Golub Mari S, Hogrefe Casey E, Germann Stacey L, Capitanio John P, Lozoff Betsy
Department of Environmental Toxicology, CNRPC, Room 1925, University of California, Davis, One Shields Avenue, Davis, CA 95616, United States.
Neurotoxicol Teratol. 2006 Jan-Feb;28(1):3-17. doi: 10.1016/j.ntt.2005.10.005. Epub 2005 Dec 15.
Human studies have shown that iron deficiency and iron deficiency anemia in infants are associated with behavioral impairment, but the periods of brain development most susceptible to iron deficiency have not been established. In the present study, rhesus monkeys were deprived of iron by dietary iron restriction during prenatal (n=14, 10 microg Fe/g diet) or early postnatal (n=12, 1.5 mg Fe/L formula) brain development and compared to controls (n=12, 100 microg Fe/g diet, 12 mg Fe/L formula) in behavioral evaluations conducted during the first four months of life in the nonhuman primate nursery. Iron deficiency anemia was detected in the pregnant dams in the third trimester and compromised iron status was seen in the prenatally iron-deprived infants at birth, but no iron deficiency was seen in either the prenatally or postnatally iron-deprived infants during the period of behavioral evaluation. Neither prenatal nor postnatal iron deprivation led to significant delays in growth, or gross or fine motor development. Prenatally deprived infants demonstrated a 20% reduced spontaneous activity level, lower inhibitory response to novel environments, and more changes from one behavior to another in weekly observation sessions. Postnatally deprived infants demonstrated poorer performance of an object concept task, and greater emotionality relative to controls. This study indicates that different syndromes of behavioral effects are associated with prenatal and postnatal iron deprivation in rhesus monkey infants and that these effects can occur in the absence of concurrent iron deficiency as reflected in hematological measures.
人体研究表明,婴儿缺铁和缺铁性贫血与行为损伤有关,但大脑发育中最易受缺铁影响的时期尚未确定。在本研究中,恒河猴在产前(n = 14,饮食中铁含量为10微克/克)或出生后早期(n = 12,配方奶中铁含量为1.5毫克/升)大脑发育期间通过饮食铁限制缺铁,并在非人灵长类动物保育室出生后的头四个月进行行为评估时与对照组(n = 12,饮食中铁含量为100微克/克,配方奶中铁含量为12毫克/升)进行比较。在孕晚期的怀孕母猴中检测到缺铁性贫血,产前缺铁的婴儿在出生时铁状态受损,但在行为评估期间,产前或产后缺铁的婴儿均未出现缺铁情况。产前和产后缺铁均未导致生长、粗大或精细运动发育显著延迟。产前缺铁的婴儿在每周观察期内自发活动水平降低20%,对新环境的抑制反应较低,且行为变化更多。产后缺铁的婴儿在物体概念任务中的表现较差,且相对于对照组情绪更不稳定。本研究表明,恒河猴婴儿产前和产后缺铁会导致不同的行为效应综合征,并且这些效应可在不存在血液学指标所反映的同时缺铁的情况下发生。