Increased NGF and BDNF in the thyroid of aged male mice exposed in fetus and during lactation to ethanol

Ethanol intoxication has been shown to elicit changes in the endocrine glands, including thyroid. In particular, during pregnancy, the hormonal systems of the mother and fetus are intricately interconnected to ensure normal fetal development. Some of the effects of maternal alcohol consumption on fetal hormone systems may contribute to the adverse effects observed in children with Fetal Alcohol Spectrum Disorder (FASD). These children may show physical, mental, behavioral and/or learning disabilities with possible lifelong implications. Reported studies suggested that ethanol consumption during pregnancy can affect neurotrophins as nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) with long-lasting damage. These neurotrophic factors have also a role in thyroid development, maintenance and activity. Thus the aim of the present study was to investigate in the thyroid of aged mice exposed in fetus and during lactation to ethanol or red wine at same ethanol concentration (11% vol) the presence of changes in NGF and BDNF. We found that the mouse thyroid exposed early only to ethanol solution had NGF and BDNF elevation although the NGF presence was higher if compared to the BDNF concentration. Interestingly no changes were elicited by red wine exposure. As ethanol exposure in fetus during pregnancy and lactation is a putative neurodevelopmental model of FASD, and given previous data that cells of target organs of ethanol intoxication change neurotrophic factors synthesis, release and utilization, these results represent a further step in the attempt to unravel the molecular events involved in cell behavior in the “FASD” thyroid.