title: Differential neurotoxic effects of methylmercury and mercuric sulfide in rats.
abstract: Methylmercury (MeHg) is an environmental toxicant, while mercuric sulfide (HgS) is a main active component of cinnabar, a Chinese mineral medicine used as a sedative. Because the neurotoxicological effects of HgS were not clearly understood, in this study, we attempted to compare HgS with MeHg in various physiological responses in Sprague-Dawley rats. After oral administration (2 mg/(kg day)) for consecutive 5 and 14 days, MeHg reversibly decreased both of motor nerve conduction velocity (MNCV) and tail flick response, whereas irreversibly inhibited all of the motor equilibrium performance, recovery of compound muscle action potentials (CMAP) following exhaustic tetanic stimuli and Na+/K+-ATPase activity of the isolated sciatic nerve. These toxic effects of MeHg were found in well correlation of Hg contents of various tissues (blood, cerebral cortex, liver and kidney) in rats. For comparison, a dose of 1g/(kg day) of HgS was orally administered to the rats based on our previous findings on ototoxicity of HgS. The results revealed that HgS only reversibly delayed the recovery of suppressed CMAP and inhibited sciatic nerve Na+/K+-ATPase activity in accordance to the lower Hg contents of the tissues. These findings provide the important information on the differential susceptibility of various nervous tissues to MeHg and HgS. The neruotoxic effects produced by HgS was estimated to be about 1000 of those induced by MeHg found in this study and our previous reports.
authors.affiliation: Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan.
authors.forename: Jiunn-Jye
authors.initials: JJ
authors.lastname: Chuu
authors.forename: Shing-Hwa
authors.initials: SH
authors.lastname: Liu
authors.forename: Shoei-Yn
authors.initials: SY
authors.lastname: Lin-Shiau
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D002540:Cerebral Cortex / Q000378:metabolism; D066298:In Vitro Techniques; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D017669:Mercury Compounds / Q000097:blood / Q000493:pharmacokinetics / Q000633:toxicity*; D020262:Mercury Poisoning, Nervous System / Q000097:blood / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology*; D008767:Methylmercury Compounds / Q000097:blood / Q000493:pharmacokinetics / Q000633:toxicity*; D009046:Motor Neurons / Q000187:drug effects; D009132:Muscles / Q000187:drug effects; D009431:Neural Conduction / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012584:Sciatic Nerve / Q000187:drug effects / Q000201:enzymology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects; D013623:Tail / Q000187:drug effects
chemical_list: D017669:Mercury Compounds; D008767:Methylmercury Compounds; D000254:Sodium-Potassium-Exchanging ATPase; C004925:methylmercuric chloride; C034211:cinnabar