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Effect of N-Acetyl Cysteine and α-Linolenic Acid on Sulfur Mustard Caused Impairment of In Vitro Endothelial Tube Formation
Sulfur mustard (SM), an alkylating chemical warfare agent, leads to tissue damage, including inflammation, blister formation, and impaired wound healing. Especially wound healing is of concern because after SM exposure, wound healing is prolonged. In this study, we focused on the effect of SM (30 an...
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| Published in: | Toxicological sciences 2010-12, Vol.118 (2), p.521-529 |
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| creator | Steinritz, Dirk Bölck, Birgit Schwarz, Jana Balszuweit, Frank Dühr, Sandra Ibrahim, Marwa Bloch, Wilhelm Thiermann, Horst Kehe, Kai |
| description | Sulfur mustard (SM), an alkylating chemical warfare agent, leads to tissue damage, including inflammation, blister formation, and impaired wound healing. Especially wound healing is of concern because after SM exposure, wound healing is prolonged. In this study, we focused on the effect of SM (30 and 100μM) on endothelial tube formation, apoptosis, and proliferation in mouse embryoid bodies (EBs), which provide an appropriate model for investigating vasculogenesis and angiogenesis. EBs were exposed to SM for 30 min on day 0, 3, or 6 of EBs’ growth, were allowed to grow until day 7, then fixed, and immunostained (PECAM-1, Ki67, and activated caspase-3). SM significantly decreased endothelial tube formation compared with unexposed EBs. Additionally, we observed a significant increase of apoptosis. As the formation of reactive oxygen species (ROS) is discussed to be involved in the pathophysiology of SM toxicity, we evaluated the effect of ROS scavengers (α-linolenic acid [ALA] and N-acetyl cysteine [NAC]) in the same experimental setup. Temporary effects of both scavengers could be detected, in particular NAC seemed to have temporary significant positive effects on endothelial tube formation in 100μM SM–exposed EBs. ALA augmented proliferation when administered after 30μM SM exposure on day 3, whereas NAC treatment on day 0 decreased apoptosis induced by 100μM SM. Taken together, our findings pointed to a negative effect of SM on vascularization and endothelial tube formation. ROS scavengers NAC and ALA showed temporary, but not long-lasting, rescuing effects regarding endothelial tube formation after SM exposure. |
| doi_str_mv | 10.1093/toxsci/kfq271 |
| format | article |
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Especially wound healing is of concern because after SM exposure, wound healing is prolonged. In this study, we focused on the effect of SM (30 and 100μM) on endothelial tube formation, apoptosis, and proliferation in mouse embryoid bodies (EBs), which provide an appropriate model for investigating vasculogenesis and angiogenesis. EBs were exposed to SM for 30 min on day 0, 3, or 6 of EBs’ growth, were allowed to grow until day 7, then fixed, and immunostained (PECAM-1, Ki67, and activated caspase-3). SM significantly decreased endothelial tube formation compared with unexposed EBs. Additionally, we observed a significant increase of apoptosis. As the formation of reactive oxygen species (ROS) is discussed to be involved in the pathophysiology of SM toxicity, we evaluated the effect of ROS scavengers (α-linolenic acid [ALA] and N-acetyl cysteine [NAC]) in the same experimental setup. Temporary effects of both scavengers could be detected, in particular NAC seemed to have temporary significant positive effects on endothelial tube formation in 100μM SM–exposed EBs. ALA augmented proliferation when administered after 30μM SM exposure on day 3, whereas NAC treatment on day 0 decreased apoptosis induced by 100μM SM. Taken together, our findings pointed to a negative effect of SM on vascularization and endothelial tube formation. 