Exposure to low dose of cinnabar (a naturally occurring mercuric sulfide (HgS)) caused neurotoxicological effects in offspring mice
Journal
Journal of Biomedicine and Biotechnology
Journal Volume
2012
Date Issued
2012
Author(s)
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.
SDGs
Other Subjects
adenosine triphosphatase (potassium sodium); mercury sulfide; nitric oxide; adenosine triphosphatase (potassium sodium); mercury; mercury derivative; mercury sulfide; neurotoxin; animal model; animal tissue; article; blood level; body weight; brain; cognitive defect; controlled study; dose response; drug brain level; drug exposure; enzyme activity; exposure; female; hearing disorder; litter size; locomotion; male; mouse; neurotoxicity; neurotoxicology; nonhuman; perinatal development; progeny; sleep time; animal; animal behavior; auditory threshold; blood; drug effect; enzymology; hearing; Institute for Cancer Research mouse; metabolism; nervous system; newborn; pathology; pathophysiology; pregnancy; prenatal exposure; sleep; time; Animals; Animals, Newborn; Auditory Threshold; Behavior, Animal; Body Weight; Brain; Female; Hearing; Litter Size; Locomotion; Male; Mercury; Mercury Compounds; Mice; Mice, Inbred ICR; Nervous System; Neurotoxins; Nitric Oxide; Pregnancy; Prenatal Exposure Delayed Effects; Sleep; Sodium-Potassium-Exchanging ATPase; Time Factors
Type
journal article