Abstract
Cinnabar, a naturally occurring mercuric sulfide (HgS), has long been used in Chinese mineral medicine for more than 2000 years. Although mercury is well-known for its toxicity, whether cinnabar induces neurotoxicity, especially in infants and children, is unknown. The purpose of this study was to explore the neurotoxic effects of low-dose of cinnabar (10mg/kg/day) on developing mice. The results revealed neurobehavioral defects in F1-C-Cin group, which were associated with Hg accumulation, increased NOx levels in whole blood, and Na +/K +-ATPase activities in brain tissues. F1- and F2-Cin-V groups were found to increase brain Hg contents and prominent neurobehavioral defects compared with F1-C-V group, suggesting that the fetal brain was more susceptible to irreversible effects for cinnabar-induced damage. Moreover, F1- and F2-Cin-Cin groups had severely neurobehavioral dysfunctions, closely correlated with the further alteration of NO x levels and Na +/K +-ATPase activities than F1- and F2-C-Cin groups. Effects in F2-Cin-Cin group were more significant than those in F1-Cin-Cin group. In conclusion, this study demonstrates that exposure to low-dose of cinnabar during the perinatal and developmental stages results in irreversible and severe injuries of the neurotoxicity in offspring, and NO x and Na +/K +-ATPase activities may exist potential and useful biomarkers for neurotoxicity-induced by low-doses of mercuric compounds. © Copyright 2012 Chun-Fa Huang et al.
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CITATION STYLE
Huang, C. F., Hsu, C. J., Liu, S. H., & Lin-Shiau, S. Y. (2012). Exposure to low dose of cinnabar (a naturally occurring mercuric sulfide (HgS)) caused neurotoxicological effects in offspring mice. Journal of Biomedicine and Biotechnology, 2012. https://doi.org/10.1155/2012/254582
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