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溴酸钾引起的DNA氧化:直接机制还是与脂质过氧化有关?

DNA oxidation by potassium bromate; a direct mechanism or linked to lipid peroxidation?

作者信息

Chipman J K, Davies J E, Parsons J L, Nair J, O'Neill G, Fawell J K

机构信息

School of Biochemistry, The University of Birmingham, Edgbaston, UK.

出版信息

Toxicology. 1998 Mar 13;126(2):93-102. doi: 10.1016/s0300-483x(97)00174-1.

Abstract

Following incubation of calf thymus DNA with potassium bromate (KBrO3) and glutathione (GSH), a statistically significant increase in the concentration of 8-oxodeoxyguanosine (8-oxodG) relative to deoxyguanosine was measured. This was GSH-dependent and was associated with loss of GSH during incubation. In contrast, 8-oxodG was not found to be elevated significantly in either total tissue DNA or mitochondrial DNA isolated from Sprague-Dawley rat kidney perfused in situ with KBrO3 (5 mM) for 15 min or 1 h. There was also no associated increase in the level of renal lipid peroxidation or reduced or oxidised GSH. Following intraperitoneal administration of KBrO3 to Sprague-Dawley rats, a dose of 100 mg/kg (maximum tolerated) gave evidence for oxidative stress in the kidney at 24 h as indicated by a significant increase in lipid peroxidation (P < 0.05) and oxidised GSH (P < 0.05). This was associated with a greater than 2-fold, significant (P < 0.01) increase in the level of 8-oxodG in kidney total DNA and a 57% (not statistically significant) increase in kidney mitochondrial 8-oxodG. Pretreatment of rats with diethylmaleate (DEM) to deplete GSH, elevated the toxicity of 100 mg/kg KBrO3. However, at a dose of 20 mg/kg, no change in any of the parameters indicative of kidney oxidative stress (including indicators of oxidative DNA damage; 8-oxodG or etheno-DNA adducts, which can be produced by lipid peroxides) was seen either with or without DEM pretreatment with the exception of a small but statistically significant (P < 0.05) increase in mitochondrial 8-oxodG when KBrO3 was given following DEM pretreatment. DNA oxidation in the kidney is therefore not inhibited by GSH depletion (contrasting with in vitro findings) and requires a sustained exposure at a near-toxic concentration of KBrO3 which is associated with lipid peroxidation and GSH oxidation. The results do not support a role, in rat kidney, of a direct, GSH-mediated mechanism for KBrO3-induced DNA oxidation as seen in vitro.

摘要

将小牛胸腺DNA与溴酸钾(KBrO₃)和谷胱甘肽(GSH)一起孵育后,相对于脱氧鸟苷,8-氧代脱氧鸟苷(8-oxodG)的浓度出现了具有统计学意义的增加。这依赖于GSH,并且与孵育过程中GSH的损失有关。相比之下,在原位用KBrO₃(5 mM)灌注15分钟或1小时的Sprague-Dawley大鼠肾脏分离的总组织DNA或线粒体DNA中,未发现8-oxodG有显著升高。肾脏脂质过氧化水平、还原型或氧化型GSH也没有相应增加。给Sprague-Dawley大鼠腹腔注射KBrO₃后,100 mg/kg(最大耐受剂量)的剂量在24小时时显示出肾脏存在氧化应激,表现为脂质过氧化(P < 0.05)和氧化型GSH(P < 0.05)显著增加。这与肾脏总DNA中8-oxodG水平增加超过2倍且具有统计学意义(P < 0.01)以及肾脏线粒体8-oxodG增加57%(无统计学意义)相关。用马来酸二乙酯(DEM)预处理大鼠以耗尽GSH,会提高100 mg/kg KBrO₃的毒性。然而,在20 mg/kg的剂量下,无论是否进行DEM预处理,任何指示肾脏氧化应激的参数(包括氧化DNA损伤指标;8-oxodG或乙烯基-DNA加合物,其可由脂质过氧化物产生)均未发生变化,但在DEM预处理后给予KBrO₃时,线粒体8-oxodG有小幅但具有统计学意义(P < 0.05)的增加除外。因此,肾脏中的DNA氧化不受GSH耗竭的抑制(与体外研究结果相反),并且需要在接近毒性浓度的KBrO₃下持续暴露,这与脂质过氧化和GSH氧化相关。结果不支持在大鼠肾脏中存在如体外所见的由GSH介导的KBrO₃诱导DNA氧化的直接机制。

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