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Glutathione esters

Martensson, J., Steinherz, R, Jain, A. and Meister, A. (1989). Glutathione ester prevents buthionine sulfoxamine-induced cataracts and lens epithelial damage. Proc. Natl Acad. Sci. USA 86, 8727-8731. [Pg.140]

I. Grattagliono, P. Wieland, C. Schranz, B. H. Lauterburg, Disposition of Glutathione Monoethyl Ester in the Rat Glutathione Ester Is a Slow Release Form of Extracellular Glutathione , J. Pharmacol. Exp. Ther. 1995, 272, 484-488. [Pg.536]

Andrew, D.J., Lindsay, C.D. (1998). Protection of human upper respiratory tract cell lines against sulphur mustard toxicity by glutathione esters. Hum. Exp. Toxicol. 17 387-95. [Pg.623]

Glutathione esters have been shown to increase the levels of GSH in the liver and kidney of mice. Administration of y-glutamylcysteinylglycine monomethyl or monoethyl esters at doses of 10 mmol/kg intraperitoneally raised GSH levels 4-fold in mice with GSH levels depleted by prior treatment with l-buthionine sulphoxime (Puri and Meister 1983). The improved uptake of the esters, and their subsequent intracellular hydrolysis to GSH may be explained by improved permeability through lysosomal membranes, and by specific hydrolysis by lysosomal esterases (Goldman 1973, Goldman and Naider 1974). [Pg.276]

FIGURE 12. A comparison of the proliferation (" H-thymidine incorporation) response of HCPC-1 cells following treatment with ascorbic acid and other agents (70 p-M, 6hr). The groups were as follows 1) untreated, 2) (i-carotene, 3) ascorbic acid, 4) a-tocopherol acid succinate, 5) retinyl palmitate, 6) canthaxanthin, 7) glutathione (ester), 8) glutathione (reduced), 9) glutathione (oxidized). Ascorbic acid treatment produced a profound reduction in proliferation at this dose and incubation period. [Pg.244]

The only disorder of the y-glutamyl cycle for which treatment principles have been developed is glutathione synthetase deficiency (9.2) [1]. The initial symptoms in the neonatal period may be metabolic acidosis and jaundice. Acidosis usually needs to be corrected with sodium bicarbonate, THAM or sodium citrate. Patients may benefit from oral administration of vitamin E (10 mg/kg/day) and vitamin C (100 mg/kg/day). Trials have also been made with N-acetylcysteine and glutathione esters which increased glutathione in leukocytes and plasma. Both these compounds lead to increased intracellular levels of glutathione. However, no decrease in the excretion of 5-oxoprolinuria has been reported. [Pg.241]

Sultatos LG, Huang GJ, Jackson O, et al. 1991. The effect of glutathione monoethyl ester on the potentiation of the acute toxicity of methyl parathion, methyl paraoxon or fenitrothion by diethyl maleate in the mouse. Toxicol Lett 55 77-83. [Pg.233]

The degradation of vinyl chloride and ethene has been examined in Mycobacterium sp. strain JS 60 (Coleman and Spain 2003) and in Nocardioides sp. strain JS614 (Mattes et al. 2005). For both substrates, the initially formed epoxides underwent reaction with reduced coenzyme M and, after dehydrogenation and formation of the coenzyme A esters, reductive loss of coenzyme M acetate resulted in the production of 5-acetyl-coenzyme A. The reductive fission is formally analogous to that in the glutathione-mediated reaction. [Pg.307]

Neuschwander-Tetri, B.A., Ferrell, L.D., Sukhabote, R.J. and Grendell, J.H. (1992). Glutathione monoethyl ester ameliorates caerulein-induced pancreatitis in the mouse. J. Clin. Invest. 89, 109-116. [Pg.168]

Figure 1.62 SATA can react with available amine groups in proteins and other molecules via its NHS ester end to form protected sulfhydryl derivatives. The illustrated protein is glutathione-S-transferase (E.C.2.5.1.18) (Ji et al., 1995). Figure 1.62 SATA can react with available amine groups in proteins and other molecules via its NHS ester end to form protected sulfhydryl derivatives. The illustrated protein is glutathione-S-transferase (E.C.2.5.1.18) (Ji et al., 1995).
The reactions of glutathione and cysteine esters have been modeled by the reaction of methanethiol with A-formyloxy-A-methoxyformamide 40 at the BP/ DN //6-31G level.45 The transition state (Fig. 24) possesses similar characteristics... [Pg.87]

Substrates for the sulfotransferases include such varied compounds as primary and secondary alcohols, hydroxysteroids, phenols, organic hydroxylamines, and amines. As is the case with formation of glutathione and glucuronide conjugates, the formation of a sulfate ester usually renders a substance more polar and more readily excreted. Several reviews on the multiple forms of sulfotransferases and their specificities and properties are available (133-135). [Pg.357]


See other pages where Glutathione esters is mentioned: [Pg.33]    [Pg.36]    [Pg.120]    [Pg.907]    [Pg.96]    [Pg.61]    [Pg.33]    [Pg.36]    [Pg.120]    [Pg.907]    [Pg.96]    [Pg.61]    [Pg.446]    [Pg.490]    [Pg.555]    [Pg.318]    [Pg.305]    [Pg.117]    [Pg.100]    [Pg.40]    [Pg.571]    [Pg.153]    [Pg.161]    [Pg.175]    [Pg.144]    [Pg.364]    [Pg.364]    [Pg.300]    [Pg.830]    [Pg.86]    [Pg.87]    [Pg.143]    [Pg.240]    [Pg.245]    [Pg.292]    [Pg.293]    [Pg.343]   
See also in sourсe #XX -- [ Pg.907 ]

See also in sourсe #XX -- [ Pg.61 , Pg.145 ]




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