EFFECTS OF MILD ZINC-DEFICIENCY, PLUS OR MINUS AN ACUTE-PHASE RESPONSE, ON GALACTOSAMINE-INDUCED HEPATITIS IN RATS

Zn deficiency is hypothesized to produce poor resistance to injury inv olving oxidative stress. This could occur by impairing Zn antioxidant function(s) or by indirectly limiting adaptive protective mechanisms s uch as a rise in acute-phase proteins. The present study examined rats fed diets adequate or moderately low in Zn (4 or 25 mu g/g diet) for 9 d. The lower intake produced a mild Zn deficiency based on body weig ht, plasma Zn and plasma alkaline phosphatase (EC 3.1.3.1) activity. G alactosamine injection, an oxidative stress, produced much more liver injury in the mildly Zn-deficient rats. However, injury was strongly i nhibited in rats from each dietary group by an acute-phase response du e to turpentine-induced leg inflammation, Mild Zn deficiency did not p revent a rise in levels of the acute-phase protein caeruloplasmin (EC 1. 16.3. 1), but did limit the usual inflammation-induced rise in hepa tic Levels of metallothionein, a Zn protein with possible antioxidant function. In conclusion, high degrees of galactosamine-induced hepatit is were associated with mild Zn deficiency, but the liver injury was b locked by prior stimulation of an acute-phase response, regardless of Zn status.