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Especially wound healing is of concern because after SM exposure, wound healing is prolonged. In this study, we focused on the effect of SM (30 and 100μM) on endothelial tube formation, apoptosis, and proliferation in mouse embryoid bodies (EBs), which provide an appropriate model for investigating vasculogenesis and angiogenesis. EBs were exposed to SM for 30 min on day 0, 3, or 6 of EBs’ growth, were allowed to grow until day 7, then fixed, and immunostained (PECAM-1, Ki67, and activated caspase-3). SM significantly decreased endothelial tube formation compared with unexposed EBs. Additionally, we observed a significant increase of apoptosis. As the formation of reactive oxygen species (ROS) is discussed to be involved in the pathophysiology of SM toxicity, we evaluated the effect of ROS scavengers (α-linolenic acid [ALA] and N-acetyl cysteine [NAC]) in the same experimental setup. Temporary effects of both scavengers could be detected, in particular NAC seemed to have temporary significant positive effects on endothelial tube formation in 100μM SM–exposed EBs. ALA augmented proliferation when administered after 30μM SM exposure on day 3, whereas NAC treatment on day 0 decreased apoptosis induced by 100μM SM. Taken together, our findings pointed to a negative effect of SM on vascularization and endothelial tube formation. ROS scavengers NAC and ALA showed temporary, but not long-lasting, rescuing effects regarding endothelial tube formation after SM exposure.</description><subject>Acetylcysteine - pharmacology</subject><subject>alpha-Linolenic Acid - pharmacology</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Chemical Warfare Agents - toxicity</subject><subject>Drug Administration Schedule</subject><subject>Embryoid Bodies - drug effects</subject><subject>Embryoid Bodies - metabolism</subject><subject>embryoid body</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - pathology</subject><subject>endothelial progenitor cells</subject><subject>Free Radical Scavengers - pharmacology</subject><subject>Ki-67 Antigen - metabolism</subject><subject>Mice</subject><subject>Mustard Gas - toxicity</subject><subject>N-acetyl cysteine</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Neovascularization, Physiologic - physiology</subject><subject>Platelet Endothelial Cell Adhesion Molecule-1 - metabolism</subject><subject>sulfur mustard</subject><subject>Time Factors</subject><subject>wound healing</subject><subject>Wound Healing - drug effects</subject><subject>Wound Healing - physiology</subject><subject>α-linolenic acid</subject><issn>1096-6080</issn><issn>1096-0929</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNpFkE1v1DAQQC0EoqVw5Ip84xQ6sRPbOa6i3XbRFg4UqLhYjj-EaWJvbUfqSvwp_gi_iS27lNOMZp7e4SH0uoZ3NXT0vMT7rP35rbsjvH6CTvdHVkFHuqfHnYGAE_Qi5x8Adc2ge45OCAhKOfBT9HPpnNUFR4c_VAtty27E_S4X64PFKhj8-1e18SGONniNF9obHAP-NI9uTvhqzkUlg3s1Z2vwetoqnyYb_urWAX_xJUW8DCaW73b0asTX82DxKqZJFR_DS_TMqTHbV8d5hj6vltf9ZbX5eLHuF5tKN1CXygjTdowS1jaNEiAI4R3nTAnbccEUsW4YgAARA9GqbWlHDGguaKNaTZxh9Ay9PXi3Kd7NNhc5-aztOKpg45ylaNneR-GBrA6kTjHnZJ3cJj-ptJM1yIfe8tBbHnrv-TdH8zxM1jzS_wL_F_p90_vHv0q3knHKW3l5802-71c3zerqq2zoH-wajXY</recordid><startdate>20101201</startdate><enddate>20101201</enddate><creator>Steinritz, Dirk</creator><creator>Bölck, Birgit</creator><creator>Schwarz, Jana</creator><creator>Balszuweit, Frank</creator><creator>Dühr, Sandra</creator><creator>Ibrahim, Marwa</creator><creator>Bloch, Wilhelm</creator><creator>Thiermann, Horst</creator><creator>Kehe, Kai</creator><general>Oxford University Press</general><scope>BSCLL</scope><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>7U7</scope><scope>C1K</scope></search><sort><creationdate>20101201</creationdate><title>Effect of N-Acetyl Cysteine and α-Linolenic Acid on Sulfur Mustard Caused Impairment of In Vitro Endothelial Tube Formation</title><author>Steinritz, Dirk ; Bölck, Birgit ; Schwarz, Jana ; Balszuweit, Frank ; Dühr, Sandra ; Ibrahim, Marwa ; Bloch, Wilhelm ; Thiermann, Horst ; Kehe, Kai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c401t-d8d596326544a8082279776a8e9786a2efbb02028b2ca55392d0c7834a5c2fd63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Acetylcysteine - pharmacology</topic><topic>alpha-Linolenic Acid - pharmacology</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Proliferation - drug effects</topic><topic>Cells, Cultured</topic><topic>Chemical Warfare Agents - toxicity</topic><topic>Drug Administration Schedule</topic><topic>Embryoid Bodies - drug effects</topic><topic>Embryoid Bodies - metabolism</topic><topic>embryoid body</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelial Cells - pathology</topic><topic>endothelial progenitor cells</topic><topic>Free Radical Scavengers - pharmacology</topic><topic>Ki-67 Antigen - metabolism</topic><topic>Mice</topic><topic>Mustard Gas - toxicity</topic><topic>N-acetyl cysteine</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Neovascularization, Physiologic - physiology</topic><topic>Platelet Endothelial Cell Adhesion