{"id":{"repo_id":"westminster","oai_identifier":"oai:westminsterresearch.westminster.ac.uk:wy80y"},"canonical_url":"https://search.dev.ndltd.org/etd/westminster/oai:westminsterresearch.westminster.ac.uk:wy80y","repository":{"repo_id":"westminster","name":"University of Westminster","base_url":"https://westminsterresearch.westminster.ac.uk/oai2"},"display":{"title":"The role of Biophotons in cellular senescence.","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.","abstract_html":"Senescence is the irreversible arrest of cell proliferation. While serving as a natural barrier against mutation progression, senescence&#x27;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 &lt; 0.0001), MCF7 (0.0042% per second; P &lt; 0.0001) and A549 cells (0.0017% per second; P &lt; 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.","abstract_has_math":false,"creators":["Kalampouka, Ifigeneia"],"institution":"University of Westminster","degree_name":"Ph.D.","degree_level":"PhD thesis","degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":["Thomas, E.L.","Bell, J.D.","Mould, R."],"committee_chairs":[],"committee_members":[],"year":2025,"date_issued":"2025","date_published":"2025","updated_at":"2026-07-24T06:01:07Z","subjects":[],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["oai:westminsterresearch.westminster.ac.uk:wy80y"],"render_values":[{"text":"oai:westminsterresearch.westminster.ac.uk:wy80y","href":null,"code":true}]}]},"links":{"outbound_url":"https://doi.org/10.34737/wy80y","outbound_label":"DOI","outbound_source":"dc:identifier.doi"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Thomas, E.L.","Bell, J.D.","Mould, R."]},{"key":"dc:creator","label":"Author","values":["Kalampouka, Ifigeneia"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2025"]},{"key":"dc:date.issued","label":"Date","values":["2025"]},{"key":"dc:publisher","label":"Institution","values":["University of Westminster"]},{"key":"dc:publisher.department","label":"Dc Publisher Department","values":["Life Sciences"]},{"key":"dc:publisher.institution","label":"Dc Publisher Institution","values":["University of Westminster"]},{"key":"dc:relation","label":"Dc Relation","values":["https://westminsterresearch.westminster.ac.uk/item/wy80y/the-role-of-biophotons-in-cellular-senescence"]},{"key":"dc:relation.isreferencedby","label":"Dc Relation Isreferencedby","values":["https://westminsterresearch.westminster.ac.uk/item/wy80y/the-role-of-biophotons-in-cellular-senescence"]},{"key":"dc:type","label":"Dc Type","values":["Thesis or dissertation"]},{"key":"dc:type.qualificationlevel","label":"Dc Type Qualificationlevel","values":["PhD thesis"]},{"key":"dc:type.qualificationname","label":"Dc Type Qualificationname","values":["Ph.D."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["oai:westminsterresearch.westminster.ac.uk:wy80y"]},{"key":"dc:identifier.doi","label":"DOI","values":["https://doi.org/10.34737/wy80y"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://westminsterresearch.westminster.ac.uk/download/ba0e8a82aa41f09def3324dd4232195a3418f5aefc219e4fff5613c47cee3941/2456789/Thesis-Ifigeneia-Kalampouka.pdf"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["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."]},{"key":"dc:description.abstract","label":"Abstract","values":["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."]},{"key":"dc:title","label":"Title","values":["The role of Biophotons in cellular senescence."]}]}],"canonical_facts":{"dc:contributor.advisor":["Thomas, E.L.","Bell, J.D.","Mould, R."],"dc:creator":["Kalampouka, Ifigeneia"],"dc:date":["2025"],"dc:date.issued":["2025"],"dc:description":["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."],"dc:description.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."],"dc:identifier":["oai:westminsterresearch.westminster.ac.uk:wy80y"],"dc:identifier.doi":["https://doi.org/10.34737/wy80y"],"dc:identifier.uri":["https://westminsterresearch.westminster.ac.uk/download/ba0e8a82aa41f09def3324dd4232195a3418f5aefc219e4fff5613c47cee3941/2456789/Thesis-Ifigeneia-Kalampouka.pdf"],"dc:publisher":["University of Westminster"],"dc:publisher.department":["Life Sciences"],"dc:publisher.institution":["University of Westminster"],"dc:relation":["https://westminsterresearch.westminster.ac.uk/item/wy80y/the-role-of-biophotons-in-cellular-senescence"],"dc:relation.isreferencedby":["https://westminsterresearch.westminster.ac.uk/item/wy80y/the-role-of-biophotons-in-cellular-senescence"],"dc:title":["The role of Biophotons in cellular senescence."],"dc:type":["Thesis or dissertation"],"dc:type.qualificationlevel":["PhD thesis"],"dc:type.qualificationname":["Ph.D."]},"updated_at":"2026-07-24T06:01:07Z"}