Smolen A, Smolen T N, Collins A C
Pharmacol Biochem Behav. 1982 Jul;17(1):91-7. doi: 10.1016/0091-3057(82)90268-4.
The effect of pregnancy on chemically-induced seizures in mice was studied. Latencies to myoclonic and clonic seizures induced by inhalation of flurothyl were significantly reduced at days 12 through 18 of gestation. Parturition resulted in a return of seizure susceptibility to control levels. The possibility that this effect might be mediated by decreased neurotransmitter levels subsequent to the decreased vitamin B6 levels which are known to occur during pregnancy was suggested. A pregnancy-associated liver cytosolic aldehyde dehydrogenase (pi-AlDH) utilized pyridoxal as a substrate, and the peak of pi-AlDH activity was shown to coincide with the peak of seizure susceptibility. The activity of aldehyde oxidase, the major enzyme normally responsible for the metabolism of pyridoxal, was reduced in pregnant animals. The pyridoxal 5'-phosphate synthesizing enzymes, pyridoxal kinase and pyridoxamine phosphate oxidase, were marginally increased in activity during pregnancy. It was suggested that the increased activity of pi-AlDH was indirectly responsible for the increased seizure susceptibility due to increased metabolism of pyridoxal.
研究了妊娠对化学诱导小鼠癫痫发作的影响。在妊娠第12至18天，吸入氟烷诱导的肌阵挛性和阵挛性癫痫发作的潜伏期显著缩短。分娩后癫痫易感性恢复到对照水平。有人提出，这种效应可能是由妊娠期间已知会降低的维生素B6水平导致神经递质水平降低所介导的。一种与妊娠相关的肝细胞质醛脱氢酶（pi-AlDH）利用吡哆醛作为底物，且pi-AlDH活性峰值与癫痫易感性峰值一致。醛氧化酶是通常负责吡哆醛代谢的主要酶，其活性在妊娠动物中降低。吡哆醛5'-磷酸合成酶，即吡哆醛激酶和磷酸吡哆胺氧化酶，在妊娠期间活性略有增加。有人认为，pi-AlDH活性增加是由于吡哆醛代谢增加导致癫痫易感性增加的间接原因。
