{"title":"芹菜籽油中的天然邻苯二甲酸:对过氧化氢和叔丁基过氧化氢诱导的HepG2和CaCo-2人细胞系毒性的影响。","authors":"J. Woods, C. Jewell, N. O'Brien","doi":"10.1089/109793301753407984","DOIUrl":null,"url":null,"abstract":"Sedanolide is a natural compound occurring in edible umbelliferous plants. Celery seed oil, a significant source of sedanolide, is used as an herbal remedy to treat inflammatory-associated conditions such as gout and rheumatism. The objective of this study was to assess the potential protective properties of sedanolide against hydrogen peroxide (H(2)O(2))- and tert-butyl hydroperoxide (tBOOH)-induced toxicity in HepG2 and CaCo-2 cells. Viability of HepG2 and CaCo-2 cells was unaffected by a 24-h exposure to sedanolide (7-500 microM), however, when the cells were cultured in sedanolide-free medium for a further two cell cycles (72 h), a decrease in cell viability was observed for HepG2 cells previously exposed to 500 microM of the compound. Cells pretreated with sedanolide (100 microM for 24 h) and exposed to either H(2)O(2) or tBOOH did not exhibit statistically significant difference in viability from controls. A significant increase (p < 0.05) in DNA strand breaks, as measured by the comet assay, was observed in HepG2 but not CaCo-2 cells following a 24-h incubation with 500 microM sedanolide. Sedanolide did not modulate H(2)O(2)- and tBOOH-induced DNA damage. Sedanolide is relatively nontoxic to cells in culture, however, the protection it afforded against H(2)O(2)- and tBOOH-induced toxicity was not statistically significant.","PeriodicalId":80284,"journal":{"name":"In vitro & molecular toxicology","volume":"14 3 1","pages":"233-40"},"PeriodicalIF":0.0000,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/109793301753407984","citationCount":"29","resultStr":"{\"title\":\"Sedanolide, a natural phthalide from celery seed oil: effect on hydrogen peroxide and tert-butyl hydroperoxide-induced toxicity in HepG2 and CaCo-2 human cell lines.\",\"authors\":\"J. Woods, C. Jewell, N. O'Brien\",\"doi\":\"10.1089/109793301753407984\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Sedanolide is a natural compound occurring in edible umbelliferous plants. Celery seed oil, a significant source of sedanolide, is used as an herbal remedy to treat inflammatory-associated conditions such as gout and rheumatism. The objective of this study was to assess the potential protective properties of sedanolide against hydrogen peroxide (H(2)O(2))- and tert-butyl hydroperoxide (tBOOH)-induced toxicity in HepG2 and CaCo-2 cells. Viability of HepG2 and CaCo-2 cells was unaffected by a 24-h exposure to sedanolide (7-500 microM), however, when the cells were cultured in sedanolide-free medium for a further two cell cycles (72 h), a decrease in cell viability was observed for HepG2 cells previously exposed to 500 microM of the compound. Cells pretreated with sedanolide (100 microM for 24 h) and exposed to either H(2)O(2) or tBOOH did not exhibit statistically significant difference in viability from controls. A significant increase (p < 0.05) in DNA strand breaks, as measured by the comet assay, was observed in HepG2 but not CaCo-2 cells following a 24-h incubation with 500 microM sedanolide. Sedanolide did not modulate H(2)O(2)- and tBOOH-induced DNA damage. Sedanolide is relatively nontoxic to cells in culture, however, the protection it afforded against H(2)O(2)- and tBOOH-induced toxicity was not statistically significant.\",\"PeriodicalId\":80284,\"journal\":{\"name\":\"In vitro & molecular toxicology\",\"volume\":\"14 3 1\",\"pages\":\"233-40\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2001-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1089/109793301753407984\",\"citationCount\":\"29\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"In vitro & molecular toxicology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1089/109793301753407984\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"In vitro & molecular toxicology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1089/109793301753407984","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Sedanolide, a natural phthalide from celery seed oil: effect on hydrogen peroxide and tert-butyl hydroperoxide-induced toxicity in HepG2 and CaCo-2 human cell lines.
Sedanolide is a natural compound occurring in edible umbelliferous plants. Celery seed oil, a significant source of sedanolide, is used as an herbal remedy to treat inflammatory-associated conditions such as gout and rheumatism. The objective of this study was to assess the potential protective properties of sedanolide against hydrogen peroxide (H(2)O(2))- and tert-butyl hydroperoxide (tBOOH)-induced toxicity in HepG2 and CaCo-2 cells. Viability of HepG2 and CaCo-2 cells was unaffected by a 24-h exposure to sedanolide (7-500 microM), however, when the cells were cultured in sedanolide-free medium for a further two cell cycles (72 h), a decrease in cell viability was observed for HepG2 cells previously exposed to 500 microM of the compound. Cells pretreated with sedanolide (100 microM for 24 h) and exposed to either H(2)O(2) or tBOOH did not exhibit statistically significant difference in viability from controls. A significant increase (p < 0.05) in DNA strand breaks, as measured by the comet assay, was observed in HepG2 but not CaCo-2 cells following a 24-h incubation with 500 microM sedanolide. Sedanolide did not modulate H(2)O(2)- and tBOOH-induced DNA damage. Sedanolide is relatively nontoxic to cells in culture, however, the protection it afforded against H(2)O(2)- and tBOOH-induced toxicity was not statistically significant.