Molecule-1 - metabolism</topic><topic>sulfur mustard</topic><topic>Time Factors</topic><topic>wound healing</topic><topic>Wound Healing - drug effects</topic><topic>Wound Healing - physiology</topic><topic>α-linolenic acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Steinritz, Dirk</creatorcontrib><creatorcontrib>Bölck, Birgit</creatorcontrib><creatorcontrib>Schwarz, Jana</creatorcontrib><creatorcontrib>Balszuweit, Frank</creatorcontrib><creatorcontrib>Dühr, Sandra</creatorcontrib><creatorcontrib>Ibrahim, Marwa</creatorcontrib><creatorcontrib>Bloch, Wilhelm</creatorcontrib><creatorcontrib>Thiermann, Horst</creatorcontrib><creatorcontrib>Kehe, Kai</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Toxicological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Steinritz, Dirk</au><au>Bölck, Birgit</au><au>Schwarz, Jana</au><au>Balszuweit, Frank</au><au>Dühr, Sandra</au><au>Ibrahim, Marwa</au><au>Bloch, Wilhelm</au><au>Thiermann, Horst</au><au>Kehe, Kai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of N-Acetyl Cysteine and α-Linolenic Acid on Sulfur Mustard Caused Impairment of In Vitro Endothelial Tube Formation</atitle><jtitle>Toxicological sciences</jtitle><addtitle>Toxicol Sci</addtitle><date>2010-12-01</date><risdate>2010</risdate><volume>118</volume><issue>2</issue><spage>521</spage><epage>529</epage><pages>521-529</pages><issn>1096-6080</issn><eissn>1096-0929</eissn><notes>ark:/67375/HXZ-JCFX4FMW-4</notes><notes>istex:C75A131A231DBE0C3F34932EE80EC7E41E220AD3</notes><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-1</notes><notes>content type line 23</notes><abstract>Sulfur mustard (SM), an alkylating chemical warfare agent, leads to tissue damage, including inflammation, blister formation, and impaired wound healing. Especially wound healing is of concern because after SM exposure, wound healing is prolonged. In this study, we focused on the effect of SM (30 and 100μM) on endothelial tube formation, apoptosis, and proliferation in mouse embryoid bodies (EBs), which provide an appropriate model for investigating vasculogenesis and angiogenesis. EBs were exposed to SM for 30 min on day 0, 3, or 6 of EBs’ growth, were allowed to grow until day 7, then fixed, and immunostained (PECAM-1, Ki67, and activated caspase-3). SM significantly decreased endothelial tube formation compared with unexposed EBs. Additionally, we observed a significant increase of apoptosis. As the formation of reactive oxygen species (ROS) is discussed to be involved in the pathophysiology of SM toxicity, we evaluated the effect of ROS scavengers (α-linolenic acid [ALA] and N-acetyl cysteine [NAC]) in the same experimental setup. Temporary effects of both scavengers could be detected, in particular NAC seemed to have temporary significant positive effects on endothelial tube formation in 100μM SM–exposed EBs. ALA augmented proliferation when administered after 30μM SM exposure on day 3, whereas NAC treatment on day 0 decreased apoptosis induced by 100μM SM. Taken together, our findings pointed to a negative effect of SM on vascularization and endothelial tube formation. ROS scavengers NAC and ALA showed temporary, but not long-lasting, rescuing effects regarding endothelial tube formation after SM exposure.</abstract><cop>United States</cop><pub>Oxford University Press</pub><pmid>20833707</pmid><doi>10.1093/toxsci/kfq271</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | Full-Text Journals in Chemistry (Open access); Oxford Journals |
| subjects | Acetylcysteine - pharmacology alpha-Linolenic Acid - pharmacology Animals Apoptosis - drug effects Caspase 3 - metabolism Cell Proliferation - drug effects Cells, Cultured Chemical Warfare Agents - toxicity Drug Administration Schedule Embryoid Bodies - drug effects Embryoid Bodies - metabolism embryoid body Endothelial Cells - drug effects Endothelial Cells - metabolism Endothelial Cells - pathology endothelial progenitor cells Free Radical Scavengers - pharmacology Ki-67 Antigen - metabolism Mice Mustard Gas - toxicity N-acetyl cysteine Neovascularization, Physiologic - drug effects Neovascularization, Physiologic - physiology Platelet Endothelial Cell Adhesion Molecule-1 - metabolism sulfur mustard Time Factors wound healing Wound Healing - drug effects Wound Healing - physiology α-linolenic acid |
| title | Effect of N-Acetyl Cysteine and α-Linolenic Acid on Sulfur Mustard Caused Impairment of In Vitro Endothelial Tube Formation |
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