We studied the effects of coenzyme Q(10) (CoQ(10)) on mice with acute myocarditis inoculated with the encephalomyocarditis (EMC) virus with the analysis of indices of effects of oxidative injury and DNA damage in the myocardium. The mice were treated as follows: CoQ(10) group (n = 118); CoQ(10) 1.0 mg (0.1 mL)x2/d (0.1 mg/g/d), control group (n = 128); sham-liquid 0.1 mL x 2/d. The mice were injected intraperitoneally 1 day before and daily for 12 days after EMC virus inoculation. The expression of thioredoxin, a marker of oxidative stress overload, as well as 8-hydroxy-2'-deoxyguanosine, an established marker of DNA damage, in the myocardium was investigated. The survival rate was significantly higher (P < 0.01) in the CoQ(10) group (46.8%, 29/62) than in the control group (14.3%, 10/70). There were significant increases of CoQ(9) and CoQ(10) in the heart, which are the biologically active forms of CoQ in mice, and significant decrease of serum creatine kinase (CK)-MB in the CoQ(10), group as compared with the control group. Histologic examination showed that the severity of myocarditis was less severe (P < 0.01) in the CoQ(10) group than in the control group. In addition, the upregulation of myocardial thioredoxin with DNA damage, which was induced by the inflammatory stimuli by the virus, was suppressed by the CoQ(10) treatment, which may reflect the anti-oxidant effects of CoQ(10) treatment. Thus, pretreatment with CoQ(10) may reduce the severity of viral myocarditis in mice associated with decreasing oxidative stress in the condition.