Cancela J M, Bralet J, Beley A
Laboratoire de Pharmacodynamie, Faculté de Pharmacie, Dijon, France.
Neurochem Res. 1994 Jul;19(7):833-7. doi: 10.1007/BF00967452.
The effects of iron-induced lipid peroxidation and of lactic acidosis on [3H]choline uptake were investigated on crude synaptosomes prepared from rat cerebral cortices. Fe(2+)-induced lipid peroxidation as evidenced from the production of thiobarbituric acid reactives substances (TBARS) was correlated with a decrease in high-affinity choline uptake (HACU). Trolox C, a free radical scavenger, prevented both Fe(2+)-induced TBARS production and decrease in HACU. Lactic acidosis (pH 6.0 for 30 or 60 min) increased the TBARS production with concomitant decrease in HACU (-48%, -78%, respectively). The acidosis dependent decrease was not reversible following pH 7.4 readjustment after 60 min acidosis. It was not prevented by trolox C, although trolox C inhibited the acidosis-induced production of TBARS. The results suggest that the contribution of acidosis to peroxidative damages is probably of less importance in comparison to other cytotoxic mechanisms.
研究了铁诱导的脂质过氧化和乳酸酸中毒对从大鼠大脑皮层制备的粗制突触体中[3H]胆碱摄取的影响。从硫代巴比妥酸反应性物质（TBARS）的产生证明，Fe(2+)诱导的脂质过氧化与高亲和力胆碱摄取（HACU）的降低相关。自由基清除剂Trolox C可防止Fe(2+)诱导的TBARS产生和HACU降低。乳酸酸中毒（pH 6.0，持续30或60分钟）会增加TBARS的产生，同时HACU降低（分别为-48%，-78%）。在酸中毒60分钟后将pH值重新调整至7.4后，酸中毒依赖性降低是不可逆的。尽管Trolox C抑制了酸中毒诱导的TBARS产生，但它并不能阻止这种降低。结果表明，与其他细胞毒性机制相比，酸中毒对过氧化损伤的作用可能不太重要。
