求一段英文的英翻汉,希望翻译得精准些The hepatopulmonary syndrome (HPS) occurs when intrapulmonary dilatation causes hypoxemia in cirrhosis.The free radicals mayplay a significant contributory role in the progression of HPS,and flavono

求一段英文的英翻汉,希望翻译得精准些The hepatopulmonary syndrome (HPS) occurs when intrapulmonary dilatation causes hypoxemia in cirrhosis.The free radicals mayplay a significant contributory role in the progression of HPS,and flavono
求一段英文的英翻汉,
希望翻译得精准些
The hepatopulmonary syndrome (HPS) occurs when intrapulmonary dilatation causes hypoxemia in cirrhosis.The free radicals may
play a significant contributory role in the progression of HPS,and flavonoid agents could protect against deleterious effects of free radicals.
The flavonoid quercetin was evaluated in an experimental model of biliary cirrhosis induced by bile duct ligation (BDL) in rats.Quercetin
was administered at 50 mg/kg for 14 days to cirrhotic and non-cirrhotic rats.Bone marrow was extracted from animals to analyze micronuclei.
Lung,liver and blood were extracted to detect DNA damage using the comet assay.The results showed that the micronuclei and
DNA damages to lung and liver were increased in BDL rats.Quercetin caused no damage to the DNA while decreasing the occurrence
of micronucleated cells in bone marrow as well asDNA damage to lung and liver in cirrhotic rats.Quercetin showed antimutagenic activity
against hydroperoxides as evaluated by the oxidative stress sensitive bacterial strains TA102 Salmonella typhimurium and IC203 Escherichia
coli,suggesting protection by free radical scavenging.In Saccharomyces cerevisie yeast strains lacking mitochondrial or cytosolic superoxide
dismutase,these results indicate that quercetin protects cells by induction of antioxidant enzymes.The present study is the first report of
genotoxic/antigenotoxic effects of quercetin in a model of animal cirrhosis.In this model,quercetin was not able to induce genotoxicity and,
conversely,it increased the genomic stability in the cirrhotic rats,suggesting beneficial effects,probably by its antioxidant properties.

求一段英文的英翻汉,希望翻译得精准些The hepatopulmonary syndrome (HPS) occurs when intrapulmonary dilatation causes hypoxemia in cirrhosis.The free radicals mayplay a significant contributory role in the progression of HPS,and flavono
这个太专业了,不当之处请见谅：
肺内扩张导致肝硬化部位血氧供应不足时就会发生肝肺综合症,自由基在肝肺综合症进程中可能扮演了一个极其显著的角色,类黄酮剂能够防止自由基的毒害作用..在老鼠身上进行胆管结扎诱导胆囊硬化的实验模式中进行了槲皮黄酮测试,对肝硬化和非肝硬化的老鼠进行了14天50 mg/kg剂量的槲皮黄酮治疗.从动物身上抽取了骨髓来分析微核.对肺脏、肝脏活检和抽取的血液用慧核实验来探明DNA的损害.结果显示在作了胆管结扎的老鼠中肺脏和肝脏的微核和DNA损害显著上升.槲皮黄酮对DNA没有产生损害,同时还减少了骨髓中微核细胞的发生以及对肝硬化老鼠的DNA损害.通过对氧化力特别敏感的TA102沙门氏菌落和IC203埃希氏菌属的测试,槲皮黄酮显示出了对过氧化氢物的抗诱变性.显示了它有清除自由基的保护作用.在酵母菌株缺乏线粒体或细胞溶质过氧化歧化酶的情况下,这些结果显示了通过诱导抗氧化酶,槲皮黄酮能保护细胞.现在的研究是第一次报告在动物肝硬化模式中的基因毒化/抗基因毒化作用,槲皮黄酮不能导致基因毒性作用,反而它会增进在肝硬化的老鼠中的基因的稳定性,可能由于其抗氧化的特性,显示出其有益的作用.

当intrapulmonary 扩张在肝硬变里引起hypoxemia时，hepatopulmonary综合症(HPS)发生。 自由基可能在HPS的前进扮演重要角色，和其他能防止有毒自由基的效应的黄酮类化合物内。 黄酮类化合物quercetin在一实验以胆汁导管ligation(BDL)引起在老鼠内的biliary 肝硬变的模式内评价。 Quercetin在50毫克/ 千克管理适合14日子在cirr...

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当intrapulmonary 扩张在肝硬变里引起hypoxemia时，hepatopulmonary综合症(HPS)发生。 自由基可能在HPS的前进扮演重要角色，和其他能防止有毒自由基的效应的黄酮类化合物内。 黄酮类化合物quercetin在一实验以胆汁导管ligation(BDL)引起在老鼠内的biliary 肝硬变的模式内评价。 Quercetin在50毫克/ 千克管理适合14日子在cirrhotic和非cirrhotic的老鼠。 骨髓被从动物中提炼分析micronuclei。 肺，肝和血被拔出使用彗星分析发现DNA 损害。 结果显示micronuclei 和DNA 对肺和肝的损害被在BDL老鼠里增加。 Quercetin在减少时没有引起对DNA 的损害 micronucleated 细胞的事件在骨髓也asDNA对的损害肺和肝在cirrhotic老鼠。 Quercetin象以氧化的压力敏感的细菌的负担TA102 typhimurium 和IC203 Escherichia coli 沙门氏菌评价的那样在hydroperoxides上显示antimutagenic 活动， 通过自由基清除建议保护。 在缺乏mitochondrial或者cytosolic superoxide dismutase的Saccharomyces cerevisie酵母劳累方面，这些结果表明quercetin通过抗氧化的酶的就职保护细胞。 目前的研究用一个动物肝硬变的模型是quercetin的genotoxic/antigenotoxic 影响的第一个报告。 用这个模型，quercetin不能引起genotoxicity，和，相反，它在cirrhotic里增加genomic 稳定 老鼠，建议有利的效应，或许通过它的抗氧化的特性。

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