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. 2012:2012:254582.
doi: 10.1155/2012/254582. Epub 2012 Jul 19.

Exposure to low dose of cinnabar (a naturally occurring mercuric sulfide (HgS)) caused neurotoxicological effects in offspring mice

Chun-Fa Huang  1 , Chuan-Jen Hsu, Shing-Hwa Liu, Shoei-Yn Lin-Shiau
Affiliations

Exposure to low dose of cinnabar (a naturally occurring mercuric sulfide (HgS)) caused neurotoxicological effects in offspring mice

Chun-Fa Huang et al. J Biomed Biotechnol. 2012.

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 (10 mg/kg/day) on developing mice. The results revealed neurobehavioral defects in F1-C-Cin group, which were associated with Hg accumulation, increased NO(x) 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.

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Figures

Figure 1
Figure 1
Schedule of oral administration of cinnabar (10 mg/kg/day) to offsprings during maternal gestation, weaning, or after weaning.
Figure 2
Figure 2
Decrease of litter number induced by cinnabar. Cinnabar (10 mg/kg/day) was treated with the dams by oral gavage during gestation period. Numbers of newborn pups were recorded at postnatal day 1 (PND 1) as described in the section of Materials and Methods. All data are presented as mean ± S.E. (n = 12–15/group). *P < 0.05 as compared with F1 control vehicle (F1-C-V) group.
Figure 3
Figure 3
Effects of cinnabar on body weight gain of offspring mice. After weaning, the offspring mice were randomly selected as representatives of their respective litters (n = 12–15/group), and body weights were determined in various experimental groups after 49 consecutively treated days as described in Figure 1. Data are presented as mean ± SE. *P < 0.05 as compared with F1-C-V group.
Figure 4
Figure 4
Changes in locomotor activities and motor equilibrium performance of offspring mice treated with cinnabar. Experimental mice were treated with cinnabar (10 mg/kg/day) or distilled water as described in Figure 1. Spontaneous locomotor activities (ambulatory distance (a), stereotypy-1 episodes (b) and Jump (c)) and motor equilibrium performance (retention times on rotating rod, 60 rpm (d)) of all groups were recorded and analyzed as described of Materials and Methods. Data are presented as mean ± SE (n = 12–15/group). *P < 0.05 as compared with F1-C-V group; &P < 0.05 as compared with F1- or F2-Cin-V group; #P < 0.05 as compared with F1-C-Cin group, respectively.
Figure 5
Figure 5
Prolongation of pentobarbital-induced sleeping time by cinnabar in offspring mice. Offspring mice were administered with distilled water or cinnabar (10 mg/kg/day, oral application by gavage) as described in Figure 1. Sleeping time was measured at the end of 49 days after weaning as described in Materials and Methods. Data are presented as mean ± S.E. (n = 12–15/group). *P < 0.05 as compared with F1-C-V group; #P < 0.05 as compared with F1- or F2-Cin-V group; &P < 0.05 as compared with F1-C-Cin group, respectively.
Figure 6
Figure 6
Chronological change of hearing thresholds and the absolute and the interwave latencies of ABRs waveforms in offspring mice treated with cinnabar. Offspring mice were orally gavaged with either cinnabar (10 mg/kg/day) or distilled water as described in Figure 1. The hearing thresholds (a), absolute wave (I, III, and V) (b), and the interwave latencies (I–III, I–V, and III–V) (c) of ABRs waveforms were recorded as described in Materials and Methods. Data are presented as mean ± SE (n = 12–15/group). *P < 0.05 as compared with F1-C-V group; &P < 0.05 as compared with F1- or F2-Cin-V group; #P < 0.05 as compared with F1-C-Cin group, respectively.
Figure 7
Figure 7
Nitric oxide (NOx) levels of the whole blood of offspring mice treated with cinnabar. Experimental mice were orally gavaged with cinnabar (10 mg/kg/day) as described in Figure 1. Whole blood samples were acquired, de-proteinized, and NOx levels were determined as described in Materials and Methods. All data are presented as mean ± SE (n = 12–15/group). *P < 0.05 as compared with compared with F1-C-V group; &P < 0.05 as compared with F1- or F2-Cin-V group; #P < 0.05 as compared with F1-C-Cin group, respectively.
Figure 8
Figure 8
Alteration of Na+/K+-ATPase activities in the brain tissues of offspring mice treated with cinnabar. Experimental mice were orally administrated with distilled water or cinnabar (10 mg/kg/day) as described in Figure 1. Na+/K+-ATPase activities of the cerebral cortex, cerebellar cortex and brainstem were determined as described in the section of Materials and Methods. All data are presented as mean ± S.E. (n = 12–15/group). *P < 0.05 as compared with F1-C-V group; &P < 0.05 as compared with F1- or F2-Cin-V group; #P < 0.05 as compared with F1-C-Cin group, respectively.
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