Bilenko M V, Kagan V E, Velikhanova D M, Komarov P G
Biull Eksp Biol Med. 1983 Apr;95(4):30-2.
One-hour ischemia followed by rat liver reoxygenation brings about the accumulation of endogenous products of lipid peroxidation (LPO) and deterioration of the monooxygenase system (the drop of cytochrome P-450 content, amidopyrine N-demethylase and NADP X H cytochrome reductase activity). Application of the antioxidant ionol inhibited LPO and protected the monooxygenase system from reoxygenation but not from ischemic injuries. Phenobarbital alone and combined with ionol did not protect the monooxygenase system from ischemic and reoxygenation injuries but provided the retention of high absolute indicators of the system. Ionol and its combination with phenobarbital also increased the survival of rats with ischemized liver.
大鼠肝脏缺血1小时后再给氧,会导致脂质过氧化(LPO)内源性产物的积累以及单加氧酶系统的恶化(细胞色素P - 450含量下降、氨基比林N - 脱甲基酶和NADP X H细胞色素还原酶活性降低)。抗氧化剂离子醇的应用可抑制LPO,并保护单加氧酶系统免受再给氧损伤,但不能防止缺血性损伤。单独使用苯巴比妥以及与离子醇联合使用,均不能保护单加氧酶系统免受缺血和再给氧损伤,但能使该系统保持较高的绝对指标。离子醇及其与苯巴比妥的组合还提高了肝脏缺血大鼠的存活率。