiation and BC participated separately and jointly in triggering necrosis and apoptosis in a programmed way. Oxidative-antioxidant action activated mitochondrial anti-apoptotic BCL2a gene expression after 24 h irradiation and exposure to BC. After irradiation of the cells for 48 h, expression of FASR cell death receptors was activated, precipitating the onset of pro-apoptotic phenomena and expression and intracellular activity of caspase-3 in the mitochondrial pathways, all of which can lead to cell death. Our results indicate that the interaction between BC and RF modifies the immune response in the human promyelocytic cell line and that these cells had two fates mediated by different pathways: necrosis and mitochondria-caspase dependent apoptosis. The findings may be important in regard to antimicrobial, inflammatory and autoimmune responses in humans. Conclusions Combined exposure to 2.45 Ghz RF and to BC over a period of 48 h caused very high levels of toxicity in a HL-60 cell line and triggered an antiproliferative effect that was dependent on the BC dose and exposure time. Activation the expression of antioxidant BCL2a and initial expression of the FAS cell death receptors, with no apparent activation of caspase-8, indicated mitochondrial cell damage due to triggering of apoptosis through a caspase-dependent pathway (increased caspase-3). However, cell death did not seem to be mediated by apoptosis alone, at least not caspase-dependent apoptosis, in any of the groups. This leads us to consider that other forms of programmed cell death may be activated by one or both stressors (Barati et al., 2021). The cell damage induced in vitro by the combination of both RF and BC in promyelocytic cells indicate ineffective antimicrobial function and increased immune or autoimmune tolerance (Glencross et al., 2020). pubmed.ncbi.nlm.nih.gov

AI evidence extraction

Main findings

In HL-60 cells exposed to 2.45 GHz RF in a GTEM chamber at sub-thermal SAR levels and/or black carbon (BC), RF and BC each induced moderate cell damage at early timepoints (8–24 h) and greater damage after 48 h and higher BC dose. ROS/oxidative stress increased with radiation time, BC dose, and combined exposure; both stressors separately and jointly were associated with necrosis and apoptosis-related signaling (including BCL2a induction at 24 h and FASR/caspase-3 activation at 48 h), and the RF–BC interaction was reported to enhance toxicity.

Outcomes measured

• cell damage/toxicity
• oxidative stress / ROS production
• necrosis
• apoptosis
• antiproliferative effect
• gene expression (BCL2a, FASR)
• caspase-3 activity

Limitations

• In vitro cell-line model (HL-60); findings may not generalize to humans or in vivo conditions
• Specific absorption rate (SAR) described as sub-thermal but numerical SAR values not provided in abstract
• Exposure/dose details for black carbon and full experimental design/sample sizes not reported in abstract
• Co-exposure design (RF plus particulate matter) may limit attribution to RF alone

Suggested hubs

• school-wi-fi (0.55)
  Uses 2.45 GHz RF, a frequency commonly associated with Wi‑Fi; study examines biological effects at this frequency (in vitro).

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    "study_type": "in_vitro",
    "exposure": {
        "band": "RF",
        "source": null,
        "frequency_mhz": 2450,
        "sar_wkg": null,
        "duration": "8–48 h (reported timepoints include 8, 24, 48 h)"
    },
    "population": "HL-60 human promyelocytic cell line",
    "sample_size": null,
    "outcomes": [
        "cell damage/toxicity",
        "oxidative stress / ROS production",
        "necrosis",
        "apoptosis",
        "antiproliferative effect",
        "gene expression (BCL2a, FASR)",
        "caspase-3 activity"
    ],
    "main_findings": "In HL-60 cells exposed to 2.45 GHz RF in a GTEM chamber at sub-thermal SAR levels and/or black carbon (BC), RF and BC each induced moderate cell damage at early timepoints (8–24 h) and greater damage after 48 h and higher BC dose. ROS/oxidative stress increased with radiation time, BC dose, and combined exposure; both stressors separately and jointly were associated with necrosis and apoptosis-related signaling (including BCL2a induction at 24 h and FASR/caspase-3 activation at 48 h), and the RF–BC interaction was reported to enhance toxicity.",
    "effect_direction": "harm",
    "limitations": [
        "In vitro cell-line model (HL-60); findings may not generalize to humans or in vivo conditions",
        "Specific absorption rate (SAR) described as sub-thermal but numerical SAR values not provided in abstract",
        "Exposure/dose details for black carbon and full experimental design/sample sizes not reported in abstract",
        "Co-exposure design (RF plus particulate matter) may limit attribution to RF alone"
    ],
    "evidence_strength": "low",
    "confidence": 0.7800000000000000266453525910037569701671600341796875,
    "peer_reviewed_likely": "yes",
    "keywords": [
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        "2.45 GHz",
        "radiofrequency",
        "RF",
        "GTEM chamber",
        "sub-thermal SAR",
        "black carbon",
        "particulate matter",
        "oxidative stress",
        "ROS",
        "necrosis",
        "apoptosis",
        "BCL2a",
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