Bartolome J, Chait E A, Trepanier P, Whitmore W L, Weigel S, Slotkin T A
Toxicol Lett. 1982 Oct;13(3-4):267-76. doi: 10.1016/0378-4274(82)90222-3.
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.
为确定新生大鼠暴露于氢氧化甲基汞（CH3HgOH）后对其潜在靶组织生化发育的器官特异性，利用鸟氨酸脱羧酶（ODC）活性的个体发育模式（细胞成熟紊乱的早期指标），比较了其对大鼠脑、肝、心和肾的影响。从出生开始，每天给予CH3HgOH，持续21天，采用三个剂量水平（1、2.5或5mg/kg皮下注射）。在脑中，CH3HgOH处理导致ODC活性最初降低，随后升高，这种成熟模式已知与细胞发育延迟有关。与CH3HgOH对脑的影响相反，在肝脏中观察到的模式是最初升高，随后下降，这通常与细胞发育时间进程的压缩有关。在心脏和肾脏中，CH3HgOH使ODC持续升高，代表快速组织生长和发育的发育期延长；这些模式与组织肥大有关，在断奶前阶段，两个组织的肥大持续存在，在肾脏中则持续到断奶后很长一段时间。用ODC获得的结果清楚地表明，新生大鼠CH3HgOH中毒会导致器官特异性生化损伤，这可能在随后对整体组织发育的影响中起作用。
