Objective: To explore the target organ for the acute toxicity of cantharidin (CTD) by establishing a cantharidin-inducing acute failure mouse model. Method: Balb/c mice were treated with different doses of cantharidin(2

3

4 mg·kg-1)

and their activities were speculated. After that

the remaining mice were treated with the acute toxic dose by gavage for 3 hours

their blood samples were collected for biochemical analyses

and tissue samples were collected from livers

intestines

kidneys

and hearts for histopathological analyses. For another group

CTD was measured after treatment with 4 mg·kg-1 cantharidin for 3 h

and animals were anaesthetized with pentobarbital sodium. Result: Compared with the control group

poisoning response of the CTD mice deteriorated with the increase of concentration. The acute toxicity dose of CTD was 4 mg·kg-1

and the average death time was (4.64±1.33) h. After the administration at the acute toxicity dose

compared with control group

ECG of the mice showed abnormally upward J point and slowdown in heart rate. Cantharidin led to significant increases in the levels of alanine aminotransferase (ALT) (P<0.05)

aspartate aminotransferase (AST) (P<0.05)

rea nitrogen (BUN) (P<0.05)

creatine kinase (CK) (P<0.01)

lactate dehydrogenase (LDH) (P<0.01)

and cardiac troponin (cTn) (P<0.05). Cantharidin caused inflammatory cell infiltration and myocardial injury in heart. Conclusion: Heart is the target organ of cantharidin at the acute toxic dose. Cantharidin could induce myocardial injury and cardiac structural damage.