摘要
大白鼠喂饲克山病区粮和非病区粮,并分别加 1000ppm 锰。实验分4组,A 组非病区粮,B 组病区粮,C 组非病区粮+锰,D 组病区粮+锰,喂8周后处死。结果表明,B 和 D 组大鼠全血、心肌和肝脏的 GSH—Px 活性均明显下降,心肌、肝脏和血清脂质过氧化物含量升高,该两组间比较无明显差异。而 C 组大鼠的 GSH—Px 活性和脂质过氧化物含量与 A 组比较也无明显差异,提示过量锰(1000ppm)对动物体的 GSH—Px 活性和脂质过氧化物水平无明显影响。加锰组(C 和 D)大鼠心肌的线粒体肿胀和空泡变明显,电镜细胞化学显示心肌线粒体的细胞色素氧化酶和琥珀酸脱氢酶活性降低,D 组降低更明显、提示过量锰引起心肌损伤的主要环节可能是损害线粒体的功能与结构。并使喂饲病区粮大鼠心肌损害加重。
In this study,the rats were fed on diet with grains produced in Keshandisease endemic region or grains prduced in non-endemic region,and the samediet besides manganese were added respectively.experimental animals weredivided in to four groups:group A non-endemic region diet;group B endemicregion diet;group C non-endemic region diet+manganese(Mn);group D ende-mic region diet+Mn.The resuts showed the activity of GSH-Px in blood,heartand liver were apparently lower in the groups B and D,compared with thosein the groups A and C.The level of MDA in heart,liver and serum wereapparently higher in the groups B and D,compared with those in the groupsA and C.The activity of GSH-Px and the level of MDA were insignificant diff-erence between the groups B and D.Those were also insignificant difference bet-ween the groups A and C.It is suggested that the excess manganese can′t exerteffects on activity of GSH-Px and level of MDA in animal.Swelling and vesic-ular change of myocardial mitochondria were recognized in the observation ofconventional electron microscopy in the groups C and D.Activity of cytochemi-cal reaction was decreased in mitochondria of the groups C and D in cytochromeoxidase and succinate dehydrogenese.Those in mitochondria of the group Dremarkably was decreased。those results suggested that A key link of cardiac lesions induced by excess manganes can be lesions of function and structureof myocardial mitochondria.
出处
《中国地方病学杂志》
CAS
CSCD
1990年第5期281-284,共4页
Chinese Jouranl of Endemiology
基金
国家自然科学基金
关键词
锰
心肌损伤
克山病
Manganese
GSH—Px
MDA
Cytochrome oxidase
Succinate dehydrogenase
