Loading…
Hematoporphyrin monomethyl ether photodynamic damage on HeLa cells by means of reactive oxygen species production and cytosolic free calcium concentration elevation
Hematoporphyrin monomethyl ether (HMME) is a novel and promising porphyrin-related photosensitizer for photodynamic therapy (PDT). HMME-PDT-induced cell death and its mechanisms were investigated in HeLa cells. We demonstrated that HMME-PDT could induce cell death through both necrosis and apoptosis...
Saved in:
| Published in: | Cancer letters 2004-12, Vol.216 (1), p.43-54 |
|---|---|
| Main Authors: | , , , , , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that this one cites Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c452t-c11d675ddf9991c945d5c0c669f752f34daa5c7029b4a9344a625a3edebb50223 |
|---|---|
| cites | cdi_FETCH-LOGICAL-c452t-c11d675ddf9991c945d5c0c669f752f34daa5c7029b4a9344a625a3edebb50223 |
| container_end_page | 54 |
| container_issue | 1 |
| container_start_page | 43 |
| container_title | Cancer letters |
| container_volume | 216 |
| creator | Ding, Xinmin Xu, Qinzhi Liu, Fanguang Zhou, Pingkun Gu, Ying Zeng, Jing An, Jing Dai, Weide Li, Xiaosong |
| description | Hematoporphyrin monomethyl ether (HMME) is a novel and promising porphyrin-related photosensitizer for photodynamic therapy (PDT). HMME-PDT-induced cell death and its mechanisms were investigated in HeLa cells. We demonstrated that HMME-PDT could induce cell death through both necrosis and apoptosis. Sodium azide (the singlet oxygen quencher) or
d-mannitol (the hydroxyl radical scavenger) could protect HeLa cells from the apoptosis and necrosis induced by HMME-PDT, showing that reactive oxygen species (ROS), such as singlet oxygen and hydroxyl radical, played a decisive role in HMME-PDT-induced HeLa cells death. Sodium azide or
d-mannitol also inhibited HMME-PDT-mediated [Ca
2+]
i elevation. Cytochrome C (Cyto C) release from mitochondria into cytosol and Caspase-3 activation after HMME-PDT were inhibited by BAPTA/AM (an intracellular calcium chelator). These results demonstrated that ROS generated in HeLa cells by HMME-PDT-induced apoptosis may be through [Ca
2+]
i elevation which mediates Cyto C release and Caspase-3 activition and initiates the subsequent late stages of apoptosis. |
| doi_str_mv | 10.1016/j.canlet.2004.07.005 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67004263</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0304383504005361</els_id><sourcerecordid>67004263</sourcerecordid><originalsourceid>FETCH-LOGICAL-c452t-c11d675ddf9991c945d5c0c669f752f34daa5c7029b4a9344a625a3edebb50223</originalsourceid><addsrcrecordid>eNp9kd9qHCEYxaW0NJu0b1CKUMjdTHVG589NoYQmW1jITXstjn6TdRl1qs7SeZ8-aNzsQqEXvVHB3zl-noPQB0pKSmjz-VAq6SZIZUUIK0lbEsJfoQ3t2qpo-468RhtSE1bUXc2v0HWMB5IJ1vK36IpyTkjPug36swUrk599mPdrMA5b77yFtF8nnFcIeN775PXqpDUKa2nlE2Dv8BZ2EiuYpoiHFVuQLmI_4gBSJXPMyO_1CRyOMygDEc_B6yXfZKV0Gqs1-ein7DgGAKzkpMxisfJOgUtBvoAwwfHl9A69GeUU4f1lv0E_77_9uNsWu8eH73dfd4VivEqFolQ3Ldd67Pueqp5xzRVRTdOPLa_GmmkpuWpJ1Q9M9jVjsqm4rEHDMHBSVfUNuj375ml_LRCTsCae_igd-CWKps1RV02dwU__gAe_BJdnE5QTXjcdbVim2JlSwccYYBRzMFaGVVAiTh2Kgzh3KE4dCtKK3FCWfbyYL4MF_Vd0KS0DX84A5CyOBoKIOeOcnDYBVBLam_-_8AzmjrNF</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1505368164</pqid></control><display><type>article</type><title>Hematoporphyrin monomethyl ether photodynamic damage on HeLa cells by means of reactive oxygen species production and cytosolic free calcium concentration elevation</title><source>ScienceDirect Freedom Collection</source><creator>Ding, Xinmin ; Xu, Qinzhi ; Liu, Fanguang ; Zhou, Pingkun ; Gu, Ying ; Zeng, Jing ; An, Jing ; Dai, Weide ; Li, Xiaosong</creator><creatorcontrib>Ding, Xinmin ; Xu, Qinzhi ; Liu, Fanguang ; Zhou, Pingkun ; Gu, Ying ; Zeng, Jing ; An, Jing ; Dai, Weide ; Li, Xiaosong</creatorcontrib><description>Hematoporphyrin monomethyl ether (HMME) is a novel and promising porphyrin-related photosensitizer for photodynamic therapy (PDT). HMME-PDT-induced cell death and its mechanisms were investigated in HeLa cells. We demonstrated that HMME-PDT could induce cell death through both necrosis and apoptosis. Sodium azide (the singlet oxygen quencher) or
d-mannitol (the hydroxyl radical scavenger) could protect HeLa cells from the apoptosis and necrosis induced by HMME-PDT, showing that reactive oxygen species (ROS), such as singlet oxygen and hydroxyl radical, played a decisive role in HMME-PDT-induced HeLa cells death. Sodium azide or
d-mannitol also inhibited HMME-PDT-mediated [Ca
2+]
i elevation. Cytochrome C (Cyto C) release from mitochondria into cytosol and Caspase-3 activation after HMME-PDT were inhibited by BAPTA/AM (an intracellular calcium chelator). These results demonstrated that ROS generated in HeLa cells by HMME-PDT-induced apoptosis may be through [Ca
2+]
i elevation which mediates Cyto C release and Caspase-3 activition and initiates the subsequent late stages of apoptosis.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2004.07.005</identifier><identifier>PMID: 15500948</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Apoptosis ; Binding sites ; Calcium - metabolism ; Calcium - pharmacokinetics ; Cell Death ; Clinical trials ; Cytosolic free calcium concentration ; Endoplasmic reticulum ; Female ; HeLa Cells ; Hematoporphyrin monomethyl ether ; Hematoporphyrins - pharmacology ; Humans ; Light ; Necrosis ; Oxygen ; Photochemotherapy ; Photodynamic therapy ; Reactive Oxygen Species ; Studies</subject><ispartof>Cancer letters, 2004-12, Vol.216 (1), p.43-54</ispartof><rights>2004</rights><rights>Copyright Elsevier Limited Dec 8, 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-c11d675ddf9991c945d5c0c669f752f34daa5c7029b4a9344a625a3edebb50223</citedby><cites>FETCH-LOGICAL-c452t-c11d675ddf9991c945d5c0c669f752f34daa5c7029b4a9344a625a3edebb50223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15500948$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ding, Xinmin</creatorcontrib><creatorcontrib>Xu, Qinzhi</creatorcontrib><creatorcontrib>Liu, Fanguang</creatorcontrib><creatorcontrib>Zhou, Pingkun</creatorcontrib><creatorcontrib>Gu, Ying</creatorcontrib><creatorcontrib>Zeng, Jing</creatorcontrib><creatorcontrib>An, Jing</creatorcontrib><creatorcontrib>Dai, Weide</creatorcontrib><creatorcontrib>Li, Xiaosong</creatorcontrib><title>Hematoporphyrin monomethyl ether photodynamic damage on HeLa cells by means of reactive oxygen species production and cytosolic free calcium concentration elevation</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>Hematoporphyrin monomethyl ether (HMME) is a novel and promising porphyrin-related photosensitizer for photodynamic therapy (PDT). HMME-PDT-induced cell death and its mechanisms were investigated in HeLa cells. We demonstrated that HMME-PDT could induce cell death through both necrosis and apoptosis. Sodium azide (the singlet oxygen quencher) or
d-mannitol (the hydroxyl radical scavenger) could protect HeLa cells from the apoptosis and necrosis induced by HMME-PDT, showing that reactive oxygen species (ROS), such as singlet oxygen and hydroxyl radical, played a decisive role in HMME-PDT-induced HeLa cells death. Sodium azide or
