叔丁基对苯二酚对亚砷酸钠诱导的细胞毒性和氧化损伤的保护作用

Q3 Medicine

中华地方病学杂志 Pub Date : 2011-09-20 DOI:10.3760/CMA.J.ISSN.1000-4955.2011.05.005

L. Bing, L. Xin, B. Zhu, Xinyu Zhang, Xiaoyue Xing, Dan Liu, Xin Wang, Gui-fan Sun

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On the other hand, Chang liver cells were pretreated with tBHQ[0(control), 5, 25 μmol/L] for24 h,and then co-treated with tBHQ(5 μmol/L) together with NaAsO2[0(control), 40, 50 μmol/L] for another 24 h,and the levels of cellular reactive oxygen species(ROS) were detected by staining cells with 2',7'-dichlorofluorescin diacetate(DCFH-DA), the results were expressed as the relative ratio of mean fluorescence intensity between the experimental group and the control group. Results Cell viability decreased dramatically by treatment with NaAsO2(30, 40, 50, 60 μmol/L), while relieved to some extent by pretreatment with 5, 25 μmol/L tBHQ, the main effects of NaAsO2 and tBHQ, as well as their interaction were all statistically significant(F =566.57, 55.09, 14.50,all P ＜ 0.05) ; the cell viability of NaAsO2(30, 40, 50, 60 μmol/L) pretreated with tBHQ(5, 25 mol/L) were 0.75 ±0.02, 0.70 ± 0.04, 0.59 ± 0.03, 0.43 ± 0.03 and 0.75 ± 0.02, 0.73 ± 0.03, 0.65 ± 0.02, 0.50 ± 0.02, respectively,all significantly higher than corresponding NaAsO2 alone groups(0.70 ± 0.03, 0.64 ± 0.03, 0.43 ± 0.03, 0.33 ±0.01, all P ＜ 0.05), the cell viability of NaAsO2(50, 60 μmol/L) pretreated with 25 μmol/L tBHQ was higher than corresponding 5 μmol/L tBHQ pretreatment groups(all P ＜ 0.05). On the other hand, 40, 50 μmol/L of NaAsO2 significantly induced hepatocellular ROS generation, while tBHQ(5, 25 μ mol/L) pretreatment significantly decreased NaAsO2-induced intracellular ROS levels, the main effects of NaAsO2 and tBHQ, as well as their interaction were all statistically significant (F =181.78, 60.55, 4.93, all P ＜ 0.05) ; the ROS levels of NaAsO2(40, 50 μ mol/L) pretreated with tBHQ(5, 25 μmol/L) were 1.87 ± 0.09, 1.80 ± 0.07 and 1.36 ± 0.11, 1.44 ± 0.12,all significantly decreased than corresponding NaAsO2 alone groups(2.30 ± 0.18, 2.18 ± 0.17, all P ＜ 0.05),the ROS levels of NaAsO2(40, 50 μmol/L) pretreated with 25 μmol/L tBHQ decreased than corresponding 5 μmol/L tBHQ pretreatment groups (all P ＜ 0.05). Conclusion tBHQ has a certain antagonism on arsenic induced cytotoxicity and oxidative injuries. \n \nKey words: \nArsenites; Tert-butylhydroquinone; Reactive oxygen species","PeriodicalId":55880,"journal":{"name":"中华地方病学杂志","volume":"34 1","pages":"489-492"},"PeriodicalIF":0.0000,"publicationDate":"2011-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Protective effects of tert-butylhydroquinone on sodium arsenite-induced cytotoxicity and oxidative injuries\",\"authors\":\"L. Bing, L. Xin, B. Zhu, Xinyu Zhang, Xiaoyue Xing, Dan Liu, Xin Wang, Gui-fan Sun\",\"doi\":\"10.3760/CMA.J.ISSN.1000-4955.2011.05.005\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Objective To study the protective effects of tert-butylhydroquinone(tBHQ) on sodium arsenite (NaAsO2)-induced cytotoxicity and oxidative injuries. 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On the other hand, 40, 50 μmol/L of NaAsO2 significantly induced hepatocellular ROS generation, while tBHQ(5, 25 μ mol/L) pretreatment significantly decreased NaAsO2-induced intracellular ROS levels, the main effects of NaAsO2 and tBHQ, as well as their interaction were all statistically significant (F =181.78, 60.55, 4.93, all P ＜ 0.05) ; the ROS levels of NaAsO2(40, 50 μ mol/L) pretreated with tBHQ(5, 25 μmol/L) were 1.87 ± 0.09, 1.80 ± 0.07 and 1.36 ± 0.11, 1.44 ± 0.12,all significantly decreased than corresponding NaAsO2 alone groups(2.30 ± 0.18, 2.18 ± 0.17, all P ＜ 0.05),the ROS levels of NaAsO2(40, 50 μmol/L) pretreated with 25 μmol/L tBHQ decreased than corresponding 5 μmol/L tBHQ pretreatment groups (all P ＜ 0.05). 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引用次数: 0

