The effects of dietary zinc on hepatic collagen and prolyl hydroxylase activity in normal and alcoholic rats has been investigated in four groups of pair-fed male Wistar rats given either liquid ethanol or a control diet for 12 wk. Each group of pair-fed animals received a diet with a different zinc concentration (standard diet, 7.6 mg/L; low-zinc diet, 3 . 4 mg/L; zinc-supplemented diet, 76 mg/L; and zincextrasupplemented, 300 mg/L. There were no significant differences in hepatic collagen concentration and prolyl hydroxylase activity between alcoholic and normal rats receiving a standard diet (collagen, 77 f 6 and 73 k 6 &ng protein; and prolyl hydroxylase; 37 f 28 and 38 f 22 cpndmg protein). Alcoholic rats fed alow-zinc diet showed increased prolyl hydroxylase activity (76 k 10 cpndmg protein, p < 0.06), although no changes in hepatic collagen (77 f 10 pglmg protein) were observed in comparison with rats fed a standard alcoholic diet. By contrast, hepatic collagen was sigdilcantly lower in alcoholic rats fed a zincsupplemented diet (66 f 4 and 63 f 3 pglmg protein, p < 0.06 and p < 0.01, respectively), and hepatic prolyl hydmxylaae activity was particularly lower in rats receiving zinc 300 mg/L (18 & 20 cpndmg protein). Similar effects were observed in normal rats. W e conclude that dietary zinc influences hepatic prolyl hydmxylaae activity and collagen deposition in alcoholic rats, and in consequence, the control of dietary zinc is neci88881y to assess the effects of alcohol on collagen m e t a b o h in rats. (&PATOLOGY 1992;16816-
819.)
Marked alterations of hepatic collagen metabolism and progressive collagen deposition leading to cirrhosis are characteristic features of alcoholic liver disease. The pathogenic mechanism whereby long-term alcohol consumption alters collagen metabolism and the contributory role of other associated factors such as nutritional deficiencies are not well understood. Although development of fibrosis and cirrhosis has been demonstrated