EFFECT OF 3-METHYLINDOLE ON RESPIRATORY ETHANE PRODUCTION IN SELENIUM AND VITAMIN-E DEFICIENT RATS

EFFECT OF 3-METHYLINDOLE ON RESPIRATORY ETHANE PRODUCTION IN SELENIUM AND VITAMIN-E DEFICIENT RATS
复制标题

DOI:
10.1016/s0006-291x(88)81127-6
复制
发表时间:
1988-06-16
影响因子:
3.1
通讯作者:
HOEKSTRA, WG
HOEKSTRA, WG
中科院分区:
生物学4区
文献类型:
--
作者:
KIORPES, AL;SWORD, JW;HOEKSTRA, WG

文献摘要

被引文献

相似文献

脂质过氧化被认为是3-甲基吲哚肺毒性的机制。在这份报告中,脂质过氧化测定超过16小时清醒大鼠给予400毫克/公斤的ip 3-甲基吲哚或其载体,Cremophore EL。对大鼠进行了为期8周的研究,这些大鼠被喂食维生素E和硒充足或缺乏的饮食。呼吸乙烷的产生被用作脂质过氧化的指标。3-甲基吲哚对喂饲充足饮食的大鼠的脂质过氧化没有影响。对于缺乏饮食的大鼠,3-甲基吲哚抑制脂质过氧化的50%的控制。这些结果表明,脂质过氧化不是3-甲基吲哚肺毒性的机制,并支持3-甲基吲哚可能作为抗氧化剂的结论。
Lipid peroxidation has been proposed as a mechanism of 3-methylindole pneumotoxicity. In this report, lipid peroxidation was measured over 16 h in awake rats given 400 mg/kg i.p. 3-methylindole or its carrier, Cremophore EL. Rats were studied after 8 weeks of feeding a diet either adequate or deficient in vitamin E and selenium. Respiratory ethane production was used as the index of lipid peroxidation. 3-methylindole had no effect on lipid peroxidation for rats fed the adequate diet. For rats on the deficient diet, 3-methylindole suppressed lipid peroxidation by 50% of control. These results indicate that lipid peroxidation is not a mechanism of 3-methylindole pneumotoxicity and support the conclusion that 3-methylindole may act as an antioxidant.