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【medical-news】新的喹诺酮类药物抗菌作用机理
Novel pathway for antibiotic-induced cell death
Published: Tuesday, 13-Mar-2007
Scientists have identified unforeseen mechanisms by which quinolones - a family of broad-spectrum antibiotics among the most widely prescribed - induce bacterial cell death.
The study is published online this week in Molecular Systems Biology.
It is well-known that quinolones inhibit bacterial DNA gyrase - an enzyme essential to DNA replication - and induce cell death by stimulating DNA damage, impeding lesion repair and blocking replication processes. Using a systems biology approach, Jim Collins and colleagues reveal that, in addition to the expected DNA damage response, gyrase inhibition surprisingly triggers a genetic program characteristic of responses to oxidative stress and promotes the generation of deleterious hydroxyl radicals.
The authors confirm their findings by showing that chemical or genetic prevention of gyrase inhibitor-induced oxidative damage protects from the bactericidal action of quinolone antibiotics. This work will facilitate the identification of antibacterial therapies with improved bactericidal activity.
http://www.nature.com/msb and http://www.bu.edu 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 Novel pathway for antibiotic-induced cell death
抗生素诱导细胞死亡的新途径
Published: Tuesday, 13-Mar-2007
发表日期：2007年3月13日，星期二
Scientists have identified unforeseen mechanisms by which quinolones - a family of broad-spectrum antibiotics among the most widely prescribed - induce bacterial cell death. The study is published online this week in Molecular Systems Biology. 科学家们已经找出了以前不知道的喹诺酮类药物诱导细菌细胞死亡的一些作用机理。喹诺酮类药物是最常使用的广谱抗生素处方药之一。该研究于本周在《分子系统生物学》上网上发表。
It is well-known that quinolones inhibit bacterial DNA gyrase - an enzyme essential to DNA replication - and induce cell death by stimulating DNA damage, impeding lesion repair and blocking replication processes. Using a systems biology approach, Jim Collins and colleagues reveal that, in addition to the expected DNA damage response, gyrase inhibition surprisingly triggers a genetic program characteristic of responses to oxidative stress and promotes the generation of deleterious hydroxyl radicals. 众所周知，喹诺酮类药物可抑制细菌的DNA回旋酶—DNA复制所必需的一种酶—并通过促使DNA损伤，阻碍伤处修复及阻止复制过程而诱导细胞死亡。Jim Collins 及其同事通过使用系统生物学的方法发现，除了预料中的DNA损伤反应外，对回旋酶的抑制还令人惊讶地触发了一种基因程序，其特征是对氧化应激出现反应，并促使产生有害的羟基自由基。
The authors confirm their findings by showing that chemical or genetic prevention of gyrase inhibitor-induced oxidative damage protects from the bactericidal action of quinolone antibiotics. This work will facilitate the identification of antibacterial therapies with improved bactericidal activity. 使用化学或基因学的方法防止回旋酶抑制剂诱导的氧化损伤，即可对喹诺酮类抗生素的杀菌作用产生保护作用，研究者们由此证实了他们的发现。这一工作将有助于找到杀菌作用更好的抗生素治疗方法。
编译：
标题：科学家发现了抗生素诱导细胞死亡的新途径
科学家们已经找出了使喹诺酮类药物能诱导细菌细胞死亡的某些新的作用机理。喹诺酮类药物是最常使用的广谱抗生素处方药之一。该研究于2007年3月份在《分子系统生物学》上网上发表。
对于喹诺酮类药物的作用机理，过去人们知道的是：它们可抑制细菌的DNA回旋酶，这是一种DNA复制所必需的酶，并使细菌DNA损伤，阻碍伤处修复及阻止DNA复制过程，从而导致细菌细胞死亡。Jim Collins 及其同事通过使用系统生物学的方法惊讶地发现，喹诺酮类药物除了通过损伤细菌的DNA而起作用外，由于其对DNA回旋酶的抑制，还触发了某种基因程序，使细菌对氧化应激出现反应，并促使细菌体内产生有害的羟基自由基。
倘若使用化学或基因学的方法防止因回旋酶抑制剂诱导的氧化损伤，就能保护细菌，研究者们由此证实了他们的发现。这一工作将有助于找到杀菌作用更好的抗生素治疗方法。 [标签:content1][标签:content2]
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作者:admin@医学,生命科学 2011-05-30 19:24
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