Effect of maternal cadmium (Cd) exposure and high-fructose diet (HFrD) on essential metals in offspring mouse liver
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Background and Purpose: Environmental exposure to pollutants combined with unhealthy diet can increase the risk of adverse health effects. Such effects can be more serious if the exposure scenario occurs during early life stages. This study evaluated the effects of maternal Cd exposure and consumption of a HFrD on essential metals in the offspring.
Methods: Female CD-1 mice were given 0.5 or 5 ppm Cd in drinking water with or without a 60% HFrD for 2 weeks prior to pregnancy, during pregnancy, and lactation. Controls animals received deionized water and calorie-matching diet. Dams were maintained on the same diets until postnatal day (PND) 16. Offspring mice were sacrificed at gestational day (GD) 18, PND22, PND188, and PND360 timepoints. Essential metals (Ca, Cd, Cu, Fe, Mg, Mn, Mo, Na, Rb, Se, Sr, and Zn) were determined in the offspring liver using High Resolution - Inductively Coupled Plasma Mass Spectrometry (HR-ICPMS) after acid-digestion of the biospecimen.
Results: Cd concentrations in maternal, fetal (GD18), and neonatal (PND22), and adult (PND188, 360) liver increased in a dose-dependent manner. Only a small fraction (0.023%) of the maternal Cd level was measured in the fetal liver, due to limited placental transfer. Approximately 0.065% of maternal Cd reached the offspring via lactation, totaling 0.08% of the maternal liver. About 45% of Cd was found in the liver of adult offspring, after reaching a peak level at weaning age, consistent with a biological half-life of 6 months. HFrD did not alter the hepatic bioaccumulation of Cd and other metal ions except for Rb which showed decreased level in fetal and neonatal liver. Offspring sex showed no effect in Cd bioaccumulation. Though neonatal liver showed sex specific differences in Fe, Mn, Mo, and Zn concentrations, there was not a consistent effect induced either by dose or diet.
Conclusion: Study results did not support a change of hepatic metal homeostasis in mouse offspring after maternal exposure to Cd, in part due to low doses and brevity of exposure. Furthermore, HFrD did not impact absorption or burden of Cd in either the dam or their offspring.