Effects of a melanogenic bicyclic monoterpene diol on cell cycle, p53, TNF-α, and PGE2 are distinct from those of UVB
Purpose: Bicyclic monoterpene (BMT) diols are small‐molecule compounds that mimic ultraviolet radiation (UVR) by inducing melanogenesis. The objective of this study was to compare the effects of 2,2‐dimethyl‐3‐propanyldiol‐norbornane (AGI‐1140), a novel BMT diol, and ultraviolet B (UVB) on additiona...
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| Veröffentlicht in: | Photodermatology, photoimmunology & photomedicine photoimmunology & photomedicine, 2003-12, Vol.19 (6), p.295-302 |
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| creator | Kraus, Eliyahu Galvin, Jason W. Boumakis, Stavroula Boamah, Ernest K. Canning, Matthew T. Yarosh, Daniel B. Brown, David A. |
| description | Purpose: Bicyclic monoterpene (BMT) diols are small‐molecule compounds that mimic ultraviolet radiation (UVR) by inducing melanogenesis. The objective of this study was to compare the effects of 2,2‐dimethyl‐3‐propanyldiol‐norbornane (AGI‐1140), a novel BMT diol, and ultraviolet B (UVB) on additional cellular responses.
Methods: S91 mouse melanoma cells were treated with a range of concentrations of AGI‐1140, and examined for induction of melanogenesis and nitric oxide (NO). The effect of AGI‐1140 on dendrite outgrowth from human melanocytes was examined by quantitative microscopy. The effect of AGI‐1140 and UVB on phosphorylation of p53 serine 15 in human keratinocytes was examined by Western blotting, while the release of tumor necrosis factor‐α (TNF‐α) and prostaglandin E2 (PGE2) was determined by enzyme‐linked immunosorbent assay. The effects of AGI‐1140 and UVB on cell cycle arrest of human melanocytes, keratinocytes, fibroblasts, and endothelial cells were compared using fluorescence‐activated cell sorting.
Results: Similar to UVB, AGI‐1140 induced both melanogenesis and NO in melanoma cells. AGI‐1140 also induced dendrite outgrowth from melanocytes, indicative of differentiation. However, whereas UVB induced G2 cell cycle arrest with phosphorylation of p53 at serine 15, AGI‐1140 induced G1 cell cycle arrest without this phosphorylation. Additionally, unlike UVB, AGI‐1140 did not increase the secretion of TNF‐α or PGE2, mediators of UVB‐induced immunosuppressive and inflammatory responses in the skin that may contribute to carcinogenesis.
Conclusion: This study shows that melanogenesis can be induced by AGI‐1140 without many of the deleterious effects associated with UVB. |
| doi_str_mv | 10.1046/j.1600-0781.2003.00061.x |
| format | Article |
| fullrecord | <record><control><sourceid>istex_pubme</sourceid><recordid>TN_cdi_pubmed_primary_14617104</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>ark_67375_WNG_DNVBRS37_Q</sourcerecordid><originalsourceid>FETCH-LOGICAL-i2441-3605a616e92abfa6b17022788cbb9576069b81e69b6ef283ef6f5509134eef3b3</originalsourceid><addsrcrecordid>eNpFkctu2zAQRYmgReMk_YWCm-wsdSg-JC2yaBw_CgSO08bOkqDoYSNHD0NSUvuz-iP9plJ1HhtygHvuDHAvIZRByECor5uQKYAA4oSFEQAPAUCxcHdEBm_CBzKAFGQgeMKPyUnbbjwkBLBP5JgJxWK_aUCex86h7VpaO2poiYWp6l9Y5ZZmud3bwg9lXdUdNluskK7zuqB1RS0WBe11HNKt5EN6N58Ef_8MqanWdDEdR9Q0Pd12eWU76pq6pN1D3WJ_Z7m6PCMfnSla_Pzyn5LlZHw3mgXXN9Pvo2_XQR4JwQKuQBrFFKaRyZxRGYshiuIksVmWyliBSrOEoX8Vuijh6JSTElLGBaLjGT8lXw57t09ZiWu9bfLSNHv9GoAHzl8A01pTuMZUNm_fORklQrLUcxcH7nde4P5dB90Xoje6z133ueu-EP2_EL3Ti9li4SfvDw5-Hwnu3vymedQq5rHU9_OpvpqvLn_85LG-5f8AyNyLpw</addsrcrecordid><sourcetype>Index Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Effects of a melanogenic bicyclic monoterpene diol on cell cycle, p53, TNF-α, and PGE2 are distinct from those of UVB</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Kraus, Eliyahu ; Galvin, Jason W. ; Boumakis, Stavroula ; Boamah, Ernest K. ; Canning, Matthew T. ; Yarosh, Daniel B. ; Brown, David A.</creator><creatorcontrib>Kraus, Eliyahu ; Galvin, Jason W. ; Boumakis, Stavroula ; Boamah, Ernest K. ; Canning, Matthew T. ; Yarosh, Daniel B. ; Brown, David A.</creatorcontrib><description>Purpose: Bicyclic monoterpene (BMT) diols are small‐molecule compounds that mimic ultraviolet radiation (UVR) by inducing melanogenesis. The objective of this study was to compare the effects of 2,2‐dimethyl‐3‐propanyldiol‐norbornane (AGI‐1140), a novel BMT diol, and ultraviolet B (UVB) on additional cellular responses.
