Nordenberg J, Beery E, Klein S, Kaplansky M, Frucht H, Beitner R
Department of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.
Biochem Med Metab Biol. 1987 Dec;38(3):278-91. doi: 10.1016/0885-4505(87)90092-2.
ATP, added externally to the incubation medium of rat diaphragm muscles, abolished the decrease in the levels of glucose-1,6-bisphosphate (Glc-1,6-P2), the powerful regulator of carbohydrate metabolism, induced by phospholipase A2, local anesthetics, Ca2+ ionophore A23187, or lithium. Concomitantly to the changes in Glc-1,6-P2, the potent activator of phosphofructokinase (the rate-limiting enzyme in glycolysis) and phosphoglucomutase, the activities of these enzymes were reduced by the myotoxic agents and restored by exogenous ATP, when assayed under conditions in which these enzymes are sensitive to regulation by Glc-1,6-P2. These findings suggest that ATP may have broad therapeutic action, as it may stimulate the impaired glycolysis in muscle induced by various drugs and conditions which cause muscle weakness or damage.
向大鼠膈肌的孵育培养基中外加ATP,可消除由磷脂酶A2、局部麻醉剂、Ca2+离子载体A23187或锂诱导的1,6-二磷酸葡萄糖(Glc-1,6-P2)水平的降低,Glc-1,6-P2是碳水化合物代谢的强效调节剂。与Glc-1,6-P2的变化同时发生的是,磷酸果糖激酶(糖酵解中的限速酶)和磷酸葡萄糖变位酶的强效激活剂,在这些酶对Glc-1,6-P2调节敏感的条件下进行测定时,这些酶的活性被肌毒性剂降低,并被外源性ATP恢复。这些发现表明,ATP可能具有广泛的治疗作用,因为它可能刺激由各种导致肌肉无力或损伤的药物和条件所诱导的肌肉中受损的糖酵解。