Zinc-deficiency increases infarct size following permanent middle cerebral artery occlusion in rats

Abstract In view of the potential relationship between cerebral ischemia and zinc status, this study was designed to examine whether dietary zinc-deficiency would affect the outcome of focal cerebral ischemia in rats. Forty-five male Sprague-Dowley rats were randomly divided into five groups: (1) eight rats received a semi-purified zinc-deficient diet containing less than 0.38mg/100g of zinc for 1 week (ZD-1w); (2) eleven rats received the same diet as described as above for 2 weeks (ZD-2w); (3) ten rats, named pair-fed control group (PF-2w), received a zinc-supplemented diet and matched by the amount of diet equal to that consumed by ZD-2w group for 2 weeks; (4) ad libitum-fed control group received the same diet as taken by PF-2w animals for 1 week (AF-1w, n=6) and (5) the remaining 10 rats were named as no-fed (NF) group, in which the rats were directly subjected to cerebral ischemia without entering the feeding process. After experiencing the dieting stage for 1 or 2 weeks, or without (NF group), respectively, the animals were subjected to permanent occlusion of the middle cerebral artery (MCA). Plasma zinc concentration and the cerebral infarct volume were determined at 24 hours of ischemia. The final level of zinc in NF and AF-1w rats was 139±5 and 127±6 μg/100 ml, respectively. The zinc-deficient diet reduced the concentration by 52% in ZD-1w and by 64% in ZD-2w group. The increment in infarct size in ZD-1w group was inconspicuous. However, treatment with zinc-deficient diet for 2 weeks increased the total infarct volume by 118%, 88%, 58% and 47% as compared with NF, AF-1w, PF-2w and ZD-1w rats, respectively. Especially, the cortical infarct volume (206±35 mm 3 ) in ZD-2w group was 98–227% larger than those in the other groups (p