Methods: S91 mouse melanoma cells were treated with a range of concentrations of AGI‐1140, and examined for induction of melanogenesis and nitric oxide (NO). The effect of AGI‐1140 on dendrite outgrowth from human melanocytes was examined by quantitative microscopy. The effect of AGI‐1140 and UVB on phosphorylation of p53 serine 15 in human keratinocytes was examined by Western blotting, while the release of tumor necrosis factor‐α (TNF‐α) and prostaglandin E2 (PGE2) was determined by enzyme‐linked immunosorbent assay. The effects of AGI‐1140 and UVB on cell cycle arrest of human melanocytes, keratinocytes, fibroblasts, and endothelial cells were compared using fluorescence‐activated cell sorting.
Results: Similar to UVB, AGI‐1140 induced both melanogenesis and NO in melanoma cells. AGI‐1140 also induced dendrite outgrowth from melanocytes, indicative of differentiation. However, whereas UVB induced G2 cell cycle arrest with phosphorylation of p53 at serine 15, AGI‐1140 induced G1 cell cycle arrest without this phosphorylation. Additionally, unlike UVB, AGI‐1140 did not increase the secretion of TNF‐α or PGE2, mediators of UVB‐induced immunosuppressive and inflammatory responses in the skin that may contribute to carcinogenesis.
Conclusion: This study shows that melanogenesis can be induced by AGI‐1140 without many of the deleterious effects associated with UVB.</description><identifier>ISSN: 0905-4383</identifier><identifier>EISSN: 1600-0781</identifier><identifier>DOI: 10.1046/j.1600-0781.2003.00061.x</identifier><identifier>PMID: 14617104</identifier><language>eng</language><publisher>Oxford, UK: Munksgaard International Publishers</publisher><subject>Animals ; Biological and medical sciences ; Blotting, Western ; cell cycle ; Cell Cycle - drug effects ; Cell Cycle - radiation effects ; Cell Line, Tumor - drug effects ; Cell Line, Tumor - metabolism ; Cell Line, Tumor - radiation effects ; cytokine ; Dendrites - drug effects ; Dendrites - metabolism ; Dendrites - radiation effects ; Dermatology ; Dinoprostone - biosynthesis ; Dose-Response Relationship, Drug ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Endothelial Cells - radiation effects ; Enzyme-Linked Immunosorbent Assay ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; Fibroblasts - radiation effects ; Investigative techniques, diagnostic techniques (general aspects) ; keratinocyte ; Keratinocytes - drug effects ; Keratinocytes - metabolism ; Keratinocytes - radiation effects ; Medical sciences ; melanocyte ; Melanocytes - drug effects ; Melanocytes - metabolism ; Melanocytes - radiation effects ; Melanoma, Experimental - pathology ; Mice ; monoterpene ; Monoterpenes - administration & dosage ; Monoterpenes - pharmacology ; Nitric Oxide - biosynthesis ; Norbornanes - administration & dosage ; Norbornanes - pharmacology ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; prostaglandin ; Skin Pigmentation - drug effects ; Skin Pigmentation - radiation effects ; Tumor Necrosis Factor-alpha - biosynthesis ; ultraviolet ; Ultraviolet Rays</subject><ispartof>Photodermatology, photoimmunology & photomedicine, 2003-12, Vol.19 (6), p.295-302</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1600-0781.2003.00061.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45556</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15284519$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14617104$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kraus, Eliyahu</creatorcontrib><creatorcontrib>Galvin, Jason W.</creatorcontrib><creatorcontrib>Boumakis, Stavroula</creatorcontrib><creatorcontrib>Boamah, Ernest K.</creatorcontrib><creatorcontrib>Canning, Matthew T.</creatorcontrib><creatorcontrib>Yarosh, Daniel B.</creatorcontrib><creatorcontrib>Brown, David A.</creatorcontrib><title>Effects of a melanogenic bicyclic monoterpene diol on cell cycle, p53, TNF-α, and PGE2 are distinct from those of UVB</title><title>Photodermatology, photoimmunology & photomedicine</title><addtitle>Photodermatol Photoimmunol Photomed</addtitle><description>Purpose: Bicyclic monoterpene (BMT) diols are small‐molecule compounds that mimic ultraviolet radiation (UVR) by inducing melanogenesis. The objective of this study was to compare the effects of 2,2‐dimethyl‐3‐propanyldiol‐norbornane (AGI‐1140), a novel BMT diol, and ultraviolet B (UVB) on additional cellular responses.
