Figure 8

Ethanol-induced craniofacial abnormalities are rescued by concurrent NAC dosage. (A,B) Flatmounts of 5 dpf wildtype craniofacial skeleton displaying the linear measurements used with anterior to the left. (A) Viscerocranium and (B) neurocranium. The cartilaginous elements that were measured: m: Meckel’s length, cl: ceratohyal length, tl: Trabeculae length, tw: Intertrabecular width, el: Ethmoid plate length, ew: Ethmoid plate width, an: Anterior neurocranium length, pn: Posterior neurocranium length. (C–J) Embryo were unexposed, exposed to 1% EtOH from 6–24 hpf, or exposed to 1% EtOH +1 mM NAC from 6–24 hpf. Fish were then grown to 5 dpf for morphometric analyses. Graphs depict craniofacial measurements across each cartilaginous element in all groups (Two-way ANOVA with multiple comparisons, black bars depict range, n = 5 per group, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). In nearly every instance in which ethanol caused a significant reduction in length or width in nnt mutants, the co-exposure with NAC restored the size back to that of wildtype (C,D,G-I). The only exception being posterior neurocranium length, where the co-exposure is not significantly different from wildtype or ethanol-exposed nnt mutants. Ctrl: control, EtOH: ethanol, NAC: N-acetyl Cysteine, Mut: mutant, Wt: wildtype.