Abstract
Objective: The present study attempts to determine whether developmental thiamine (B1 vitamin) deficiency and developmental ethanol exposure disturb eye opening in Wistar rat pups. Methods: During gestation and lactation, Wistar rat dams were exposed to the following treatments: (1) Prenatal thiamine-deficient dams; (2) perinatal thiamine-deficient dams; (3) postnatal thiamine-deficient dams; (4) 12% alcohol/water drinking mothers; (5) mothers drinking 12% alcohol/water + thiamine hydrochloride mixture; (6) ad libitum control dams. Pair-feeding treatments controlled malnutrition related to thiamine deficiency: (7) Prenatal pair-fed dams; (8) perinatal pair-fed dams; (9) postnatal pair-fed dams and included also the control of alcohol consummation: (10) pair-fed saccharose dams. After birth, from postnatal day 10 (P10) to P18, eye opening was observed in the pups bred by ten different experimental dams. Results: The present experiments showed eye opening to be delayed strongly in perinatal thiamine-deficient pups only. Consequently, our study suggests perinatal thiamine deficiency to interfere with photoreceptors differentiation in the rat retina. In addition, our results reveal that developmental alcohol exposure-induced premature eye opening contrasted paradoxically with perinatal thiamine deficiency-induced delayed opening. Conclusions: The results suggest differential actions of alcohol and thiamine deficiency on cellular genesis in the rat retina.
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