Organ specificity of neonatal methyl mercury hydroxide poisoning in the rat: effects of ornithine decarboxylase activity in developing tissues.

To determine the organ specificity of neonatal mercury hydroxide (CH3HgOH) exposure on biochemical development of its potential target tissues, effects on rat brain, liver, heart and kidney were compared utilizing the ontogenetic pattern of ornithine decarboxylase (ODC) activity, an early index of perturbation of cellular maturation. CH3HgOH was given daily beginning at birth for up to 21 days, using three dose levels (1, 2.5 or 5 mg/kg s.c.). In the brain, CH3HgOH treatment resulted in an initial reduction in ODC followed by a subsequent elevation of activity, a maturational pattern known to be associated with delayed cellular development. In contrast to the effects of CH3HgOH on brain, the pattern obtained in the liver, an initial elevation followed by a subsequent decline, is usually associated with compression of the time couse of cellular development. In the heart and kidney, CH3HgOH produced sustained elevations of ODC representing prolongation of the developmental period of rapid tissue growth and development; these patterns were associated with tissue hypertrophy which was sustained through the preweaning stage for both tissues and well into the postweaning period for the kidney. The results obtained with ODC clearly demonstrate that neonatal CH3HgOH poisoning causes organ-specific biochemical lesions which can play a role in subsequent effects on overall tissue development.