Trace element distribution in heart tissue sections studied by nuclear microscopy is changed in coxsackie virus B3 myocarditis in methyl mercury-exposed nice

Methyl mercury (MeHg) has been shown to change Coxsackie virus type B3 (CB3 ) myocarditis in a direction compatible with the development of chronic dis ease. Murine models of CB3 myocarditis closely mimic the pathogenesis in hu mans. There are also indications that metals, such as mercury, and trace el ements may interact and adversely affect viral replication and development of inflammatory lesions. The effects of low-dose MeHg exposure on myocardia l trace element distribution, as determined by means of nuclear microscopy, was studied in CB3 myocarditis. Balb/c mice were fed a MeHg-containing die t (3.9 mg/kg diet) for 12 wk prior to infection. Areas of inflammatory lesi ons in the myocardium were identified by traditional histologic examination , and serial tissue sections in these selected areas were used for immune h istology (macrophages), in situ hybridization of virus genomes, and nuclear microscopy of tissue trace element distribution. Areas with no inflammatio n or virus were compared with areas of ongoing inflammation and viral repli cation. In the inflammatory lesions of MeHg-exposed mice as compared to non exyosed mice, the myocardial contents of calcium (Ca), manganese (Mn), and iron (Fe) were significantly increased, whereas the zinc (Zn) content was d ecreased. The increased Ca and decreased Zn contents in the inflamed heart may partly explain a more severe disease in MeHg-exposed individuals. Altho ugh not significant in the present study, with a limited number of mice, th e inflammatory and necrotic lesions in the ventricular myocardium on d 7 of the infection was increased by 50% (from 2.2% tb 3.3% of the tissue sectio n area) in MeHg-exposed mice and, also, there was a tendency of increased p ersistence of virus with MeHg exposure. No increased MeHg uptake, either in the inflammatory lesions or in the areas of noninflamed heart tissue in in fected mice, could be detected. The present results indicate that a "compet ition" exists between potentially toxic heavy metals from the environment/d iet and important trace elements in the body and that a disturbed trace ele ment balance adversely influences the development of pathophysiologic chang es in inflammatory heart disease.