Prohaska J R, Lukasewycz O A
Department of Biochemistry, University of Minnesota, Duluth 55812.
J Nutr. 1989 Jun;119(6):922-31. doi: 10.1093/jn/119.6.922.
Dietary copper (Cu) was restricted in Swiss albino mice during five discrete intervals over a 9-wk period of perinatal development: gestation only (G), lactation only (L), 3 wk postlactation (PL), 1 wk after birth through postlactation (2/3L + PL), and lactation plus postlactation (L + PL). Biochemical and immunological status of mice in copper-deficient (-Cu) treatment groups in models G and L did not differ from that of copper-adequate (+Cu) controls. Signs of severe copper deficiency, such as low liver copper levels, and significant reductions in activity of plasma ceruloplasmin and splenocyte Cu-Zn superoxide dismutase were most evident in 6-wk-old mice from two groups, -Cu 2/3L + PL and -Cu L + PL. Mice in these groups were anemic and had small thymuses and enlarged spleens compared to controls receiving +Cu treatment. The -Cu mice demonstrated impaired antibody (plaque-forming cells, PFC) response to sheep erythrocytes, and the attenuation was proportional to copper deficiency, as judged by liver copper levels. Total plasma IgM levels were not greatly altered by -Cu treatment except in model L + PL. Total IgG levels were markedly reduced in this group and in the -Cu 2/3L + PL group. The PFC response of mice in the -Cu PL group was normal even though signs of copper deficiency were evident; however, the PFC response was reduced when -Cu treatment was extended to 5 wk and was reversible by switching to +Cu treatment. Splenocyte reactivity to B- and T-cell mitogens was not greatly different between groups. Incorporation of thymidine into DNA in the absence of mitogen was higher in -Cu mice. It is evident that severity of copper deficiency is related to degree of impaired immunity. Furthermore, severity of copper deficiency is dependent on duration and time of initiation of dietary copper restriction.
在围产期发育的9周期间，对瑞士白化小鼠的膳食铜（Cu）进行了五个不同阶段的限制：仅妊娠期（G）、仅哺乳期（L）、哺乳期后3周（PL）、出生后1周直至哺乳期后（2/3L + PL）以及哺乳期加哺乳期后（L + PL）。在模型G和L中，铜缺乏（-Cu）治疗组小鼠的生化和免疫状态与铜充足（+Cu）对照组无差异。严重铜缺乏的迹象，如肝脏铜水平低，以及血浆铜蓝蛋白和脾细胞铜锌超氧化物歧化酶活性的显著降低，在 -Cu 2/3L + PL和 -Cu L + PL这两组6周龄小鼠中最为明显。与接受 +Cu治疗的对照组相比，这些组中的小鼠贫血，胸腺小且脾脏肿大。-Cu小鼠对绵羊红细胞的抗体（空斑形成细胞，PFC）反应受损，且根据肝脏铜水平判断，这种减弱与铜缺乏程度成正比。除了在模型L + PL中，-Cu治疗对总血浆IgM水平影响不大。该组以及 -Cu 2/3L + PL组中的总IgG水平显著降低。-Cu PL组小鼠的PFC反应正常，尽管铜缺乏迹象明显；然而，当 -Cu治疗延长至5周时，PFC反应降低，且通过改用 +Cu治疗可逆转。各组之间脾细胞对B细胞和T细胞有丝分裂原的反应性差异不大。在无有丝分裂原的情况下，-Cu小鼠中胸苷掺入DNA的水平较高。显然，铜缺乏的严重程度与免疫受损程度相关。此外，铜缺乏的严重程度取决于膳食铜限制开始的持续时间和时间点。
