Pulse Radiolytic Study of Hydrogen Transfer from Glutathione to Organic Radicals

Baker, M.Z.; Badiello, R.; Tamba, Maurizio; Quintiliani, M.; Gorin, George

doi:10.1080/09553008214550691

Cited by 45 publications

(19 citation statements)

References 7 publications

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“…These values agree with previous, pulse radiolytically determined rate constants for thiyl radical-mediated hydrogen abstraction from various model alcohols and ethers [74,78,79]. In contrast, the reverse reaction, hydrogen transfer from thiols to carbohydrate radicals, proceeds with k À29 > 10 6 M À1 s À1 [80,81], indicating that equilibrium (3.29) is normally located far to the left-hand side.…”

Section: ð3:26þsupporting

confidence: 89%

Hydrogen Atom Transfer in Model Reactions

Schöneich

2006

Hydrogen‐Transfer Reactions

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Section: ð3:26þsupporting

confidence: 89%

Hydrogen Atom Transfer in Model Reactions

Schöneich

2006

Hydrogen‐Transfer Reactions

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“…However, several studies have reported that GSH content decreases after ischemia and/or reperfusion in rat brain without a concomitant increase in GSSG (2,3,28). Other studies have suggested that GSH in the absence of GSH peroxidase can act as a free radical scavenger (29)(30)(31). From these results, it is suggested that the decrease in GSH levels following cerebral ischemia is caused by GSH not only serving as a substrate for GSH peroxidase but also scavenging free radicals.…”

Section: Methodsmentioning

confidence: 50%

Attenuation of focal cerebral ischemic injury in transgenic mice overexpressing CuZn superoxide dismutase.

Kinouchi

Epstein

Mizui

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

542

244

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Oxygen-derived free radicals have been implicated in the pathogenesis of vasogenic edema and infarction caused by ischeria and reperfusion injury. In earlier studies, exogenously supplied liposome-entrapped CuZn superoxide dismutase (CuZn-SOD) ameliorated ischemic brain edema and infarction in rats following focal cerebral ischemla. To ascertain directly the role of SOD in the protection against superoxide radical-induced injury, we measured infarct size and water content 24 hr following focal cerebral ischemia in nontransgenic mice and in transgeic mice bearing the human SODI gene. These transgenic mice have 3.1-fold higher cellular CuZn-SOD activity in the brain than do their nontransgenic littermates. We also'measured antioxidant levels (reduced glutathione and reduced ascorbate) of contralateral cortex, infarct cortex, surrounding cortex, and striatum. Infarct size and brain edema were s ntly decreased in trenic mice compared with nontransgenic mice. Reduced glutathione and reduced ascorbate levels decreased in the ischemlc hemisphere, -but levels-in surrounding cortex and striaturm were gficantly higher in trasgenic'mice than in nontransgenic mice. These rEsults indicate that increased endogenous SOD activity in brain reduces the level of ischemic damage and support the concept that superoxide radicals play an important role in the-pathogenesis of infarction and edema following focal cerebral ischemia.The role of oxygen free radicals in the pathogenesis of infarction and edema following cerebral ischemia has been intensively investigated since the report of Flamm et al. (1).Because of technical 4ffficulties in the measurement of free radicals'in brain tissues the part played by free radicals in the pathogenesis of cerebral ischemia still remains unclear (2, 3). However, reports of decreased levels of lipid-soluble and water-soluble endogenous antioxidants and of increased levels ofconjugated dienes and lipid peroxidation (4-10) support the notion that free radicals are involved in ischemic brain injury.Indirect methods using specific antioxidants [e.g., superoxide dismutase (SOD) and catalase] have traditionally been used to implicate oxygen free radicals in physiological or pathological processes. Unfortunately, the half-life of CuZn-SOD in circulating blood is extremely short (6 min), and it is unable to pass the blood-brain barrier. Therefore, use has been made of chemically modified enzymes for work on cerebral injury (11), and it has been found that polyethylene glycol-conjugated CuZn-SOD (PEG-SOD) and PEG-catalase reduce the degree of cortical infarction resulting from focal cerebral ischemia (12). Similarly, CuZn-SOD conjugated with divinyl ether/maleic acid copolymer ameliorated delayed hippocampal neuronal death after global cerebral ischemia in the gerbil brain (13). Liposome-entrapped CuZn-SOD, which has a half life of 4.2 hr (11), reduces the severity of traumatic and ischemic injuries (14,15).Although these studies provide potential therapeutic precedents for the management of brain in...

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“…First, the initial reaction certainly occurs for simple aliphatic carbon-centered radicals ( §II.C,l.b). However when a variety of structures are tested and the extent of reaction Is determined, it has been noted that when the target radical is more biologically relevant, this reaction is quan titatively less important [44]. Furthermore, kinetic treatment of these data suggests that when competing reactions vie for the Initially formed target radical, including intramolecular reactions, only a subset of the reaction products may be susceptible to this "repair" reaction [437].…”

Section: B Thiols and Free Radical Reactionsmentioning

confidence: 99%

Chemical protection against ionizing radiation. Final report

Livesey¹,

Reed²,

Adamson³

1984

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Section II reviews the contributions of various natural factors which influence the inherent radiosensitivity of biological systems. Included in the list of these factors are water, oxygen, thiols, vitamins and antioxi-«• dants. Brief attention is given to the model describing competition between oxygen and natural radioprotective substances (principally, thiols) in deter mining the net cellular radiosensitivity. Several theories of the mechanism(s) of action of radioprotective drugs are described in Section III. These mechanisms include the production of hypoxia, detoxication of radiochemical reactive species, stabilization of the radiobiological target and the enhancement of damage repair processes. Section IV describes the current strategies for the treatment of radiation injury. Likely areas in which fruitful research might be performed are described in Section V. Appendices are devoted to lists of currently-funded research projects involving chemical radiation protection and a brief compendium of compounds which have been tested for radioprotective activity.

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Pulse Radiolytic Study of Hydrogen Transfer from Glutathione to Organic Radicals

Cited by 45 publications

References 7 publications

Hydrogen Atom Transfer in Model Reactions

Hydrogen Atom Transfer in Model Reactions

Attenuation of focal cerebral ischemic injury in transgenic mice overexpressing CuZn superoxide dismutase.

Chemical protection against ionizing radiation. Final report

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