Yáskara Veruska Ribeiro Barros, Amanda Onduras de Andrade, Larissa Pereira Dantas da Silva, Lucas Aleixo Leal Pedroza, Iverson Conrado Bezerra, Iago Dillion Lima Cavalcanti, Mariane Cajuba de Britto Lira Nogueira, Kristiana Cerqueira Mousinho, Angelo Roberto Antoniolli, Luiz Carlos Alves, José Luiz de Lima Filho, Alexandre Varão Moura, Álex Aparecido Rosini Silva, Andréia de Melo Porcari, Priscila Gubert
{"title":"蜂毒对 MDA-MB-231 乳腺癌细胞和蜗牛的毒性作用","authors":"Yáskara Veruska Ribeiro Barros, Amanda Onduras de Andrade, Larissa Pereira Dantas da Silva, Lucas Aleixo Leal Pedroza, Iverson Conrado Bezerra, Iago Dillion Lima Cavalcanti, Mariane Cajuba de Britto Lira Nogueira, Kristiana Cerqueira Mousinho, Angelo Roberto Antoniolli, Luiz Carlos Alves, José Luiz de Lima Filho, Alexandre Varão Moura, Álex Aparecido Rosini Silva, Andréia de Melo Porcari, Priscila Gubert","doi":"10.2174/0118715206291634240312062957","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Bee venom has therapeutics and pharmacological properties. Further toxicological studies on animal models are necessary due to the severe allergic reactions caused by this product.</p><p><strong>Method: </strong>Here, <i>Caenorhabditis elegans</i> was used as an <i>in vivo</i> toxicity model, while breast cancer cells were used to evaluate the pharmacological benefits. The bee venom utilized in this research was collected from <i>Apis mellifera</i> species found in Northeast Brazil. The cytotoxicity caused by bee venom was measured by MTT assay on MDA-MB-231 and J774 A.1 cells during 24 - 72 hours of exposure. <i>C. elegans</i> at the L4 larval stage were exposed for three hours to M9 buffer or bee venom. Survival, behavioral parameters, reproduction, DAF-16 transcription factor translocation, the expression of superoxide dismutase (SOD), and metabolomics were analyzed. Bee venom suppressed the growth of MDA-MB-231 cancer cells and exhibited cytotoxic effects on macrophages. Also, decreased <i>C. elegans</i> survival impacted its behaviors by decreasing <i>C. elegans</i> feeding behavior, movement, and reproduction.</p><p><strong>Results: </strong>Bee venom did not increase the expression of SOD-3, but it enhanced DAF-16 translocation from the cytoplasm to the nucleus. <i>C. elegans</i> metabolites differed after bee venom exposure, primarily related to aminoacyl- tRNA biosynthesis, glycine, serine and threonine metabolism, and sphingolipid and purine metabolic pathways. Our findings indicate that exposure to bee venom resulted in harmful effects on the cells and animal models examined.</p><p><strong>Conclusion: </strong>Thus, due to its potential toxic effect and induction of allergic reactions, using bee venom as a therapeutic approach has been limited. The development of controlled-release drug strategies to improve this natural product's efficacy and safety should be intensified.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":"798-811"},"PeriodicalIF":2.6000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Bee Venom Toxic Effect on MDA-MB-231 Breast Cancer Cells and <i>Caenorhabditis Elegans</i>.\",\"authors\":\"Yáskara Veruska Ribeiro Barros, Amanda Onduras de Andrade, Larissa Pereira Dantas da Silva, Lucas Aleixo Leal Pedroza, Iverson Conrado Bezerra, Iago Dillion Lima Cavalcanti, Mariane Cajuba de Britto Lira Nogueira, Kristiana Cerqueira Mousinho, Angelo Roberto Antoniolli, Luiz Carlos Alves, José Luiz de Lima Filho, Alexandre Varão Moura, Álex Aparecido Rosini Silva, Andréia de Melo Porcari, Priscila Gubert\",\"doi\":\"10.2174/0118715206291634240312062957\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Bee venom has therapeutics and pharmacological properties. Further toxicological studies on animal models are necessary due to the severe allergic reactions caused by this product.