St Omer V E, Bolon B
Department of Veterinary Biomedical Services, College of Veterinary Medicine, University of Missouri, Columbia 65211.
Neurotoxicol Teratol. 1990 Mar-Apr;12(2):85-90. doi: 10.1016/0892-0362(90)90117-u.
Suckling mice exposed to secalonic acid D (SAD) mycotoxin postnatally (by gavaging dams with 0, 15 or 25 mg/kg on postgestational days 1 to 10) or prenatally (by gavaging with 25 mg/kg on gestational day 13 to produce a positive behavioral teratogenic control group) manifested subtle preweaning neurobehavioral, neurochemical and growth deficits. Gestational length, maternal weight gain, neonatal sex ratio and physical appearance of pups at birth were unaffected by treatment. Prenatal SAD (25 mg/kg) delayed (p less than 0.05) ontogeny of swimming on postnatal days (PND) 11 and 13 and reduced norepinephrine (NE) and dopamine (DA) levels in prosencephalon on PND 7 and in cerebellum-pons on PND 7-16. In the postnatal treatment groups, pup body weight gains were decreased from PND 9-22. Swimming was delayed in the 15 mg/kg postnatal exposure group on PND 11 and 13, while 25 mg/kg delayed swimming on PND 11-15. Postnatal exposure to 25 mg/kg also reduced NE and DA levels in prosencephalon and cerebellum-pons on PND 7-16. SAD thus caused concomitant ontogenetic delays in growth, swimming behavior and brain catecholamine levels following either prenatal (transplacental) or early postnatal (transmammary) exposure. These data indicate that both in utero and lactational exposures must be considered when assessing potential risks posed to developing mammals by environmental neurotoxicants.
出生后（通过在妊娠第1至10天给母鼠灌胃0、15或25 mg/kg的剂量）或出生前（通过在妊娠第13天灌胃25 mg/kg以建立阳性行为致畸对照组）暴露于黑麦烯酸D（SAD）霉菌毒素的乳鼠表现出细微的断奶前神经行为、神经化学和生长缺陷。治疗对妊娠期长度、母鼠体重增加、新生鼠性别比例和出生时幼崽的外观没有影响。产前SAD（25 mg/kg）使出生后第11天和13天的游泳发育延迟（p小于0.05），并使出生后第7天前脑以及出生后第7至16天小脑-脑桥中的去甲肾上腺素（NE）和多巴胺（DA）水平降低。在出生后治疗组中，幼崽体重增加从出生后第9天至22天减少。出生后暴露于15 mg/kg组在出生后第11天和13天游泳延迟，而25 mg/kg组在出生后第11至15天游泳延迟。出生后暴露于25 mg/kg还使出生后第7至16天前脑和小脑-脑桥中的NE和DA水平降低。因此，无论是产前（经胎盘）还是出生后早期（经乳腺）暴露，SAD都会导致生长、游泳行为和脑儿茶酚胺水平的发育延迟。这些数据表明，在评估环境神经毒物对发育中哺乳动物构成的潜在风险时，必须同时考虑子宫内和哺乳期暴露。