摘要

目的研究叔丁基对苯二酚(tBHQ)对亚砷酸钠(NaAsO2)诱导的细胞毒性和氧化损伤的保护作用。方法以tBHQ[0(对照)、5、25 μmol/L]预处理长肝细胞24 h，再以tBHQ(5 μmol/L)与NaAsO2[0(对照)、30、40、50、60 μmol/L]共处理24 h，以Alamar蓝还原率评价细胞活力，结果以实验组与对照组Alamar蓝还原率的相对比值表示。另以tBHQ[0(对照)、5、25 μmol/L]预处理长肝细胞24 h，再以tBHQ(5 μmol/L)与NaAsO2[0(对照)、40、50 μmol/L]共处理24 h，用2′，7′-二氯荧光素双乙酸酯(DCFH-DA)染色检测细胞活性氧(ROS)水平，结果用实验组与对照组平均荧光强度的相对比值表示。结果NaAsO2(30、40、50、60 μmol/L)处理后细胞活力显著降低，5、25 μmol/L tBHQ预处理后细胞活力有所缓解，NaAsO2和tBHQ的主要作用及其相互作用均有统计学意义(F =566.57、55.09、14.50，均P < 0.05);NaAsO2细胞生存能力(30、40、50、60μmol / L)使用特丁基对苯二酚(5,25 mol / L)分别为0.75±0.02、0.70±0.04、0.59±0.03、0.43±0.03、0.75±0.02、0.73±0.03、0.65±0.02、0.50±0.02,分别都明显高于相应的单独NaAsO2组(0.70±0.03,0.64±0.03,0.43±0.03,0.33±0.01,P < 0.05),所有细胞的可行性NaAsO2(50, 60μmol / L)使用25μmol / L特丁基对苯二酚高于对应5μmol / L特丁基对苯二酚预处理组(P < 0.05)。另一方面，40、50 μmol/L NaAsO2显著诱导肝细胞ROS生成，而tBHQ(5、25 μmol/L)预处理显著降低NaAsO2诱导的细胞内ROS水平，NaAsO2与tBHQ的主要作用及其交互作用均有统计学意义(F =181.78、60.55、4.93，均P < 0.05);tBHQ(5、25 μmol/L)预处理的NaAsO2(40、50 μmol/L) ROS水平分别为1.87±0.09、1.80±0.07和1.36±0.11、1.44±0.12，均显著低于单独NaAsO2处理组(2.30±0.18、2.18±0.17，均P < 0.05)， 25 μmol/L tBHQ预处理的NaAsO2(40、50 μmol/L) ROS水平均低于相应的5 μmol/L tBHQ预处理组(P < 0.05)。结论四溴六酚对砷致细胞毒性和氧化损伤具有一定的拮抗作用。关键词:亚砷酸盐;Tert-butylhydroquinone;活性氧

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Protective effects of tert-butylhydroquinone on sodium arsenite-induced cytotoxicity and oxidative injuries

