Formaldehyde stress

被引:88
作者
He RongQiao [1 ]
Lu Jing [1 ,2 ]
Mia JunYe [1 ,2 ]
机构
[1] Chinese Acad Sci, Inst Biophys, State Key Lab Brain & Cognit Sci, Beijing 100101, Peoples R China
[2] Chinese Acad Sci, Grad Univ, Beijing 100049, Peoples R China
基金
中国国家自然科学基金;
关键词
formaldehyde; Alzheimer's disease; senile dementia; stress; cognition; impairment; hyperphosphorylation; ALZHEIMERS-DISEASE; ALCOHOL-DEHYDROGENASE; TAU-PROTEIN; CLASS-III; GENE; HYPERPHOSPHORYLATION; PHOSPHORYLATION; LOCALIZATION; DEGENERATION; DEFICITS;
D O I
10.1007/s11427-010-4112-3
中图分类号
Q [生物科学];
学科分类号
090105 [作物生产系统与生态工程];
摘要
Formaldehyde, one of the most toxic organic compounds, is produced and processed in human cells. The level of human endogenous formaldehyde is maintained at a low concentration (0.01-0.08 mmol L-1 in blood) under physiological conditions, but the concentration increases during ageing (over 65 years old). Clinical trials have shown that urine formaldehyde concentrations are significantly different between elderly Alzheimer's patients (n=91) and normal elderly volunteers (n=38) (P<0.001). Abnormally high levels of intrinsic formaldehyde lead to dysfunction in cognition such as learning decline and memory loss. Excess extracellular and intracellular formaldehyde could induce metabolic response and abnormal modifications of cellular proteins such as hydroxymethylation and hyperphosphorylation, protein misfolding, nuclear translocation and even cell death. This cellular response called formaldehyde stress is dependent upon the concentration of formaldehyde. Chronic impairments of the brain resulted from formaldehyde stress could be one of the mechanisms involved in the process of senile dementia during ageing.
引用
收藏
页码:1399 / 1404
页数:6
相关论文
共 71 条
[1]
Tissue activity and cellular localization of human semicarbazide-sensitive amine oxidase [J].
Andrés, N ;
Lizcano, JM ;
Rodríguez, MJ ;
Romera, M ;
Unzeta, M ;
Mahy, N .
JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY, 2001, 49 (02) :209-217
[2]
Anwar R, 1996, J NEUROCHEM, V66, P1774
[3]
Mapping the Altered Patterns of Cerebellar Resting-State Function in Longitudinal Amnestic Mild Cognitive Impairment Patients [J].
Bai, Feng ;
Liao, Wei ;
Watson, David R. ;
Shi, Yongmei ;
Yuan, Yonggui ;
Cohen, Alexander D. ;
Xie, Chunming ;
Wang, Yi ;
Yue, Chunxian ;
Teng, Yuhuan ;
Wu, Di ;
Jia, Jianping ;
Zhang, Zhijun .
JOURNAL OF ALZHEIMERS DISEASE, 2011, 23 (01) :87-99
[4]
Kinetics of cytochrome P450 2E1-catalyzed oxidation of ethanol to acetic acid via acetaldehyde [J].
Bell-Parikh, LC ;
Guengerich, FP .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (34) :23833-23840
[5]
Bertoni-Freddari C, 1997, Ann N Y Acad Sci, V826, P479, DOI 10.1111/j.1749-6632.1997.tb48508.x
[6]
APOE GENE DOSE IN ALZHEIMERS-DISEASE [J].
BIGNALL, J .
LANCET, 1993, 342 (8868) :426-426
[7]
BINKOVA B, 1989, CHEM LISTY, V83, P1065
[8]
Cloning of dimethylglycine dehydrogenase and a new human inborn error of metabolism, dimethylglycine dehydrogenase deficiency [J].
Binzak, BA ;
Wevers, RA ;
Moolenaar, SH ;
Lee, YM ;
Hwu, WL ;
Poggi-Bach, J ;
Engelki, UFH ;
Hoard, HM ;
Vockley, JG ;
Vockley, J .
AMERICAN JOURNAL OF HUMAN GENETICS, 2001, 68 (04) :839-847
[9]
Alzheimer's disease [J].
Scheltens, Philip ;
De Strooper, Bart ;
Kivipelto, Miia ;
Holstege, Henne ;
Chetelat, Gael ;
Teunissen, Charlotte E. ;
Cummings, Jeffrey ;
van der Flier, Wiesje M. .
LANCET, 2021, 397 (10284) :1577-1590
[10]
BOTTIGLIONIE SPL, 1955, ARCH PATOL CLIN MED, V32, P210