Dietary zinc supplementation during pregnancy prevents spatial and object recognition memory impairments caused by early prenatal ethanol exposure

Abstract

Alcohol-induced zinc (Zn) deficiency is one of the mechanisms proposed as a cause of ethanol teratogenicity. Subcutaneous Zn treatment with ethanol in early pregnancy has been shown to prevent birth abnormalities and memory impairments in mice. This study examined whether dietary Zn supplementation throughout pregnancy can prevent cognitive impairments caused by early ethanol exposure. Pregnant C57BL/6J mice were fed either a control (35 microg Zn/g) or Zn-supplemented (200 microg Zn/g) diet throughout pregnancy. On gestational day (GD) 8, mice received two intraperitoneal injections (4h apart) of either saline or 25% ethanol (0.015 mL/g). All offspring were screened for physical and behavioural defects (e.g. growth, visual, exploratory, anxiety, motor deficits). Twenty-four phenotypically-normal offspring were randomly selected from each of the four treatment groups (saline +/- Zn-supplementation, ethanol +/- Zn-supplementation) and tested at 60 d of age using a cross-maze escape task for spatial learning and memory impairments, and an object recognition task. While no differences were observed between treatments for spatial learning, offspring exposed to ethanol demonstrated spatial memory impairments at both 12 and 28 d after learning an escape task, with less correct trials and increased escape latency scores compared with saline-treated mice. Furthermore, these mice also exhibited impairments in object recognition memory. In comparison, ethanol-exposed offspring from dams fed a Zn-supplemented diet throughout pregnancy did not display spatial memory or object recognition deficits, performing at the same level as saline-treated offspring. Therefore, dietary Zn-supplementation during pregnancy prevents spatial and object recognition memory impairments caused by ethanol exposure during early pregnancy.