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退行性脑疾病中DNA修复缺陷的研究。

Studies on DNA repair defects in degenerative brain disease.

作者信息

Boerrigter M E, Vijg J

机构信息

Division on Aging, Harvard Medical School, Boston, MA 02215.

出版信息

Age Ageing. 1993 Jan;22(1):S44-52. doi: 10.1093/ageing/22.suppl_1.s44.

DOI:10.1093/ageing/22.suppl_1.s44
PMID:8438655
Abstract

Using the alkaline filter elution technique we determined the induction and disappearance of single-strand breaks (SSB) in freshly isolated peripheral blood lymphocytes (PBL) from 43 Alzheimer disease (AD) patients and from 48 healthy, age- and sex-matched control subjects following in vitro exposure to N-ethyl-N-nitrosourea (ENU), methyl methanesulphonate (MMS), or gamma (gamma)-radiation. No differences in SSB disappearance between AD patients and controls were observed after treatment of PBL with MMS or gamma-rays. After treatment with ENU, however, the amount of SSB disappearance was significantly lower in PBL from familial, but not in PBL from sporadic AD patients. ENU repair in PBL from neurological controls was comparable to that found in normal age-matched controls, indicating that the lower amount of ENU repair in familial AD patients is not a consequence of neuronal degeneration. These tentative findings are discussed in relation to the aetiology of AD.

摘要

我们运用碱性滤膜洗脱技术,测定了43例阿尔茨海默病(AD)患者以及48例年龄和性别匹配的健康对照受试者新鲜分离的外周血淋巴细胞(PBL)在体外暴露于N-乙基-N-亚硝基脲(ENU)、甲磺酸甲酯(MMS)或γ射线后单链断裂(SSB)的诱导和消失情况。在用MMS或γ射线处理PBL后,未观察到AD患者与对照之间SSB消失存在差异。然而,在用ENU处理后,家族性AD患者PBL中SSB消失的量显著低于散发性AD患者PBL中的量。神经学对照受试者PBL中的ENU修复与年龄匹配的正常对照者相当,这表明家族性AD患者中ENU修复量较低并非神经元变性的结果。我们结合AD的病因学对这些初步发现进行了讨论。

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Studies on DNA repair defects in degenerative brain disease.退行性脑疾病中DNA修复缺陷的研究。
Age Ageing. 1993 Jan;22(1):S44-52. doi: 10.1093/ageing/22.suppl_1.s44.
2
Decreased DNA repair capacity in familial, but not in sporadic Alzheimer's disease.家族性阿尔茨海默病患者的DNA修复能力下降,而散发性阿尔茨海默病患者则不然。
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Induction and disappearance of DNA strand breaks and/or alkali-labile sites in human lymphocytes exposed to N-ethyl-N-nitrosourea.暴露于N-乙基-N-亚硝基脲的人淋巴细胞中DNA链断裂和/或碱不稳定位点的诱导与消失
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