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实验用Wistar大鼠72只,随机分对照组、10ppm氟水组和30ppm氟水,于实验后组、5个月和8个月分两批处理各组动物进行检查。结果显示,长期饮用高氟水的大鼠组织中Lpo含量增多,SOD活性增强,但肝组织中Lpo及SOD无明显改变。表明Lpo水平增高可能是氟中毒时脑损伤的作用机制之一,而大脑SOD活性的增高则可能是机体对抗过氧化作用的一种代偿性保护反应。
Seventy-two experimental wistar rats were randomly divided into control group, 10 ppm fluoride water group and 30 ppm fluorine water. The animals in each group were treated in two groups after the experiment, 5 months and 8 months for examination. The results showed that the content of Lpo increased and the activity of SOD increased in rats with long-term drinking high-fluorine water, but there was no significant change in Lpo and SOD in liver tissue. It is suggested that the increase of Lpo level may be one of the mechanisms of brain injury during fluorosis, and the increase of SOD activity in the brain may be a compensatory protection response against the peroxidation of the body.