https://scholars.lib.ntu.edu.tw/handle/123456789/369121
Title: | Exposure to low dose of cinnabar (a naturally occurring mercuric sulfide (HgS)) caused neurotoxicological effects in offspring mice | Authors: | SHING-HWA LIU | Issue Date: | 2012 | Journal Volume: | 2012 | Source: | Journal of Biomedicine and Biotechnology | 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. |
URI: | http://www.scopus.com/inward/record.url?eid=2-s2.0-84864950383&partnerID=MN8TOARS http://scholars.lib.ntu.edu.tw/handle/123456789/369121 |
DOI: | 10.1155/2012/254582 | SDG/Keyword: | 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 |
Appears in Collections: | 毒理學研究所 |
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