为探讨酒精对肝细胞损伤的自由基机理,首先研究酒精对体外培养的L-02肝细胞的增殖和生化指标的影响.实验表明,酒精浓度在100mL·L^-1以上时,共培养结束后30h内细胞存活率始终低于50%;当酒精浓度控制在80mL·L^-1以下时,细胞恢复过程中存在存活率突降又上升的时间段;当酒精与细胞共培养时间为2、3、4h时,存活率突降又上升的时间段分别为18、12、6h.结果表明,酒精对肝细胞的损伤因浓度和与细胞共培养时间不同而造成化学损伤(即由酒精及其代谢产物本身的毒性直接杀死细胞)和自由基损伤.酒精引起的自由基损伤具有滞后性;随着与细胞共培养时间的延长,自由基攻击的时间会提前,并且所需的酒精浓度会降低.实验结果证实了酒精对肝细胞损伤确实与自由基有重要的关系,也为从清除自由基途径预防和治疗酒精性肝病提供一定的理论依据.
Objective this paper study on mechanism of the free radical damage caused by alcohol. Methods the effect of alcohol on cell proliferation and biochemical permanents of L - 02 cells was investigated. Results while the alcohol concentration is above 100 mL·L^-1, the rate of cell survival is always below 50% in 30 hours during incubated with alcohol. While the alcohol concentration is below 80mL·L^-1 , the rate of cell survival is keeping in the low level in 18 hours, after that the cells will recover soon. Conclusions these interesting results indicated that the damage of alcohol on the L -02 cell can be divided into two phages, including the chemical damage phage and the free radical damage phage. The free radical damage as a "second hit" is always following the chemical damage. We extend the incubation time with alcohol, the free radical damage in cells is coming earlier and lower concentration of alcohol can trigger the free radical damage. Results also proved that the free radicals play an important role in alcoholic cell damage, and also proved that intracellular free radical scavengers can be good potential drugs for alcoholic liver diseases.