Sréter I, Kiss A, Cornides A, Vereckei A, Toncsev H, Fehér J
Acta Physiol Hung. 1984;64(3-4):431-5.
The influence of a new dihydroquinoline type antioxidant on doxorubicin-induced hepatic toxicity was studied in mice (CFLP, LATI). Four groups of mice were studied: control, doxorubicin-treated, 5,6-methylen-bis (2,2,4/-trimethyl-1,2-dihydroquinoline/-disulphate (MDS)-treated, as well as doxorubicin and MDS-treated groups. Doxorubicin (15 mg/kg) was administered intraperitoneally, the MDS solution was given by a gastric tube. Liver function was assessed by the serum glutaminic-oxaloacetic-transaminase (SGOT) reaction. The lipid peroxidation in liver tissue was determined by the rate of malondialdehyd (MDA) production, the permeability of the liver lysosomal membrane was established by measuring beta-glucuronidase activity and its release from the cells. The MDS treatment proved to be effective in significantly reducing SGOT elevation, MDA production and lysosomal membrane damage in hepatic tissue. Clinical trials seem to be justified in using antioxidative substances to control doxorubicin toxicity.
在小鼠（CFLP，LATI）中研究了一种新型二氢喹啉类抗氧化剂对阿霉素诱导的肝毒性的影响。研究了四组小鼠：对照组、阿霉素处理组、5,6-亚甲基-双（2,2,4'-三甲基-1,2-二氢喹啉）-二硫酸盐（MDS）处理组以及阿霉素和MDS联合处理组。阿霉素（15mg/kg）腹腔注射，MDS溶液通过胃管给予。通过血清谷草转氨酶（SGOT）反应评估肝功能。通过丙二醛（MDA）生成速率测定肝组织中的脂质过氧化，通过测量β-葡萄糖醛酸酶活性及其从细胞中的释放来确定肝溶酶体膜的通透性。结果证明，MDS处理可有效显著降低肝组织中SGOT升高、MDA生成和溶酶体膜损伤。使用抗氧化物质来控制阿霉素毒性的临床试验似乎是合理的。
