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首页> 外文期刊>Biochemical Pharmacology >Effects of 2(RS)-n-propylthiazolidine-4(R)-carboxylic acid on extrahepatic sulfhydryl levels in mice treated with acetaminophen.
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Effects of 2(RS)-n-propylthiazolidine-4(R)-carboxylic acid on extrahepatic sulfhydryl levels in mice treated with acetaminophen.

机译：2（RS）-正丙基噻唑烷-4（R）-羧酸对对乙酰氨基酚治疗的小鼠肝外巯基水平的影响。

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The cysteine (Cys) precursor 2(RS)-n-propylthiazolidine-4(R)-carboxylic acid (PTCA) has been shown to protect against acetaminophen (APAP)-induced hepatic GSH, GSSG, and Cys depletion and hepatic necrosis. The aim of this study was to determine the effects of PTCA on the concentrations of sulfhydryl compounds in extrahepatic tissues, including renal cortex, whole blood, and brain, in C57BL/6 mice treated with hepatotoxic doses of APAP. PTCA (1-5 mmol/kg, i.p.) was administered 30 min after the administration of APAP at a dose (800 mg/kg; 5.29 mmol/kg, i.p.) that depleted hepatic GSH and Cys at 4 hr by 95 and 86%, respectively. Tissue concentrations of GSH and Cys were determined by HPLC. At 4 hr following APAP administration, renal cortical GSH and Cys concentrations were decreased to 64 and 39%, respectively, of vehicle-treated control values, and blood concentrations were decreased to 87 and 30%, respectively, of vehicle controls. Brain GSH and Cys were not depleted by APAP. PTCA at 5 mmol/kg (i) attenuated the APAP-induced depletion of GSH and Cys at 4 hr in renal cortex (78 and 65%, respectively, of vehicle controls), (ii) prevented APAP-induced Cys depletion in blood (670% of vehicle controls) with no effect on GSH concentration (94% of vehicle controls), and (iii) increased GSH and Cys concentrations in brain (119 and 411%, respectively, of vehicle controls). The results demonstrate a high degree of tissue selectivity in the APAP-induced depletion of GSH and Cys, and in the effectiveness of PTCA in maintaining and even elevating sulfhydryl levels in extrahepatic tissues of APAP-treated mice.
机译：半胱氨酸（Cys）前体2（RS）-正丙基噻唑烷-4（R）-羧酸（PTCA）已被证明可防止对乙酰氨基酚（APAP）诱导的肝GSH，GSSG以及Cys耗竭和肝坏死。这项研究的目的是确定PTCA对用肝毒性剂量APAP治疗的C57BL / 6小鼠肝外组织（包括肾皮质，全血和脑）中巯基化合物浓度的影响。在APAP给药后30分钟给予PTCA（1-5 mmol / kg，ip）（800 mg / kg; 5.29 mmol / kg，ip）的剂量在4小时时分别消耗了95％和86％的肝GSH和Cys ， 分别。通过HPLC测定GSH和Cys的组织浓度。在APAP给药后4小时，肾皮质GSH和Cys浓度分别降低至媒介物对照值的64％和39％，血液浓度分别降低至媒介物对照值的87％和30％。 APAP并未耗尽脑GSH和Cys。 5 mmol / kg的PTCA（i）在4小时时减弱了APAP诱导的肾皮质GSH和Cys的耗竭（分别为溶媒对照的78％和65％），（ii）防止了APAP诱导的血液Cys耗竭（ 670％的媒介物对照）对GSH浓度没有影响（94％的媒介物对照），并且（iii）脑中GSH和Cys的浓度增加（分别为媒介物对照的119％和411％）。结果表明，在APAP诱导的GSH和Cys耗竭中，组织选择性具有高度选择性，在PTCA维持和甚至升高APAP处理的小鼠肝组织中巯基水平方面，PTCA的有效性也很高。

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