d-mannitol also inhibited HMME-PDT-mediated [Ca
2+]
i elevation. Cytochrome C (Cyto C) release from mitochondria into cytosol and Caspase-3 activation after HMME-PDT were inhibited by BAPTA/AM (an intracellular calcium chelator). These results demonstrated that ROS generated in HeLa cells by HMME-PDT-induced apoptosis may be through [Ca
2+]
i elevation which mediates Cyto C release and Caspase-3 activition and initiates the subsequent late stages of apoptosis.</description><subject>Apoptosis</subject><subject>Binding sites</subject><subject>Calcium - metabolism</subject><subject>Calcium - pharmacokinetics</subject><subject>Cell Death</subject><subject>Clinical trials</subject><subject>Cytosolic free calcium concentration</subject><subject>Endoplasmic reticulum</subject><subject>Female</subject><subject>HeLa Cells</subject><subject>Hematoporphyrin monomethyl ether</subject><subject>Hematoporphyrins - pharmacology</subject><subject>Humans</subject><subject>Light</subject><subject>Necrosis</subject><subject>Oxygen</subject><subject>Photochemotherapy</subject><subject>Photodynamic therapy</subject><subject>Reactive Oxygen Species</subject><subject>Studies</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNp9kd9qHCEYxaW0NJu0b1CKUMjdTHVG589NoYQmW1jITXstjn6TdRl1qs7SeZ8-aNzsQqEXvVHB3zl-noPQB0pKSmjz-VAq6SZIZUUIK0lbEsJfoQ3t2qpo-468RhtSE1bUXc2v0HWMB5IJ1vK36IpyTkjPug36swUrk599mPdrMA5b77yFtF8nnFcIeN775PXqpDUKa2nlE2Dv8BZ2EiuYpoiHFVuQLmI_4gBSJXPMyO_1CRyOMygDEc_B6yXfZKV0Gqs1-ein7DgGAKzkpMxisfJOgUtBvoAwwfHl9A69GeUU4f1lv0E_77_9uNsWu8eH73dfd4VivEqFolQ3Ldd67Pueqp5xzRVRTdOPLa_GmmkpuWpJ1Q9M9jVjsqm4rEHDMHBSVfUNuj375ml_LRCTsCae_igd-CWKps1RV02dwU__gAe_BJdnE5QTXjcdbVim2JlSwccYYBRzMFaGVVAiTh2Kgzh3KE4dCtKK3FCWfbyYL4MF_Vd0KS0DX84A5CyOBoKIOeOcnDYBVBLam_-_8AzmjrNF</recordid><startdate>20041208</startdate><enddate>20041208</enddate><creator>Ding, Xinmin</creator><creator>Xu, Qinzhi</creator><creator>Liu, Fanguang</creator><creator>Zhou, Pingkun</creator><creator>Gu, Ying</creator><creator>Zeng, Jing</creator><creator>An, Jing</creator><creator>Dai, Weide</creator><creator>Li, Xiaosong</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20041208</creationdate><title>Hematoporphyrin monomethyl ether photodynamic damage on HeLa cells by means of reactive oxygen species production and cytosolic free calcium concentration elevation</title><author>Ding, Xinmin ; Xu, Qinzhi ; Liu, Fanguang ; Zhou, Pingkun ; Gu, Ying ; Zeng, Jing ; An, Jing ; Dai, Weide ; Li, Xiaosong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c452t-c11d675ddf9991c945d5c0c669f752f34daa5c7029b4a9344a625a3edebb50223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Apoptosis</topic><topic>Binding sites</topic><topic>Calcium - metabolism</topic><topic>Calcium - pharmacokinetics</topic><topic>Cell Death</topic><topic>Clinical trials</topic><topic>Cytosolic free calcium concentration</topic><topic>Endoplasmic reticulum</topic><topic>Female</topic><topic>HeLa Cells</topic><topic>Hematoporphyrin monomethyl ether</topic><topic>Hematoporphyrins - pharmacology</topic><topic>Humans</topic><topic>Light</topic><topic>Necrosis</topic><topic>Oxygen</topic><topic>Photochemotherapy</topic><topic>Photodynamic therapy</topic><topic>Reactive Oxygen