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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Horner S A, Fry J R, Clothier R H, Balls M

Xenobiotica. 1987 Jun;17(6):777-82. doi: 10.3109/00498258709043985.

A V79 cell incubation incorporating rat liver 9000 g supernatant (S9) fractions, used previously to detect the toxicity due to long-lived, stable metabolites of cyclophosphamide, has been used to study the toxicity of short-lived, reactive metabolites generated from bromobenzene. 2. Cytotoxicity was observed in the presence of S9 fractions from rats treated with phenobarbitone but not in the presence of S9 fractions from untreated or beta-naphthoflavone-treated animals. This toxicity was enhanced by depletion of the glutathione in the S9 fraction by prior treatment of the animals with diethyl maleate and was reduced by SKF 525 A, in agreement with results in vivo on the mechanism of bromobenzene-induced hepatotoxicity. 3. This study demonstrates that cytotoxicity due to the generation of short-lived, reactive metabolites can be detected in this system in vitro provided that procedures are used to modify the activating and detoxifying enzyme systems within the S9 fraction.

利用先前用于检测环磷酰胺长寿命稳定代谢产物毒性的、包含大鼠肝脏9000g上清液（S9）组分的V79细胞培养体系，来研究溴苯产生的短寿命活性代谢产物的毒性。2. 在使用苯巴比妥处理过的大鼠的S9组分存在的情况下观察到了细胞毒性，而在未处理或用β-萘黄酮处理过的动物的S9组分存在的情况下则未观察到。通过用马来酸二乙酯预先处理动物使S9组分中的谷胱甘肽耗竭，这种毒性增强了，而SKF 525 A使其降低，这与溴苯诱导肝毒性机制的体内结果一致。3. 本研究表明，只要采用程序来改变S9组分内的活化和解毒酶系统，在该体外体系中就能检测到因短寿命活性代谢产物的产生而导致的细胞毒性。

Horner S A, Fry J R, Clothier R H, Balls M

Xenobiotica. 1987 Jun;17(6):777-82. doi: 10.3109/00498258709043985.

A V79 cell incubation incorporating rat liver 9000 g supernatant (S9) fractions, used previously to detect the toxicity due to long-lived, stable metabolites of cyclophosphamide, has been used to study the toxicity of short-lived, reactive metabolites generated from bromobenzene. 2. Cytotoxicity was observed in the presence of S9 fractions from rats treated with phenobarbitone but not in the presence of S9 fractions from untreated or beta-naphthoflavone-treated animals. This toxicity was enhanced by depletion of the glutathione in the S9 fraction by prior treatment of the animals with diethyl maleate and was reduced by SKF 525 A, in agreement with results in vivo on the mechanism of bromobenzene-induced hepatotoxicity. 3. This study demonstrates that cytotoxicity due to the generation of short-lived, reactive metabolites can be detected in this system in vitro provided that procedures are used to modify the activating and detoxifying enzyme systems within the S9 fraction.

利用先前用于检测环磷酰胺长寿命稳定代谢产物毒性的、包含大鼠肝脏9000g上清液（S9）组分的V79细胞培养体系，来研究溴苯产生的短寿命活性代谢产物的毒性。2. 在使用苯巴比妥处理过的大鼠的S9组分存在的情况下观察到了细胞毒性，而在未处理或用β-萘黄酮处理过的动物的S9组分存在的情况下则未观察到。通过用马来酸二乙酯预先处理动物使S9组分中的谷胱甘肽耗竭，这种毒性增强了，而SKF 525 A使其降低，这与溴苯诱导肝毒性机制的体内结果一致。3. 本研究表明，只要采用程序来改变S9组分内的活化和解毒酶系统，在该体外体系中就能检测到因短寿命活性代谢产物的产生而导致的细胞毒性。