Neurotoxicity of mercury sulfide in the vestibular ocular reflex system ofguinea pigs

A traditional Chinese mineral medicine, cinnabar, naturally occurring mercu ric sulfide (HgS), is still occasionally prescribed, but the neurotoxic eff ects of HgS have not been elucidated. In this paper, an animal model of the purified HgS intoxication was established in guinea pigs in order to study neurotoxicity and pathophysiology of the vestibular ocular reflex system ( VOR). Guinea pigs were dosed with HgS by gastric gavage (0.01, 0.1 and 1.0 g/kg per day) for 7 consecutive days. By means of caloric testing coupled w ith the electronystagmographic (ENG) recording in guinea pigs, we have foun d that HgS at a dose of 0.1 g/kg induced reversible caloric hypofunction pa ttern and at a higher dose of 1.0 g/kg induced irreversible hypofunction of caloric test. Monitoring the mercury contents of various tissues (blood, k idney, liver and cerebellum) by continuous flow and cold vapor atomic absor ption spectrometry (AAS) revealed that a certain amount of HgS could be abs orbed from the gastrointestinal tract and was detectable in these tissues. In addition to the induced dysfunction of VOR system, HgS also caused distu rbance of motor performance in guinea pigs. In enzyme assay, Na+/K+-ATPase activity of cerebellum was also significantly inhibited by HgS. Morphologic al studies showed partial cell loss only in the cerebellar Purkinje cell la yer, but not in the granule cell layer, nor in the vestibular labyrinth. Al l of these findings suggest that cerebellar Purkinje cells are the sensitiv e target site responsible for HgS-inducing dysfunctions of both VOR system and the motor performance in guinea pigs. Thus, it is concluded that calori c test coupled with ENG recording in VOR system is certainly a sensitive bi omarker for monitoring the neurotoxicity of HgS.