The role of Biophotons in cellular senescence.

2025 · Mixed · Low evidence

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MixedLow evidencePaper 6854

Study snapshot

Publicationmanual · 2025

Study typein_vitro

Reported directionMixed

Evidence ratingLow

Abstract

Senescence is the irreversible arrest of cell proliferation. While serving as a natural barrier against mutation progression, senescence's metabolic activity and elevated ROS levels can pose significant health risks. Concurrently, cellular metabolic processes, including mitochondrial respiration, are known to emit ultra-weak photons (biophotons), primarily generated through ROS production. There is increasing evidence that cells can influence each other non-chemically via biophotons. In this study, I aim to elucidate the potential impact of both intrinsic biophotonic emissions and extrinsic light exposure on cellular senescence. To achieve this, I developed, utilising doxorubicin (Dox), four different senescence models: two cancer (MCF7 breast and A549 lung) and two non-cancer cell lines (MCF10A breast and IMR-90 lung fibroblasts). Dox-treated cells showed senescentrelated physiological changes, including decreased proliferation (P ≤ 0.05), increased betagalactosidase activity (P ≤ 0.001), increased ROS (P ≤ 0.01), mitochondrial membrane potential (P ≤ 0.01) and calcium (Ca2+) levels (P ≤ 0.01). Then, to investigate potential biophotonic communication, I utilised a customised assay to detect non-chemical signalling, showing an increasing oxygen consumption rate in isolated mitochondria from senescent MCF10A (0.0029% per second; P < 0.0001), MCF7 (0.0042% per second; P < 0.0001) and A549 cells (0.0017% per second; P < 0.0001). Additionally, photons emitted by isolated mitochondria from senescent MCF10A cells were monitored via an ultra-sensitive light detector, confirming biophotonic activity (1.86 ± 0.82 photons per 10 seconds; P ≤ 0.05). Further comparison of mitochondrial non-chemical signalling between senescent and nonsenescent cells revealed distinct biophotonic communication across the three tested senescent cell lines, with significant differences compared to their non-senescent cellular controls (MCF10A and MCF7: P ≤ 0.0001; A549: P ≤ 0.05). In addition, I have shown that cells interact with external light, as exposure to near-infrared (NIR) light (734 nm) increased senescent levels in the cancer cell lines (P ≤ 0.01), associated with increased ROS production (P ≤ 0.05), mitochondrial membrane potential (P ≤ 0.05), and intracellular Ca2+ levels (P ≤ 0.05), but not in the two non-cancer populations. My work demonstrates that biophotons and extracellular light (NIR light exposure) may play a significant role in senescence and open novel insights for non-invasively influencing cellular processes.

Machine Enhanced Logic

AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typein_vitro

Effect directionmixed

PopulationCell lines: MCF7 breast cancer, A549 lung cancer, MCF10A non-cancer breast, and IMR-90 lung fibroblasts; doxorubicin-induced senescence models with near-infrared light exposure in some experiments.

Sample sizeNot supplied

ExposureNot supplied

Evidence strengthLowConfidence: 89% · Peer reviewed: unknown

Main findings

Doxorubicin-treated cells showed senescence-related changes including decreased proliferation and increased beta-galactosidase activity, ROS, mitochondrial membrane potential, and Ca2+ levels. Isolated mitochondria from several senescent cell lines showed increased oxygen consumption and detectable photon emission, with significant differences in non-chemical signalling versus non-senescent controls. Near-infrared light exposure at 734 nm increased senescent levels and related mitochondrial/oxidative markers in cancer cell lines but not in the two non-cancer cell populations.

Outcomes measured

Cellular senescence
Cell proliferation
Beta-galactosidase activity
Reactive oxygen species (ROS)
Mitochondrial membrane potential
Intracellular Ca2+ levels
Oxygen consumption rate in isolated mitochondria
Biophotonic activity/photon emission
Non-chemical signalling/biophotonic communication

Limitations

In vitro cell-line study
Sample size not stated in the abstract
Mechanistic interpretation is framed as potential/may play a role
Findings may differ between cancer and non-cancer cell lines

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": null,
    "source": "other",
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": null
  },
  "population": "Cell lines: MCF7 breast cancer, A549 lung cancer, MCF10A non-cancer breast, and IMR-90 lung fibroblasts; doxorubicin-induced senescence models with near-infrared light exposure in some experiments.",
  "sample_size": null,
  "outcomes": [
    "Cellular senescence",
    "Cell proliferation",
    "Beta-galactosidase activity",
    "Reactive oxygen species (ROS)",
    "Mitochondrial membrane potential",
    "Intracellular Ca2+ levels",
    "Oxygen consumption rate in isolated mitochondria",
    "Biophotonic activity/photon emission",
    "Non-chemical signalling/biophotonic communication"
  ],
  "main_findings": "Doxorubicin-treated cells showed senescence-related changes including decreased proliferation and increased beta-galactosidase activity, ROS, mitochondrial membrane potential, and Ca2+ levels. Isolated mitochondria from several senescent cell lines showed increased oxygen consumption and detectable photon emission, with significant differences in non-chemical signalling versus non-senescent controls. Near-infrared light exposure at 734 nm increased senescent levels and related mitochondrial/oxidative markers in cancer cell lines but not in the two non-cancer cell populations.",
  "effect_direction": "mixed",
  "limitations": [
    "In vitro cell-line study",
    "Sample size not stated in the abstract",
    "Mechanistic interpretation is framed as potential/may play a role",
    "Findings may differ between cancer and non-cancer cell lines"
  ],
  "evidence_strength": "low",
  "confidence": 0.89,
  "peer_reviewed_likely": "unknown",
  "keywords": [
    "biophotons",
    "cellular senescence",
    "near-infrared light",
    "ROS",
    "mitochondria",
    "non-chemical signalling",
    "MCF7",
    "A549",
    "MCF10A",
    "IMR-90",
    "doxorubicin"
  ],
  "suggested_hubs": []
}

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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.34737/wy80y
PubMed: Not supplied

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