Methods: S91 mouse melanoma cells were treated with a range of concentrations of AGI‐1140, and examined for induction of melanogenesis and nitric oxide (NO). The effect of AGI‐1140 on dendrite outgrowth from human melanocytes was examined by quantitative microscopy. The effect of AGI‐1140 and UVB on phosphorylation of p53 serine 15 in human keratinocytes was examined by Western blotting, while the release of tumor necrosis factor‐α (TNF‐α) and prostaglandin E2 (PGE2) was determined by enzyme‐linked immunosorbent assay. The effects of AGI‐1140 and UVB on cell cycle arrest of human melanocytes, keratinocytes, fibroblasts, and endothelial cells were compared using fluorescence‐activated cell sorting.
Results: Similar to UVB, AGI‐1140 induced both melanogenesis and NO in melanoma cells. AGI‐1140 also induced dendrite outgrowth from melanocytes, indicative of differentiation. However, whereas UVB induced G2 cell cycle arrest with phosphorylation of p53 at serine 15, AGI‐1140 induced G1 cell cycle arrest without this phosphorylation. Additionally, unlike UVB, AGI‐1140 did not increase the secretion of TNF‐α or PGE2, mediators of UVB‐induced immunosuppressive and inflammatory responses in the skin that may contribute to carcinogenesis.
Conclusion: This study shows that melanogenesis can be induced by AGI‐1140 without many of the deleterious effects associated with UVB.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Cycle - radiation effects</subject><subject>Cell Line, Tumor - drug effects</subject><subject>Cell Line, Tumor - metabolism</subject><subject>Cell Line, Tumor - radiation effects</subject><subject>cytokine</subject><subject>Dendrites - drug effects</subject><subject>Dendrites - metabolism</subject><subject>Dendrites - radiation effects</subject><subject>Dermatology</subject><subject>Dinoprostone - biosynthesis</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - radiation effects</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - metabolism</subject><subject>Fibroblasts - radiation effects</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>keratinocyte</subject><subject>Keratinocytes - drug effects</subject><subject>Keratinocytes - metabolism</subject><subject>Keratinocytes - radiation effects</subject><subject>Medical sciences</subject><subject>melanocyte</subject><subject>Melanocytes - drug effects</subject><subject>Melanocytes - metabolism</subject><subject>Melanocytes - radiation effects</subject><subject>Melanoma, Experimental - pathology</subject><subject>Mice</subject><subject>monoterpene</subject><subject>Monoterpenes - administration & dosage</subject><subject>Monoterpenes - pharmacology</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Norbornanes - administration & dosage</subject><subject>Norbornanes - pharmacology</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>prostaglandin</subject><subject>Skin Pigmentation - drug effects</subject><subject>Skin Pigmentation - radiation effects</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>ultraviolet</subject><subject>Ultraviolet Rays</subject><issn>0905-4383</issn><issn>1600-0781</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkctu2zAQRYmgReMk_YWCm-wsdSg-JC2yaBw_CgSO08bOkqDoYSNHD0NSUvuz-iP9plJ1HhtygHvuDHAvIZRByECor5uQKYAA4oSFEQAPAUCxcHdEBm_CBzKAFGQgeMKPyUnbbjwkBLBP5JgJxWK_aUCex86h7VpaO2poiYWp6l9Y5ZZmud3bwg9lXdUdNluskK7zuqB1RS0WBe11HNKt5EN6N58Ef_8MqanWdDEdR9Q0Pd12eWU76pq6pN1D3WJ_Z7m6PCMfnSla_Pzyn5LlZHw3mgXXN9Pvo2_XQR4JwQKuQBrFFKaRyZxRGYshiuIksVmWyliBSrOEoX8Vuijh6JSTElLGBaLjGT8lXw57t09ZiWu9bfLSNHv9GoAHzl8A01pTuMZUNm_fORklQrLUcxcH7nde4P5dB90Xoje6z133ueu-EP2_EL3Ti9li4SfvDw5-Hwnu3vymedQq5rHU9_OpvpqvLn_85LG-5f8AyNyLpw</recordid><startdate>200312</startdate><enddate>200312</enddate><creator>Kraus, Eliyahu</creator><creator>Galvin, Jason W.