Methylmercury (MeHg) is a well-established environmental neurotoxicant and the primary cause of Minamata disease. Recently, α-mercuri-acetaldehyde (HgCH2CHO) and α-mercuri-acetic acid (HgCH2COOH) have been proposed to be relevant to the Minamata tragedy. However, their in vivo toxicity has not been compared with that of MeHg under identical conditions. We conducted a comparative in vivo toxicity study of HgCH2CHO and HgCH2COOH using the dosing regimen previously established for MeHg. Male Wistar rats were orally administered MeHg, HgCH2CHO, or HgCH2COOH (26.6 µmol/kg/day) for 5 days, which was followed by a 2-day drug-free period and a single repeat of this cycle. Systemic toxicity was evaluated using the change in body mass, neurobehavioral effects were assessed using the hindlimb crossing test, and the total mercury accumulation in blood and organs was quantified. MeHg exposure resulted in marked weight loss and significant neurobehavioral impairment. In contrast, rats exposed to HgCH2CHO or HgCH2COOH exhibited only mild weight loss and substantially attenuated hindlimb crossing responses. The total mercury levels in the blood, liver, brain, muscle, and spleen were considerably lower in the HgCH2CHO- and HgCH2COOH-treated groups than in the MeHg group. The renal accumulation of mercury did not differ among the groups, despite the blood mercury levels in the HgCH2CHO and HgCH2COOH groups being extremely low, suggesting distinct toxicokinetic properties. Overall, HgCH2CHO and HgCH2COOH demonstrated much lower in vivo toxicity and systemic mercury burden than MeHg under equivalent dosing conditions. These findings do not challenge the established role of MeHg as the primary causative agent of Minamata disease.
Shinoda et al. (Thu,) studied this question.