Reference

Plasma glutathione and glutathione disulfide in the rat: regulation and response to oxidative stress

Plasma glutathione and glutathione disulfide in the rat: regulation and response to oxidative stress. Adams, James D.; Bernhard, J.; Lauterburg, H.; Mitchell, Jerry R. (Inst. Lipid Res., Baylor Coll. Med., Houston, TX 77030, USA). J. Pharmacol. Exp. Ther., 227(3), 749-54 (English) 1983. CODEN: JPETAB. ISSN: 0022-3565. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Section cross-reference(s): 1 Plasma GSH [70-18-8] and GSSG [27025-41-8] concns. were examd. after the administration of compds. that deplete intracellular GSH either by adduct formation or by prodn. of oxidative stress. Control arterial plasma GSH and GSSG concns. were 16.5 and 0.3 mM, resp. Depletion of GSH by fasting or by the administration of acetaminophen [103-90-2] or di-Et maleate [141-05-9] was assocd. with a proportional decrease in the arterial plasma GSH concns. consistent with the hypothesis that the liver in vivo is a major source of plasma GSH. Diquat [2764-72-9] and tert-butylhydroperoxide [75-91-2], but not acetaminophen or di-Et maleate, elicited large increases in arterial plasma GSSG concns. (17- and 115-fold, resp.) and several-fold increases in biliary GSSG levels without markedly increasing hepatic GSSG levels (2.7- and 1.2-fold, resp.). In contrast, treatment with paraquat [4685-14-7] produced substantial increases in arterial plasma GSSG levels (22-fold) without large increases in the bile (3-fold). Assessment of the arteriovenous difference for GSSG across the lungs after paraquat administration demonstrated that the lung may be a significant source of plasma GSSG. Plasma GSH concns. appear to reflect mainly intrahepatic GSH concn., whereas plasma GSSG appears to arise from both hepatic and extrahepatic sites. Plasma GSSG concns. provide a sensitive index of whole-body oxidative stress as induced by oxidant drugs and the relative contribution from organs such as lung and liver can be estd. by detn. of arteriovenous differences in disulfide concns.

Effects of various agents on the in vivo "lipoperoxide" content of rat liver and kidney and on the "lipoperoxide" and lipid content of liver slices

Effects of various agents on the in vivo "lipoperoxide" content of rat liver and kidney and on the "lipoperoxide" and lipid content of liver slices. Agostini, C.; Di Segni, M.; Negrini, A. (Ist. Patol. Gen., Univ. Milano, Milan 20133, Italy). Res. Commun. Chem. Pathol. Pharmacol., 42(2), 349-52 (English) 1983. CODEN: RCOCB8. 13073-35-3 and 3416-24-8 which are cas registry numbers of chemicals are mentioned. ISSN: 0034-5164. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 4, 8 Lipoperoxide content increases in rat livers 2h after emetine [483-18-1] and glucosamine [3416-24-8] and 24 h after CCl4 [56-23-5], cycloheximide [66-81-9], colchicine [64-86-8], emetine and ethionine [13073-35-3] administration. Renal lipoperoxides decrease 24 h after glucosamine and 24 h and 72 h after x-rays. In liver slices, thiobarbituric acid-reactive substances (lipoperoxides) are increased by diethyl maleate [141-05-9], glucosamine and puromycin [53-79-2]. The loss in lipid content is accelerated in liver slices by cycloheximide, emetine, FeCl3 [7705-08-0] but counteracted by colchicine and EtOH [64-17-5]. .