摘要
为探讨砷中毒的肝脏损害机理，通过急性实验和亚慢性实验，研究了砷对小鼠肝脏脂质过氧化（ＬＰＯ）水平的影响。结果表明，在急性实验中，与对照组相比，低、中剂量组ＧＳＨ含量显著增高，高剂量组则显著降低；低剂量组ＳＯＤ活力显著增高，中、高剂量组则显著降低；各剂量组ＧＳＨ－Ｐｘ活力均显著降低，且呈剂量－效应关系；中、高剂量组ＭＤＡ水平显著升高。亚慢性实验中，低、高、超剂量组ＧＳＨ含量显著降低；各剂量组ＳＯＤ活力显著降低；中、高、超剂量组ＧＳＨＰｘ活力显著降低，且呈剂量－效应关系；中、高、超剂量组ＭＤＡ水平则显著升高。提示，砷可引起小鼠肝组织发生ＬＰＯ，ＬＰＯ可能是砷致肝损害的机制之一。
In
order to explore the mechanism of arsenic in liver injury,the effect of arsenic on lipid
peroxidation(LPO)in mice liver was studied by means of acute and subchronic experiments.The
results were as follows:In acute experiment,the contents of glutathione(GSH)in low and middle
dose groups were higher than those in controls,and decreased significantly in high dose group.
The activity of superoxide dismutase(SOD)in low dose group increased and markedly
decreased in middle and high dose groups.The activity of glutathione peroxidase(GSH\|Px)in all
groups decreased strikingly and showed a dose\|effect manner.The level of
malonaldehyed(MDA)in middle and high dose groups increased significantly.In subchronic
experiment,the contents of GSH in low,high and super\|high dose groups decreased
significantly.The activity of SOD in all groups decreased markedly.The activity of GSH\|Px in
middle,high and super\|high dose groups also decreased strikingly,and showed a dose\|effect
manner,The level of MDA in middle,high and super\|high dose groups increased
significantly.The results indicated that arsenic could induced LPO in mice liver.LPO might be
one of the mechanism of arsenic in liver injury.
出处
《工业卫生与职业病》
CAS
CSCD
1999年第3期145-148,共4页
Industrial Health and Occupational Diseases
