Amelioration of Doxorubicin-Induced Cardiac and Renal Toxicity by Oxycarotenoid Lutein and Its Mechanism of Action.

E. Sindhu, Thattaruparambil Raveendran Nithya, P. Binitha, R. Kuttan
{"title":"Amelioration of Doxorubicin-Induced Cardiac and Renal Toxicity by Oxycarotenoid Lutein and Its Mechanism of Action.","authors":"E. Sindhu, Thattaruparambil Raveendran Nithya, P. Binitha, R. Kuttan","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.2016014010","DOIUrl":null,"url":null,"abstract":"We set out to determine the effect of oxycarotenoid lutein on reducing cardiac and renal toxicity induced by doxorubicin (DXR). We started with oral administration in rats of lutein for 15 d before administering DXR (30 mg/kg body weight, intraperitoneally, in a single dose). Animals in all groups were sacrificed 24 h after DXR administration. Serum markers of cardiac injury lactate dehydrogenase, creatine phosphokinase, serum glutamate oxaloacetate transaminase, and serum glutamate pyruvate transaminase increased drastically after DXR but decreased after lutein treatment (p < 0.001). Elevated serum urea and creatinine in DXR-treated rats were reduced by lutein treatment (p < 0.001). Lutein increased superoxide dismutase, catalase, glutathione peroxidase, and glutathione levels in cardiac and renal tissues of DXR-treated rats. Pretreatment of lutein reduced DXR-induced rise of oxidative stress markers including lipid peroxidation, tissue hydroperoxides, and conjugated dienes in cardiac and renal tissue. These findings were supported by electrocardiogram measurements and histopathological analyses. Results confirmed the protection of lutein against cardiac and renal toxicity induced by DXR in rats.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.2016014010","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 9

Abstract

We set out to determine the effect of oxycarotenoid lutein on reducing cardiac and renal toxicity induced by doxorubicin (DXR). We started with oral administration in rats of lutein for 15 d before administering DXR (30 mg/kg body weight, intraperitoneally, in a single dose). Animals in all groups were sacrificed 24 h after DXR administration. Serum markers of cardiac injury lactate dehydrogenase, creatine phosphokinase, serum glutamate oxaloacetate transaminase, and serum glutamate pyruvate transaminase increased drastically after DXR but decreased after lutein treatment (p < 0.001). Elevated serum urea and creatinine in DXR-treated rats were reduced by lutein treatment (p < 0.001). Lutein increased superoxide dismutase, catalase, glutathione peroxidase, and glutathione levels in cardiac and renal tissues of DXR-treated rats. Pretreatment of lutein reduced DXR-induced rise of oxidative stress markers including lipid peroxidation, tissue hydroperoxides, and conjugated dienes in cardiac and renal tissue. These findings were supported by electrocardiogram measurements and histopathological analyses. Results confirmed the protection of lutein against cardiac and renal toxicity induced by DXR in rats.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
类胡萝卜素叶黄素改善阿霉素所致心脏和肾脏毒性及其作用机制。
我们着手确定类胡萝卜素叶黄素对减少阿霉素(DXR)引起的心脏和肾脏毒性的作用。我们先给大鼠口服叶黄素15天,然后给药DXR (30 mg/kg体重,腹腔注射,单剂量)。DXR给药后24 h处死各组动物。心肌损伤指标乳酸脱氢酶、肌酸磷酸激酶、谷氨酸草酰乙酸转氨酶和谷氨酸丙酮转氨酶在DXR治疗后显著升高,叶黄素治疗后显著降低(p < 0.001)。叶黄素处理降低了dxr处理大鼠血清尿素和肌酐升高(p < 0.001)。叶黄素增加了dxr处理大鼠心脏和肾脏组织中超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽水平。叶黄素预处理降低了dxr诱导的氧化应激标志物的升高,包括心脏和肾脏组织中的脂质过氧化、组织氢过氧化物和共轭二烯。这些发现得到了心电图测量和组织病理学分析的支持。结果证实叶黄素对大鼠DXR所致的心脏和肾脏毒性具有保护作用。
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 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Can the Toxic Heavy Metals Be Beneficial at Trace Levels? Understanding Their Outranged Biological Functions. Chemotherapeutic Drugs Endow Gastric Cancer Mesenchymal Stem Cells with Stronger Tumor-Promoting Ability. Comprehensive Investigation of m6A Regulators for Prognosis in Head and Neck Squamous Cell Carcinoma. Frequency of Healthy Control Genotype of VDR Gene Polymorphisms in the Saudi Population of the Ha'il Region: A Comparative Study with Worldwide Population. The Mutational and Transcriptional Landscapes of Speckle-Type POZ Protein (SPOP) and Androgen Receptor (AR) in a Single-Center pT3 Prostatectomy Cohort.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1