Oxenkrug G F, Requintina P J, Correa R M, Yuwiler A
Pineal Research Laboratory, VAMC, Providence, Rhode Island.
J Neural Transm Suppl. 1994;41:249-52. doi: 10.1007/978-3-7091-9324-2_32.
Six months of administration of the selective MAO-B inhibitor, selegiline (l-deprenyl 0.25 mg/kg, s.c.) to aged female Fisher 344N rats suppressed MAO-A as well as MAO-B activity and increased serotonin (substrate for melatonin biosynthesis) and N-acetylserotonin (immediate melatonin precursor) levels in pineal glands taken from the animals during the night. Daytime values were unchanged by the treatment. The data suggest that stimulation of pineal melatonin biosynthesis might be one of the consequences of MAO-A inhibition contributing to life span prolongation induced by chronic selegiline treatment.
对老年雌性Fisher 344N大鼠皮下注射选择性单胺氧化酶B（MAO-B）抑制剂司来吉兰（左旋司来吉兰0.25毫克/千克），持续六个月，可抑制MAO-A和MAO-B的活性，并增加夜间取自这些动物的松果体中血清素（褪黑素生物合成的底物）和N-乙酰血清素（褪黑素的直接前体）的水平。治疗对白天的值没有影响。数据表明，刺激松果体褪黑素生物合成可能是MAO-A抑制的后果之一，有助于慢性司来吉兰治疗诱导的寿命延长。
