Abstract
This study aims to determine the impact of preconception paternal alcohol consumption (PPAC) on retinal function and morphology in PPAC-offspring. Fetal alcohol spectrum disorder (FASD)-related ocular defects caused by maternal alcohol exposure has been well investigated, but the influence of PPAC on offspring eyes remains unknown. Adult C57BL/6J male mice were exposed to either 10% ethanol or water (control) for six weeks and bred to naïve females. Dark-adapted retinal light responses at two, four, and six months old were assessed using electroretinography (ERG) for the offspring born to PPAC and control males. The thicknesses of whole retinas and different retinal layers of the control and PPAC-offspring were analyzed at two and six months old. Some PPAC-offspring had only one developed eye. ERG a- and b-wave amplitudes were reduced in PPAC-offspring compared to controls, with a more pronounced effect in females. PPAC had significant effects on inner retinal function. At two months old, there was a significant thinning of the retinal inner nuclear and inner plexiform layers in PPAC-offspring. At six months old, the retinal thickness and ERG amplitudes were similar between both treatment groups. This study provides pioneering evidence that PPAC contributes to FASD-related ocular defects including negative impacts on retinal light responses and retinal thinning in young adult offspring. Thus the adverse impact of paternal alcohol consumption prior to conception on their offspring (from childhood to early adulthood) should be considered as seriously as the maternal contribution to FASD.
Published Version
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