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.

J. Woods, C. Jewell, N. O'Brien
{"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}
引用次数: 29

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.
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。
Sedanolide是一种存在于可食用伞形植物中的天然化合物。芹菜籽油是sedanolide的重要来源,被用作治疗炎症相关疾病的草药,如痛风和风湿病。本研究的目的是评估sedanolide对过氧化氢(H(2)O(2))-和过氧化叔丁基(tBOOH)-诱导的HepG2和CaCo-2细胞毒性的潜在保护作用。HepG2和CaCo-2细胞的活力不受24小时暴露于sedanolide (7-500 microM)的影响,然而,当细胞在无sedanolide的培养基中再培养两个细胞周期(72 h)时,先前暴露于500 microM化合物的HepG2细胞的活力下降。用sedanolide (100 microM)预处理24 h,并暴露于h (2)O(2)或tBOOH的细胞的活力与对照组相比没有统计学上的显著差异。用彗星法测定,HepG2细胞的DNA链断裂显著增加(p < 0.05),而CaCo-2细胞在500 μ m的sedanolide中孵育24小时后则没有。Sedanolide不调节H(2)O(2)-和tbooh诱导的DNA损伤。Sedanolide对培养的细胞相对无毒,然而,它对H(2)O(2)-和tbooh诱导的毒性的保护作用没有统计学意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信