</p><p><strong>Method: </strong>Here, <i>Caenorhabditis elegans</i> was used as an <i>in vivo</i> toxicity model, while breast cancer cells were used to evaluate the pharmacological benefits. The bee venom utilized in this research was collected from <i>Apis mellifera</i> species found in Northeast Brazil. The cytotoxicity caused by bee venom was measured by MTT assay on MDA-MB-231 and J774 A.1 cells during 24 - 72 hours of exposure. <i>C. elegans</i> at the L4 larval stage were exposed for three hours to M9 buffer or bee venom. Survival, behavioral parameters, reproduction, DAF-16 transcription factor translocation, the expression of superoxide dismutase (SOD), and metabolomics were analyzed. Bee venom suppressed the growth of MDA-MB-231 cancer cells and exhibited cytotoxic effects on macrophages. Also, decreased <i>C. elegans</i> survival impacted its behaviors by decreasing <i>C. elegans</i> feeding behavior, movement, and reproduction.</p><p><strong>Results: </strong>Bee venom did not increase the expression of SOD-3, but it enhanced DAF-16 translocation from the cytoplasm to the nucleus. <i>C. elegans</i> metabolites differed after bee venom exposure, primarily related to aminoacyl- tRNA biosynthesis, glycine, serine and threonine metabolism, and sphingolipid and purine metabolic pathways. Our findings indicate that exposure to bee venom resulted in harmful effects on the cells and animal models examined.</p><p><strong>Conclusion: </strong>Thus, due to its potential toxic effect and induction of allergic reactions, using bee venom as a therapeutic approach has been limited. 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Bee Venom Toxic Effect on MDA-MB-231 Breast Cancer Cells and Caenorhabditis Elegans.
Introduction: Bee venom has therapeutics and pharmacological properties. Further toxicological studies on animal models are necessary due to the severe allergic reactions caused by this product.
Method: Here, Caenorhabditis elegans was used as an in vivo toxicity model, while breast cancer cells were used to evaluate the pharmacological benefits. The bee venom utilized in this research was collected from Apis mellifera species found in Northeast Brazil. The cytotoxicity caused by bee venom was measured by MTT assay on MDA-MB-231 and J774 A.1 cells during 24 - 72 hours of exposure. C. elegans at the L4 larval stage were exposed for three hours to M9 buffer or bee venom. Survival, behavioral parameters, reproduction, DAF-16 transcription factor translocation, the expression of superoxide dismutase (SOD), and metabolomics were analyzed. Bee venom suppressed the growth of MDA-MB-231 cancer cells and exhibited cytotoxic effects on macrophages. Also, decreased C. elegans survival impacted its behaviors by decreasing C. elegans feeding behavior, movement, and reproduction.
Results: Bee venom did not increase the expression of SOD-3, but it enhanced DAF-16 translocation from the cytoplasm to the nucleus. C. elegans metabolites differed after bee venom exposure, primarily related to aminoacyl- tRNA biosynthesis, glycine, serine and threonine metabolism, and sphingolipid and purine metabolic pathways. Our findings indicate that exposure to bee venom resulted in harmful effects on the cells and animal models examined.
Conclusion: Thus, due to its potential toxic effect and induction of allergic reactions, using bee venom as a therapeutic approach has been limited. The development of controlled-release drug strategies to improve this natural product's efficacy and safety should be intensified.
期刊介绍:
Formerly: Current Medicinal Chemistry - Anti-Cancer Agents.
Anti-Cancer Agents in Medicinal Chemistry aims to cover all the latest and outstanding developments in medicinal chemistry and rational drug design for the discovery of anti-cancer agents.
Each issue contains a series of timely in-depth reviews and guest edited issues written by leaders in the field covering a range of current topics in cancer medicinal chemistry. The journal only considers high quality research papers for publication.
Anti-Cancer Agents in Medicinal Chemistry is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments in cancer drug discovery.