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D-青霉胺对氧衍生自由基介导的组织损伤模型的影响。

Effects of D-penicillamine on a model of oxygen-derived free radical mediated tissue damage.

作者信息

Betts W H, Cleland L G, Gee D J, Whitehouse M W

出版信息

Agents Actions. 1984 Feb;14(2):283-90. doi: 10.1007/BF01966654.

Abstract

In vitro studies indicate that D-penicillamine can affect the depolymerization of hyaluronate in aqueous media (induced primarily by the hydroxyl radical) in several ways. These include: Protecting the hyaluronate by quenching oxygen-derived free radicals (ODFR). Hydrated cupric ions alone and copper(II)-penicillamine complexes were equipotent in quenching ODFR but more potent than D-penicillamine alone. Initiating hyaluronate degradation by (a) directly reducing inert Fe(III) to reactive Fe(II) (which may autoxidize to produce hydroxyl radicals), a property shared with other thiols, and (b) forming reactive iron complexes that catalyse the formation of hydroxyl radicals from superoxide and hydrogen peroxide.

摘要

体外研究表明,D-青霉胺可通过多种方式影响透明质酸在水性介质中的解聚(主要由羟基自由基诱导)。这些方式包括:通过淬灭氧衍生自由基(ODFR)来保护透明质酸。单独的水合铜离子和铜(II)-青霉胺络合物在淬灭ODFR方面具有同等效力,但比单独的D-青霉胺更有效。通过以下方式引发透明质酸降解:(a)直接将惰性Fe(III)还原为活性Fe(II)(其可能自动氧化产生羟基自由基),这是其他硫醇共有的特性;(b)形成活性铁络合物,催化超氧化物和过氧化氢形成羟基自由基。

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