Prohaska J R, Bailey W R
Department of Biochemistry and Molecular Biology, School of Medicine, University of Minnesota, Duluth 55812, USA.
Proc Soc Exp Biol Med. 1995 Nov;210(2):107-16. doi: 10.3181/00379727-210-43929.
Perinatal copper (Cu) deficiency was studied in month-old female and male Sprague-Dawley rat offspring to investigate regional changes in brain cuproenzymes. Offspring of dams given the low Cu treatment beginning at Day 7 of gestation exhibited signs characteristic of Cu deficiency including a 70% reduction in liver Cu levels compared with Cu-adequate controls. Compared with Cu-adequate rats, Cu-deficient rats had lower activities of the cuproenzymes peptidylglycine alpha-amidating monooxygenase (PAM), cytochrome c oxydase (CCO), and Cu,Zn-superoxide dismutase (SOD) in all six brain regions studied. Apparent activity of dopamine-beta-monooxygenase (DBM) was higher in all regions from Cu-deficient compared with Cu-adequate rats. Activity of the selenoenzyme glutathione peroxidase (GPX) was not greatly altered in brain by Cu deficiency. Following 1 month of Cu repletion, liver but not brain Cu levels were equivalent to control. Brain CCO activity was still lower in Cu-repleted female and male rats. PAM activity was still lower in cerebrum of Cu-repleted rats. DBM activity was no longer significantly elevated in the former Cu-deficient groups except for midbrain. SOD and GPX activity were equivalent between groups. PAM activity, in vitro, is lower in the brain following perinatal Cu deficiency and activity is slow to recover following nutritional supplementation with Cu. Perhaps neuropeptide maturation is compromised by Cu deficiency.
对1月龄雌性和雄性斯普拉格-道利大鼠后代进行围产期铜（Cu）缺乏研究，以调查脑铜酶的区域变化。从妊娠第7天开始接受低铜处理的母鼠所产后代表现出铜缺乏的特征性迹象，与铜充足的对照组相比，肝脏铜水平降低了70%。与铜充足的大鼠相比，铜缺乏的大鼠在所研究的所有六个脑区中，肽基甘氨酸α-酰胺化单加氧酶（PAM）、细胞色素c氧化酶（CCO）和铜锌超氧化物歧化酶（SOD）等铜酶的活性较低。与铜充足的大鼠相比，铜缺乏大鼠所有脑区的多巴胺-β-单加氧酶（DBM）表观活性均较高。铜缺乏对脑中硒酶谷胱甘肽过氧化物酶（GPX）的活性影响不大。在补充铜1个月后，肝脏铜水平恢复到与对照组相当，但脑铜水平未恢复。补充铜的雌性和雄性大鼠的脑CCO活性仍然较低。补充铜的大鼠大脑中PAM活性仍然较低。除中脑外，先前铜缺乏组的DBM活性不再显著升高。各组之间SOD和GPX活性相当。围产期铜缺乏后，脑中PAM活性在体外较低，补充铜营养后活性恢复缓慢。也许神经肽成熟受到铜缺乏的影响。
