Hietanen E, Kilpiö J, Savolainen H
Arch Environ Contam Toxicol. 1981;10(3):339-45. doi: 10.1007/BF01055635.
Adult male rats were exposed to 0.5% manganese as MnCl2 in their drinking water for 1, 4, or 6 weeks. Manganese content was measured in brain, liver, kidney, and intestine. Peak manganese concentrations were found in all tissues after one week exposure. Hepatic aryl hydrocarbon hydroxylase, ethoxycoumarin O-deethylase, and epoxide hydrase activities increased after one week manganese exposure, while intestinal and renal activities decreased. The activities returned nearly to the control level at six weeks of exposure. The UDPglucuronosyltransferase activity increased in the liver, kidney, and intestinal mucosa after one week exposure, decreasing thereafter nearly to the control level. In the brain, most significant changes were found after six weeks exposure when the succinate dehydrogenase activity decreased. The results suggest an adaptation to manganese absorption during continuous exposure. The biotransformation enzymes respond first to manganese exposure followed by neurochemical changes in the central nervous system.
成年雄性大鼠饮用含0.5%氯化锰（MnCl₂）的水1周、4周或6周。测定脑、肝、肾和肠道中的锰含量。暴露1周后，所有组织中均发现锰浓度峰值。锰暴露1周后，肝芳烃羟化酶、乙氧基香豆素O-脱乙基酶和环氧化物水解酶活性增加，而肠道和肾脏活性降低。暴露6周时，这些活性几乎恢复到对照水平。UDP-葡萄糖醛酸基转移酶活性在暴露1周后在肝脏、肾脏和肠黏膜中增加，此后几乎降至对照水平。在脑中，暴露6周后发现最显著的变化，此时琥珀酸脱氢酶活性降低。结果表明，在持续暴露期间对锰吸收存在适应性。生物转化酶首先对锰暴露作出反应，随后中枢神经系统发生神经化学变化。