</creator><creator>Boumakis, Stavroula</creator><creator>Boamah, Ernest K.</creator><creator>Canning, Matthew T.</creator><creator>Yarosh, Daniel B.</creator><creator>Brown, David A.</creator><general>Munksgaard International Publishers</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>200312</creationdate><title>Effects of a melanogenic bicyclic monoterpene diol on cell cycle, p53, TNF-α, and PGE2 are distinct from those of UVB</title><author>Kraus, Eliyahu ; Galvin, Jason W. ; Boumakis, Stavroula ; Boamah, Ernest K. ; Canning, Matthew T. ; Yarosh, Daniel B. ; Brown, David A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i2441-3605a616e92abfa6b17022788cbb9576069b81e69b6ef283ef6f5509134eef3b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>cell cycle</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Cycle - radiation effects</topic><topic>Cell Line, Tumor - drug effects</topic><topic>Cell Line, Tumor - metabolism</topic><topic>Cell Line, Tumor - radiation effects</topic><topic>cytokine</topic><topic>Dendrites - drug effects</topic><topic>Dendrites - metabolism</topic><topic>Dendrites - radiation effects</topic><topic>Dermatology</topic><topic>Dinoprostone - biosynthesis</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelial Cells - radiation effects</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - metabolism</topic><topic>Fibroblasts - radiation effects</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>keratinocyte</topic><topic>Keratinocytes - drug effects</topic><topic>Keratinocytes - metabolism</topic><topic>Keratinocytes - radiation effects</topic><topic>Medical sciences</topic><topic>melanocyte</topic><topic>Melanocytes - drug effects</topic><topic>Melanocytes - metabolism</topic><topic>Melanocytes - radiation effects</topic><topic>Melanoma, Experimental - pathology</topic><topic>Mice</topic><topic>monoterpene</topic><topic>Monoterpenes - administration & dosage</topic><topic>Monoterpenes - pharmacology</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Norbornanes - administration & dosage</topic><topic>Norbornanes - pharmacology</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>prostaglandin</topic><topic>Skin Pigmentation - drug effects</topic><topic>Skin Pigmentation - radiation effects</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>ultraviolet</topic><topic>Ultraviolet Rays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kraus, Eliyahu</creatorcontrib><creatorcontrib>Galvin, Jason W.</creatorcontrib><creatorcontrib>Boumakis, Stavroula</creatorcontrib><creatorcontrib>Boamah, Ernest K.</creatorcontrib><creatorcontrib>Canning, Matthew T.</creatorcontrib><creatorcontrib>Yarosh, Daniel B.</creatorcontrib><creatorcontrib>Brown, David A.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Photodermatology, photoimmunology & photomedicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kraus, Eliyahu</au><au>Galvin, Jason W.</au><au>Boumakis, Stavroula</au><au>Boamah, Ernest K.</au><au>Canning, Matthew T.</au><au>Yarosh, Daniel B.</au><au>Brown, David A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of a melanogenic bicyclic monoterpene diol on cell cycle, p53, TNF-α, and PGE2 are distinct from those of UVB</atitle><jtitle>Photodermatology, photoimmunology & photomedicine</jtitle><addtitle>Photodermatol Photoimmunol Photomed</addtitle><date>2003-12</date><risdate>2003</risdate><volume>19</volume><issue>6</issue><spage>295</spage><epage>302</epage><pages>295-302</pages><issn>0905-4383</issn><eissn>1600-0781</eissn><abstract>Purpose: Bicyclic monoterpene (BMT) diols are small‐molecule compounds that mimic ultraviolet radiation (UVR) by inducing melanogenesis. The objective of this study was to compare the effects of 2,2‐dimethyl‐3‐propanyldiol‐norbornane (AGI‐1140), a novel BMT diol, and ultraviolet B (UVB) on additional cellular responses.
