Effects of methyl mercury, mercuric sulfide and cinnabar on active avoidance responses, Na+/K+-ATPase activities and tissue mercury contents in rats

This study compared the neurobehavioral toxicities of three mercurial compounds: methyl mercury (MeHg) which is soluble and organic. and mercuric sulfide (HgS) and cinnabar (naturally occurring HgS), which are insoluble and inorganic. Cinnabar, a Chinese mineral medicine, is still used as a sedative in some Asian countries, but there is relatively little toxicological information about it. These mercurial compounds were administered intraperitoneally (MeHg, 2 mg/ kg) or orally (HgS and cinnabar, 1.0 g/kg) to male rats once every day for 13 consecutive days with assays conducted during or after discontinuous administration for 1 h, 2, 8 and 33 weeks. Neurotoxicity was assessed based on the active avoid-ance response and locomotor activity. The results obtained showed that MeHg and cinnabar prominently and irreversibly caused a decrease in body weight, prolongation of latency for escape from electric shock, a decrease in the percentage for the conditioned avoidance response (CAR) to electric shock, impairment of spontaneous locomotion and inhibition of Na+/K+-ATPase activity of the cerebral cortex. In contrast. HgS reversibly inhibited spontaneous locomotion and Na+/K+-ATPase activity. It was noted that HgS significantly decreased the latency of escape from electric shock during the ad-ministration period, which lasted for 33 weeks after discontinuous administration. In fact that pretreatment with arecoline (a cholinergic receptor agonist) but not fipexide (a dopaminergic receptor agonist) could significantly shorten the prolonged latency for escape caused by MeHg and cinnabar, suggested that the deficit in the active avoidance response was perhaps, at least in part, mediated by the dysfunction of the cholinergic rather than the dopaminergic system. Determination of the Hg levels of the whole blood and cerebral cortex revealed that the tissue mercury content was highly correlated with the degree of neurobehavioral toxicity of these Hg compounds. These findings suggest that insoluble HgS and cinnabar can be absorbed from the G-I tract and distributed to the brain. The possibility that contamination due to other minerals in the cinnabar is responsible for the greater neurotoxic effects compared to HgS is under investigation.