Species</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ding, Xinmin</creatorcontrib><creatorcontrib>Xu, Qinzhi</creatorcontrib><creatorcontrib>Liu, Fanguang</creatorcontrib><creatorcontrib>Zhou, Pingkun</creatorcontrib><creatorcontrib>Gu, Ying</creatorcontrib><creatorcontrib>Zeng, Jing</creatorcontrib><creatorcontrib>An, Jing</creatorcontrib><creatorcontrib>Dai, Weide</creatorcontrib><creatorcontrib>Li, Xiaosong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ding, Xinmin</au><au>Xu, Qinzhi</au><au>Liu, Fanguang</au><au>Zhou, Pingkun</au><au>Gu, Ying</au><au>Zeng, Jing</au><au>An, Jing</au><au>Dai, Weide</au><au>Li, Xiaosong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hematoporphyrin monomethyl ether photodynamic damage on HeLa cells by means of reactive oxygen species production and cytosolic free calcium concentration elevation</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2004-12-08</date><risdate>2004</risdate><volume>216</volume><issue>1</issue><spage>43</spage><epage>54</epage><pages>43-54</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>Hematoporphyrin monomethyl ether (HMME) is a novel and promising porphyrin-related photosensitizer for photodynamic therapy (PDT). HMME-PDT-induced cell death and its mechanisms were investigated in HeLa cells. We demonstrated that HMME-PDT could induce cell death through both necrosis and apoptosis. Sodium azide (the singlet oxygen quencher) or
d-mannitol (the hydroxyl radical scavenger) could protect HeLa cells from the apoptosis and necrosis induced by HMME-PDT, showing that reactive oxygen species (ROS), such as singlet oxygen and hydroxyl radical, played a decisive role in HMME-PDT-induced HeLa cells death. Sodium azide or
d-mannitol also inhibited HMME-PDT-mediated [Ca
2+]
i elevation. Cytochrome C (Cyto C) release from mitochondria into cytosol and Caspase-3 activation after HMME-PDT were inhibited by BAPTA/AM (an intracellular calcium chelator). These results demonstrated that ROS generated in HeLa cells by HMME-PDT-induced apoptosis may be through [Ca
2+]
i elevation which mediates Cyto C release and Caspase-3 activition and initiates the subsequent late stages of apoptosis.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>15500948</pmid><doi>10.1016/j.canlet.2004.07.005</doi><tpages>12</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0304-3835 |
| ispartof | Cancer letters, 2004-12, Vol.216 (1), p.43-54 |
| issn | 0304-3835 1872-7980 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67004263 |
| source | ScienceDirect Freedom Collection |
| subjects | Apoptosis Binding sites Calcium - metabolism Calcium - pharmacokinetics Cell Death Clinical trials Cytosolic free calcium concentration Endoplasmic reticulum Female HeLa Cells Hematoporphyrin monomethyl ether Hematoporphyrins - pharmacology Humans Light Necrosis Oxygen Photochemotherapy Photodynamic therapy Reactive Oxygen Species Studies |
| title | Hematoporphyrin monomethyl ether photodynamic damage on HeLa cells by means of reactive oxygen species production and cytosolic free calcium concentration elevation |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T13%3A59%3A26IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Hematoporphyrin%20monomethyl%20ether%20photodynamic%20damage%20on%20HeLa%20cells%20by%20means%20of%20reactive%20oxygen%20species%20production%20and%20cytosolic%20free%20calcium%20concentration%20elevation&rft.jtitle=Cancer%20letters&rft.au=Ding,%20Xinmin&rft.date=2004-12-08&rft.volume=216&rft.issue=1&rft.spage=43&rft.epage=54&rft.pages=43-54&rft.issn=0304-3835&rft.eissn=1872-7980&rft_id=info:doi/10.1016/j.canlet.2004.07.005&rft_dat=%3Cproquest_cross%3E67004263%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c452t-c11d675ddf9991c945d5c0c669f752f34daa5c7029b4a9344a625a3edebb50223%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1505368164&rft_id=info:pmid/15500948&rfr_iscdi=true |