Iron depletion prevents adenine nucleotide decomposition and an increase of xanthine oxidase activity in the liver of the Long Evans Cinnamon (LEC) rat, an animal model of Wilson's disease.
Iron depletion prevents adenine nucleotide decomposition and an increase of xanthine oxidase activity in the liver of the Long Evans Cinnamon (LEC) rat, an animal model of Wilson's disease.
复制标题
铁耗竭可以防止腺嘌呤核苷酸分解，并防止长埃文斯肉桂 (LEC) 大鼠（威尔逊病动物模型）肝脏中黄嘌呤氧化酶活性的增加。
DOI：
10.1016/s0024-3205(99)00378-1
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发表时间：
1999
期刊：
影响因子：
6.1
通讯作者：
M. Tamura
中科院分区：
文献类型：
--
作者：
N. Sugawara;T. Ohta;Y. Lai;C. Sugawara;M. Yuasa;M. Nakamura;M. Tamura
Long Evans Cinnamon（LEC）大鼠在肝脏中积累了过量的Cu，与Wilson病患者一样，是一种表现出自发性肝炎的突变株。据报道，铁，像铜，在肝脏中增加，肝炎的严重程度是由饮食中的铁修改。在本实验中，研究了肝炎发病前铁增加的氧化应激。为了检查铁对肝炎进展的影响，LEC雌性大鼠从53日龄开始连续35天喂食常规铁（Fe 214 μ g/g; Fe（+）组）或限制铁（Fe 14 μ g/g; Fe（-）组）饮食。还喂养Fischer大鼠作为对照动物。腺嘌呤核苷酸分解被确定为基于黄嘌呤氧化酶活性的氧化应激指标。LEC大鼠的腺嘌呤核苷酸池（ATP + ADP + AMP）的大小明显小于Fischer大鼠。Fe（+）组的能荷（ATP +0.5ADP）/（ATP + ADP + AMP）小于Fe（-）组。在LEC大鼠肝脏中，Fe（+）组的Fe浓度是Fe（-）组的160%，并且肝脏Fe浓度与能荷之间的相关系数显著。在该菌株中，黄嘌呤氧化酶活性的增加导致黄嘌呤（次黄嘌呤在肝脏中的氧化代谢物）的增加。结果表明，铁的参与进展为肝炎的LEC大鼠，即使饮食中的铁浓度是类似的商业饮食。
The Long Evans Cinnamon (LEC) rat, which accumulates excess Cu in the liver as in patients with Wilson's disease, is a mutant strain displaying spontaneous hepatitis. It was reported that Fe, like Cu, increases in the liver and that the severity of hepatitis is modified by Fe in the diet. In this experiment, oxidative stress increased by Fe was investigated before the onset of hepatitis. To examine the effect of Fe on the progress into hepatitis, LEC female rats were fed an Fe-regular (Fe 214μg/g; Fe(+) group) or an Fe-restricted (Fe 14μg/g; Fe(−) group) diet from 53 days of age for 35 days. Fischer rats were also fed as control animals. Adenine nucleotide decomposition was determined as an index of oxidative stress based on xanthine oxidase activity. The size of the hepatic pool of adenine nucleotides (ATP + ADP + AMP) was significantly smaller in LEC rats than Fischer rats. The energy charge (ATP + 0.5ADP)/(ATP + ADP + AMP) was smaller in Fe(+) groups than in Fe(−) groups. In the LEC rat liver, the Fe concentration in the Fe(+) group was 160% of that in Fe(−) group and the correlation coefficient between the hepatic Fe concentration and the energy charge was significant. In this strain, an increase of xanthine oxidase activity resulted in an increase of xanthine, an oxidized metabolite of hypoxanthine in the liver. The results suggest the involvement of the Fe in the progression into hepatitis in the LEC rat, even if the dietary Fe concentration is similar to that of commercial diet.