Methods: S91 mouse melanoma cells were treated with a range of concentrations of AGI‐1140, and examined for induction of melanogenesis and nitric oxide (NO). The effect of AGI‐1140 on dendrite outgrowth from human melanocytes was examined by quantitative microscopy. The effect of AGI‐1140 and UVB on phosphorylation of p53 serine 15 in human keratinocytes was examined by Western blotting, while the release of tumor necrosis factor‐α (TNF‐α) and prostaglandin E2 (PGE2) was determined by enzyme‐linked immunosorbent assay. The effects of AGI‐1140 and UVB on cell cycle arrest of human melanocytes, keratinocytes, fibroblasts, and endothelial cells were compared using fluorescence‐activated cell sorting.
Results: Similar to UVB, AGI‐1140 induced both melanogenesis and NO in melanoma cells. AGI‐1140 also induced dendrite outgrowth from melanocytes, indicative of differentiation. However, whereas UVB induced G2 cell cycle arrest with phosphorylation of p53 at serine 15, AGI‐1140 induced G1 cell cycle arrest without this phosphorylation. Additionally, unlike UVB, AGI‐1140 did not increase the secretion of TNF‐α or PGE2, mediators of UVB‐induced immunosuppressive and inflammatory responses in the skin that may contribute to carcinogenesis.
Conclusion: This study shows that melanogenesis can be induced by AGI‐1140 without many of the deleterious effects associated with UVB.</abstract><cop>Oxford, UK</cop><pub>Munksgaard International Publishers</pub><pmid>14617104</pmid><doi>10.1046/j.1600-0781.2003.00061.x</doi><tpages>8</tpages></addata></record> |
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| issn | 0905-4383 1600-0781 |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Animals Biological and medical sciences Blotting, Western cell cycle Cell Cycle - drug effects Cell Cycle - radiation effects Cell Line, Tumor - drug effects Cell Line, Tumor - metabolism Cell Line, Tumor - radiation effects cytokine Dendrites - drug effects Dendrites - metabolism Dendrites - radiation effects Dermatology Dinoprostone - biosynthesis Dose-Response Relationship, Drug Endothelial Cells - drug effects Endothelial Cells - metabolism Endothelial Cells - radiation effects Enzyme-Linked Immunosorbent Assay Fibroblasts - drug effects Fibroblasts - metabolism Fibroblasts - radiation effects Investigative techniques, diagnostic techniques (general aspects) keratinocyte Keratinocytes - drug effects Keratinocytes - metabolism Keratinocytes - radiation effects Medical sciences melanocyte Melanocytes - drug effects Melanocytes - metabolism Melanocytes - radiation effects Melanoma, Experimental - pathology Mice monoterpene Monoterpenes - administration & dosage Monoterpenes - pharmacology Nitric Oxide - biosynthesis Norbornanes - administration & dosage Norbornanes - pharmacology Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques prostaglandin Skin Pigmentation - drug effects Skin Pigmentation - radiation effects Tumor Necrosis Factor-alpha - biosynthesis ultraviolet Ultraviolet Rays |
| title | Effects of a melanogenic bicyclic monoterpene diol on cell cycle, p53, TNF-α, and PGE2 are distinct from those of UVB |
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