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 μg/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.