The developing perinatal brain is vulnerable to methylmercury (MeHg) exposure. The contribution of breast milk to tissue MeHg levels in offspring is a significant public health concern because breast milk contains a certain amount of MeHg. Here, the contribution of MeHg transferred via breast milk to the Hg levels in the tissues of pups (Wistar rats) was investigated. Mated maternal rats were fed a MeHg (2 ppm)-supplemented or a control diet during pregnancy. Following parturition, male neonates from each group were cross-fostered between exposed or control dams, and they were further raised by dams fed a MeHg-supplemented diet or a control diet during lactation. Consequently, we evaluated three pup groups, which were raised by dams exposed to MeHg during pregnancy (P pups), lactation (L pups), or pregnancy and lactation (PL pups). Total mercury (THg) concentrations in the tissues of the offspring were measured at birth (postnatal day 0 [PD0]), during lactation (PD6, PD12, and PD19), and after weaning (PD29 and PD36). Blood and brain THg levels in the P and PL pups declined dramatically during lactation, however, there were no considerable differences between the two groups at PD6 and PD12. In contrast, blood and brain THg levels in the L pups increased slightly during lactation. The increase in the THg levels in the blood and brain of L pups at PD12 were approximately 3.3% and 1.5%, respectively, compared to the corresponding THg levels in the neonates in the P and PL groups. Our results suggest that if the MeHg exposure level during pregnancy is not high enough to cause neuronal development defects in the fetus, the exposure via breast milk is not a significant concern.
Keywords: Blood; Brain; Breast milk; Methylmercury; Offspring.
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