Abstract: ObjectiveTo explore the cinnabar-induced subchronic hepatotoxicity in rats by oral administration.MethodsThe Sprague-Dawley(SD)rats were randomly divided into cinnabar group and control group.The rats in the treatment group were administered with cinnabar by gavage at the dosage of 1.0 g/kg/d in 0.5% carboxymethyl cellulose sodium solution and the rats in the control group were treated with the same volume of solvent,respectively.Half of the rats in each group were sacrificed after 8 and 12 weeks of the treatment and blood and liver samples were collected for the determination of mercury content,indexes of liver function and pathological examination.ResultsAfter cinnabar exposure,the contents of mercury in both blood and liver were significantly higher than those of the control(blood mercury:13.843±3.929 vs.7.523±3.85 μg/L at 8 week,P<0.05;14.038±4.446 vs.6.829±3.258 μg/L at 12 week,P<0.05;liver mercury:0.107±0.051 vs.0.055±0.020 at 8 week,P<0.01;0.147±0.065 vs.0.045±0.028 μg/g at 12 week,P<0.05).The concentration of aspartate aminotransferase of cinnabar group was significantly higher than that of control group at 8 week(130.17±32.26 vs.95.83±17.86 U/L)(P<0.05).The contents of total protein and albumin of cinnabar group were higher than those of the control group at 12 week.Pathologieal changes in the livers of cinnabar-treated rats were observed,including hepatocyte swelling,vacuolar degeneration,and inflammatory cell infiltration.ConclusionLong-term overdose of cinnabar could cause mercury accumulation in liver and result in liver damage.Cinnabar should be used rationally in clinical practice.