Ittel T H, Paulus C P, Handt S, Hofstädter F, Sieberth H G
Department of Internal Medicine II, Aachen, FRG.
Miner Electrolyte Metab. 1992;18(1):15-23.
The intestinal absorption of aluminum (Al) appears to be enhanced in the uremic rat. Since atrophic changes of the intestinal mucosa have been observed in uremia the present study investigated whether intestinal atrophy induced by difluoromethylornithine (DFMO), a specific inhibitor of ornithine decarboxylase, could affect the absorption of Al. DFMO supplied with the drinking water (5%) to rats with normal renal function for 9 days resulted in a reduced number of microvilli with definite morphological alterations in small intestinal mucosa. Following an oral load of Al urinary excretion rates and 1-hour postload serum concentrations of Al were increased in DFMO-treated rats as compared to controls suggesting enhanced absorption of Al. Pattern and degree of urinary Al excretion as well as ultrastructural alterations of the intestinal mucosa were similar in DFMO-treated rats and uremic rats. The model of DFMO-induced intestinal alterations suggests that structural lesions of the intestine may be involved in the enhanced absorption of Al in uremia.
尿毒症大鼠对铝（Al）的肠道吸收似乎有所增强。由于在尿毒症中已观察到肠黏膜的萎缩性变化，因此本研究调查了鸟氨酸脱羧酶的特异性抑制剂二氟甲基鸟氨酸（DFMO）诱导的肠道萎缩是否会影响铝的吸收。给具有正常肾功能的大鼠饮用含5%DFMO的水9天，导致小肠黏膜微绒毛数量减少，形态发生明确改变。口服铝负荷后，与对照组相比，DFMO处理的大鼠尿铝排泄率和负荷后1小时血清铝浓度升高，提示铝吸收增强。DFMO处理的大鼠和尿毒症大鼠的尿铝排泄模式和程度以及肠黏膜的超微结构改变相似。DFMO诱导的肠道改变模型表明，肠道结构损伤可能与尿毒症时铝吸收增强有关。