Objective To study the protective effects of tert-butylhydroquinone(tBHQ) on sodium arsenite (NaAsO2)-induced cytotoxicity and oxidative injuries. Methods Chang liver cells were pretreated with tBHQ[0(control), 5, 25 μmol/L]for 24 h, and then co-treated with tBHQ(5 μmol/L) together with NaAsO2[0(control),30, 40, 50, 60 μmol/L] for another 24 h, and Alamar blue reduction rates were used to evaluate cell viability,the results were expressed as the relative ratio of Alamar blue reduction rates between the experimental group and the control group. On the other hand, Chang liver cells were pretreated with tBHQ[0(control), 5, 25 μmol/L] for24 h,and then co-treated with tBHQ(5 μmol/L) together with NaAsO2[0(control), 40, 50 μmol/L] for another 24 h,and the levels of cellular reactive oxygen species(ROS) were detected by staining cells with 2',7'-dichlorofluorescin diacetate(DCFH-DA), the results were expressed as the relative ratio of mean fluorescence intensity between the experimental group and the control group. Results Cell viability decreased dramatically by treatment with NaAsO2(30, 40, 50, 60 μmol/L), while relieved to some extent by pretreatment with 5, 25 μmol/L tBHQ, the main effects of NaAsO2 and tBHQ, as well as their interaction were all statistically significant(F =566.57, 55.09, 14.50,all P ＜ 0.05) ; the cell viability of NaAsO2(30, 40, 50, 60 μmol/L) pretreated with tBHQ(5, 25 mol/L) were 0.75 ±0.02, 0.70 ± 0.04, 0.59 ± 0.03, 0.43 ± 0.03 and 0.75 ± 0.02, 0.73 ± 0.03, 0.65 ± 0.02, 0.50 ± 0.02, respectively,all significantly higher than corresponding NaAsO2 alone groups(0.70 ± 0.03, 0.64 ± 0.03, 0.43 ± 0.03, 0.33 ±0.01, all P ＜ 0.05), the cell viability of NaAsO2(50, 60 μmol/L) pretreated with 25 μmol/L tBHQ was higher than corresponding 5 μmol/L tBHQ pretreatment groups(all P ＜ 0.05). On the other hand, 40, 50 μmol/L of NaAsO2 significantly induced hepatocellular ROS generation, while tBHQ(5, 25 μ mol/L) pretreatment significantly decreased NaAsO2-induced intracellular ROS levels, the main effects of NaAsO2 and tBHQ, as well as their interaction were all statistically significant (F =181.78, 60.55, 4.93, all P ＜ 0.05) ; the ROS levels of NaAsO2(40, 50 μ mol/L) pretreated with tBHQ(5, 25 μmol/L) were 1.87 ± 0.09, 1.80 ± 0.07 and 1.36 ± 0.11, 1.44 ± 0.12,all significantly decreased than corresponding NaAsO2 alone groups(2.30 ± 0.18, 2.18 ± 0.17, all P ＜ 0.05),the ROS levels of NaAsO2(40, 50 μmol/L) pretreated with 25 μmol/L tBHQ decreased than corresponding 5 μmol/L tBHQ pretreatment groups (all P ＜ 0.05). Conclusion tBHQ has a certain antagonism on arsenic induced cytotoxicity and oxidative injuries. Key words: Arsenites; Tert-butylhydroquinone; Reactive oxygen species

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来源期刊

中华地方病学杂志我国对人类健康危害特别严重的地方性疾病：克山病、大骨节病、碘缺乏病、地方性氟中毒、地方性砷中毒、鼠疫、布鲁氏菌病、寄生虫、新冠肺炎等疾病，同时还报道多发性自然疫源性疾病。

CiteScore

1.60

自引率

0.00%

发文量

8714

期刊介绍： The Chinese Journal of Endemiology covers predominantly endemic diseases threatening health of the people in the areas affected by the diseases including Keshan disease, Kaschin-Beck Disease, iodine deficiency disorders, endemic fluorosis, endemic arsenism, plague, epidemic hemorrhagic fever, brucellosis, parasite diseases and the diseases related to local natural and socioeconomic conditions; and reports researches in the basic science, etiology, epidemiology, clinical practice, control as well as multidisciplinary studies on the diseases.