The organic mercury compounds, methylmercury and ethylmercury, inhibited ciliary movement of ventricular ependymal cells in the mouse brain around the concentrations reported for human poisoning.
Functions of the nervous system are supported by the flow of cerebrospinal fluid (CSF), which is driven by the ciliary beating of ventricular ependymal cells. The aim of the present study was to examine whether methylmercury (MeHg), a substance with potent neurotoxicity in humans, affects the ciliary movement. The effects of another organic mercury compound, ethylmercury (EtHg), were also assessed for comparison. Toxicity of MeHg or EtHg was evaluated by measuring alterations in the ciliary beat frequency of ependymal cells lining the third ventricle of mouse brain slices. The obtained results were: (1) Both MeHg and EtHg started to inhibit ciliary motility between 1 and 3μM, the reported threshold limit of MeHg in humans. (2) An abrupt increase was observed in the inhibitory curves from 3 to 6μM for MeHg and EtHg. (3) The "give-in" concentration, i.e., concentration at which the cilia lose the ability to recover, for MeHg and EtHg was 6μM and 12μM, respectively. (4) Ciliary beating was irreversibly halted by MeHg and EtHg at concentrations above 12μM and 30μM, respectively. (5) The estimated half-maximal inhibitory concentration (IC50) for MeHg and EtHg was 5.53μM and 5.80μM, respectively. Based on these findings, we conclude that: (a) Ependymal cell cilia movement in mice was inhibited by MeHg in a concentration-dependent manner around concentrations reported to cause poisoning in humans; EtHg inhibited ciliary motility to a less extent. (b) Inhibition of CSF flow by suppression of ciliary movement is suggested to be an additional route for MeHg poisoning in humans, especially in prenatal exposure than in adult exposure.
Department of Life Science, Faculty of Science and Engineering, Kindai University, Higashi-Osaka, Japan. Electronic address: physiology@life.kindai.ac.jp.
Shigeru
S
Yoshida
Department of Life Science, Faculty of Science and Engineering, Kindai University, Higashi-Osaka, Japan.
Shinsaku
S
Matsumoto
Department of Life Science, Faculty of Science and Engineering, Kindai University, Higashi-Osaka, Japan.
Takuya
T
Kanchika
Department of Life Science, Faculty of Science and Engineering, Kindai University, Higashi-Osaka, Japan. Electronic address: hagi@life.kindai.ac.jp.
Teruki
T
Hagiwara
Department of Life Science, Faculty of Science and Engineering, Kindai University, Higashi-Osaka, Japan. Electronic address: minamita@life.kindai.ac.jp.
Takeshi
T
Minami
D000818:Animals; D001921:Brain / Q000166:cytology; D002552:Cerebral Ventricles / Q000166:cytology; D002923:Cilia / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D004805:Ependyma / Q000166:cytology*; D005035:Ethylmercury Compounds / Q000494:pharmacology*; D066298:In Vitro Techniques; D008767:Methylmercury Compounds / Q000494:pharmacology*; D051379:Mice; D008813:Mice, Inbred ICR; D013997:Time Factors
D005035:Ethylmercury Compounds; D008767:Methylmercury Compounds
Ciliary movement; Ependymal cell; Ethylmercury; Methylmercury; Methylmercury poisoning