Parsons S E, DiSilvestro R A
Human Nutrition and Food Management, Ohio State University, Columbus 43210.
Br J Nutr. 1994 Oct;72(4):611-8. doi: 10.1079/bjn19940063.
Zn deficiency is hypothesized to produce poor resistance to injury involving oxidative stress. This could occur by impairing Zn antioxidant function(s) or by indirectly limiting adaptive protective mechanisms such as a rise in acute-phase proteins. The present study examined rats fed diets adequate or moderately low in Zn (4 or 25 micrograms/g diet) for 9 d. The lower intake produced a mild Zn deficiency based on body weight, plasma Zn and plasma alkaline phosphatase (EC 3.1.3.1) activity. Galactosamine injection, an oxidative stress, produced much more liver injury in the mildly Zn-deficient rats. However, injury was strongly inhibited in rats from each dietary group by an acute-phase response due to turpentine-induced leg inflammation. Mild Zn deficiency did not prevent a rise in levels of the acute-phase protein caeruloplasmin (EC 1.16.3.1), but did limit the usual inflammation-induced rise in hepatic levels of metallothionein, a Zn protein with possible antioxidant function. In conclusion, high degrees of galactosamine-induced hepatitis were associated with mild Zn deficiency, but the liver injury was blocked by prior stimulation of an acute-phase response, regardless of Zn status.
锌缺乏被认为会导致对涉及氧化应激的损伤的抵抗力下降。这可能是通过损害锌的抗氧化功能，或者间接限制适应性保护机制，如急性期蛋白的升高来实现的。本研究检测了喂食锌含量充足或适度低（4或25微克/克饮食）的饮食9天的大鼠。根据体重、血浆锌和血浆碱性磷酸酶（EC 3.1.3.1）活性，较低的摄入量导致了轻度锌缺乏。注射半乳糖胺（一种氧化应激）在轻度锌缺乏的大鼠中造成了更多的肝损伤。然而，由于松节油诱导的腿部炎症引起的急性期反应，每个饮食组的大鼠的损伤都受到了强烈抑制。轻度锌缺乏并没有阻止急性期蛋白铜蓝蛋白（EC 1.16.3.1）水平的升高，但确实限制了通常由炎症诱导的具有可能抗氧化功能的锌蛋白金属硫蛋白在肝脏中的水平升高。总之，高度的半乳糖胺诱导的肝炎与轻度锌缺乏有关，但无论锌状态如何，急性期反应的预先刺激都能阻止肝损伤。
