Ankrah N A
Noguchi Memorial Institute for Medical Research, University of Ghana, Legon.
Vet Hum Toxicol. 1995 Feb;37(1):59-61.
Glyoxalase-I activity plays an important role in glucose metabolism and has been reported to be depressed in mice fed low levels of aflatoxin B1. In the present study examination of glyoxalase-I activity, glucose tolerance and pancreatic beta cell sensitivity was made in mice fed 0.045 ng aflatoxin B1 + 0.450 ng aflatoxin G1/g feed prenatally and for 6 mo after birth. After glucose challenge the ratios between 0-h and 2-h serum glucose levels were significantly higher than controls, indicating an increase in tolerance of glucose in the aflatoxin-fed mice with lower glyoxalase-I activity. Pancreatic beta cell sensitivity to stimulation by tolbutamide was similar in both groups. However, liver malonic dialdehyde was significantly higher in the aflatoxin-fed mice, suggesting that the altered tolerance for glucose in the aflatoxin-fed mice might be a consequence of aflatoxin mediated peroxidative actions in the liver.
乙二醛酶 -I活性在葡萄糖代谢中起重要作用,据报道,在喂食低水平黄曲霉毒素B1的小鼠中该活性会降低。在本研究中,对产前及出生后6个月喂食0.045纳克黄曲霉毒素B1 + 0.450纳克黄曲霉毒素G1/克饲料的小鼠进行了乙二醛酶 -I活性、葡萄糖耐量和胰腺β细胞敏感性检测。葡萄糖激发后,黄曲霉毒素喂养组小鼠0小时与2小时血清葡萄糖水平之比显著高于对照组,表明乙二醛酶 -I活性较低的黄曲霉毒素喂养小鼠对葡萄糖的耐受性增加。两组小鼠胰腺β细胞对甲苯磺丁脲刺激的敏感性相似。然而,黄曲霉毒素喂养组小鼠肝脏丙二醛水平显著更高,这表明黄曲霉毒素喂养小鼠对葡萄糖耐受性的改变可能是黄曲霉毒素介导的肝脏过氧化作用的结果。