抄録
While the primary source of human MeHg exposure is the consumption of fish contaminated with MeHg, it is unknown whether the toxicity of MeHg in fish is equivalent to that of MeHg chloride (MeHgCl) experimentally added to the diet. We investigated developmental and behavioral effects of MeHg derived from fish and MeHgCl added to various diets during the prenatal period in mice from GD 0 to GD 17. From 7 to 9 female C57BL/6NCr mice were assigned to each of the following exposure groups: Control (CL), CL+MeHgCl (CL+MeHg, 1.6 mgHg/kg), low MeHg tuna (LT, 0.2 mgHg/kg), LT+MeHgCl (LT+MeHg, 1.6 mgHg/kg), and high MeHg tuna (HT, 1.6 mgHg/kg). In pups, body weight was depressed and elevated by MeHg exposure in the CL+MeHg and the LT, respectively, compared with other three groups. In neurodevelopmental test, the righting reflex of 4 groups other than CL showed the facilitated developments compared to the CL. The cliff avoidance of the HT developed slower than in the CL+MeHg, LT and LT+MeHg. In water maze test, the swimming speed of the HT decreased in comparison with the CL in males but not females. The latency until falling from a rotating rod of the LT+MeHg was significantly shorter than that of the LT in males but not females. Our results are suggesting the possibility that the toxicological profiles of MeHg derived from fish and reagent MeHg are somewhat different. Our findings also provide evidence that males are more susceptible than females to prenatal MeHg exposure.
