Stability of Zinc Complexes with Glutathione and Oxidized Glutathione<sup>1</sup>

Li, Norman C.; Gawron, Oscar; Bascuas, Gloria

doi:10.1021/ja01630a058

Cited by 56 publications

(31 citation statements)

References 2 publications

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“…Since the ionizations of both carboxylic acid protons are close together and so are the ionizations of the sulfhydryl and the ammonium groups, the macroconstants determined are composite of the microscopic constants for ionization from the individual groups. Our macroscopic constants (Table 1) are in accordance with those obtained by other authors [26][27][28].…”

Section: Potentiometric Studiessupporting

confidence: 91%

Equilibrium characterization of the As(III)–cysteine and the As(III)–glutathione systems in aqueous solution

Rey

Howarth

Pereira-Maia

2004

Journal of Inorganic Biochemistry

132

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Section: Potentiometric Studiessupporting

confidence: 91%

Equilibrium characterization of the As(III)–cysteine and the As(III)–glutathione systems in aqueous solution

Rey

Howarth

Pereira-Maia

2004

Journal of Inorganic Biochemistry

132

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“…The mechanism of acidification‐induced intracellular Zn 2+ release needs to be further elucidated. Whereas Zn 2+ may be displaced from metallothioneins and other zinc‐binding ligands by protons (Li et al. 1954; Jiang et al.…”

Section: Discussionmentioning

confidence: 99%

Cytosolic acidification and intracellular zinc release in hippocampal neurons

Kiedrowski

2012

Journal of Neurochemistry

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In neurons exposed to glutamate, Ca2+ influx triggers intracellular Zn2+ release via an as yet unclear mechanism. Since glutamate induces a Ca2+-dependent cytosolic acidification, the present work tested the relationships among intracellular Ca2+ concentration ([Ca2+]i), intracellular pH (pHi), and [Zn2+]i. Cultured hippocampal neurons were exposed to glutamate and glycine (Glu/Gly), while [Zn2+]i, [Ca2+]i and pHi were monitored using FluoZin-3, Fura2-FF, and 2′,7′-bis-(2-carboxyethyl)-5(6)-carboxyfluorescein, respectively. Glu/Gly applications decreased pHi to 6.1 and induced intracellular Zn2+ release in a Ca2+-dependent manner, as expected. The pHi drop reduced the affinity of FluoZin-3 and Fura-2-FF for Zn2+. The rate of Glu/Gly-induced [Zn2+]i increase was not correlated with the rate of [Ca2+]i increase. Instead, the extent of [Zn2+]i elevations corresponded well to the rate of pHi drop. Namely, [Zn2+]i increased more in more highly acidified neurons. Inhibiting the mechanisms responsible for the Ca2+-dependent pHi drop (plasmalemmal Ca2+ pump and mitochondria) counteracted the Glu/Gly-induced intracellular Zn2+ release. Alkaline pH (8.5) suppressed Glu/Gly-induced intracellular Zn2+ release whereas acidic pH (6.0) enhanced it. A pHi drop to 6.0 (without any Ca2+ influx or glutamate receptor activation) led to intracellular Zn2+ release; the released Zn2+ (free Zn2+ plus Zn2+ bound to Fura-2FF and FluoZin-3) reached 1 μM.

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“…The acid-base properties of GSH have long been in the focus of scientific interest [8][9][10][11], and even the site-specific protonation constants of GSH [12] and GSSG [13] have been studied. Nevertheless, these values are only those of the major pathways.…”

Section: Introductionmentioning

confidence: 99%