Arkhipenko Iu V, Bilenko M V, Dobrina S K, Kagan V E, Kozlov Iu P
Biull Eksp Biol Med. 1977 Jun;83(6):683-6.
Ischemia development was accompanied by inhibition of the enzymatic transport system (ETS) of Ca2+ (reduction of the Ca2+/ATP value and of the Ca2+-dependent ATPase activity), this correlating with the accumulation of primary and secondary molecular products of lipid peroxidation (LPO) in the sarcoplasmic reticulum membranes of the skeletal muscles, in vivo. Administration of antioxidants (2,6-ditretbutyl-4-methylphenol, alpha-tocopherol) prevented the LPO activation in the ischemic muscle and partially protected the ETS of Ca2+ from damage. The blood supply restoration after prolonged ischemia led to further ETS of Ca2+ inhibition against the background of unchanges LPO products level.
缺血的发展伴随着Ca2+酶转运系统(ETS)的抑制(Ca2+/ATP值和Ca2+依赖性ATP酶活性降低),这与体内骨骼肌肌浆网膜中脂质过氧化(LPO)的一级和二级分子产物的积累相关。给予抗氧化剂(2,6-二叔丁基-4-甲基苯酚、α-生育酚)可防止缺血肌肉中的LPO激活,并部分保护Ca2+的ETS免受损伤。长时间缺血后恢复血液供应导致在LPO产物水平不变的背景下Ca2+的ETS进一步受到抑制。