Strain difference in galactokinase level and susceptibility to the teratogenic effect of dietary galactose in mice: I. Teratogenic and embryopathic effect

Congenital cataracts have been noted to occur in infants when either the mother or the mother and infant have reduced activity of the enzymes galactokinase (GK) or galactose‐1‐phosphate uridyl transferase (GALT). Studies were undertaken to elucidate the possible genetic and dietary fetomaternal interactions leading to the presumptive galactose teratogenesis noted in two inbred strains of mice differing in GK activity. Pregnant A/J (high erythrocyte GK activity 134.18 ± 17.89 mU/gm Hb) and C57BL/6J (low erythrocyte GK activity 55.05 ± 11.39 mU/gm Hb) mice were treated with a diet containing either 25% or 50% galactose throughout gestation. A significantly higher percentage of C57BL offspring (92.3%) were observed to have lens opacities when their mothers were fed a high‐galactose diet, whereas no increase in lens pathology was observed in the offspring of similarly treated A/J mothers. Additionally, reciprocal matings were carried out so that all offspring were genetically equivalent in terms of GK activity. However, when the mother had low GK activity, a significant incidence of lens opacities was present in their offspring; this was not found when the mother had high GK activity. After weaning, no difference in the incidence of lens opacities was observed when the 25% galactose diet was introduced to the offspring of these reciprocal crosses, providing additional support for a maternal dietary influence on the development of lens opacities.