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Increasing longevity by tuning up metabolism. To maximize human health and lifespan, scientists must abandon outdated models of micronutrients.通过调节新陈代谢来延长寿命。为了使人类健康和寿命最大化,科学家们必须摒弃过时的微量营养素模型。
EMBO Rep. 2005 Jul;6 Spec No(Suppl 1):S20-4. doi: 10.1038/sj.embor.7400426.
2
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3
[The ecological, biological and social hygiene factors of longevity].
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The effects of the dietary polyphenol resveratrol on human healthy aging and lifespan.白藜芦醇对人类健康衰老和寿命的影响。
Epigenetics. 2011 Jul;6(7):870-4. doi: 10.4161/epi.6.7.16499. Epub 2011 Jul 1.
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Antioxid Redox Signal. 2003 Oct;5(5):557-61. doi: 10.1089/152308603770310202.
7
Longevity and aging: role of genes and of the extracellular matrix.长寿与衰老:基因及细胞外基质的作用
Biogerontology. 2015 Feb;16(1):125-9. doi: 10.1007/s10522-014-9544-x. Epub 2014 Dec 12.
8
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J Dev Orig Health Dis. 2014 Oct;5(5):325-38. doi: 10.1017/S2040174414000294. Epub 2014 Jun 13.
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Integr Comp Biol. 2010 Nov;50(5):778-82. doi: 10.1093/icb/icq136. Epub 2010 Sep 21.

引用本文的文献

1
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2
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Vitamin D, folate, and potential early lifecycle environmental origin of significant adult phenotypes.维生素 D、叶酸和潜在的重要成年表型的早期生命周期环境起源。
Evol Med Public Health. 2014 Jan;2014(1):69-91. doi: 10.1093/emph/eou013. Epub 2014 Apr 2.
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Hormesis in aging and neurodegeneration-a prodigy awaiting dissection.衰老与神经退行性变中的兴奋效应——一个有待剖析的非凡现象。
Int J Mol Sci. 2013 Jun 25;14(7):13109-28. doi: 10.3390/ijms140713109.
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Prevention of mutation, cancer, and other age-associated diseases by optimizing micronutrient intake.通过优化微量营养素摄入预防突变、癌症及其他与年龄相关的疾病。
J Nucleic Acids. 2010 Sep 22;2010:725071. doi: 10.4061/2010/725071.
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Reduced expression of mitochondrial frataxin in mice exacerbates diet-induced obesity.小鼠线粒体铁调素表达降低会加剧饮食诱导的肥胖。
Proc Natl Acad Sci U S A. 2007 Apr 10;104(15):6377-81. doi: 10.1073/pnas.0611631104. Epub 2007 Apr 2.
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Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage.微量营养素摄入不足可能通过“应急分配”稀缺的微量营养素,加速衰老相关的退行性疾病。
Proc Natl Acad Sci U S A. 2006 Nov 21;103(47):17589-94. doi: 10.1073/pnas.0608757103. Epub 2006 Nov 13.

本文引用的文献

1
Nutritional treatment of genome instability: a paradigm shift in disease prevention and in the setting of recommended dietary allowances.基因组不稳定的营养治疗:疾病预防及推荐膳食摄入量设定方面的范式转变
Nutr Res Rev. 2003 Jun;16(1):109-22. doi: 10.1079/NRR200359.
2
Dietary zinc modulation of COX-2 expression and lingual and esophageal carcinogenesis in rats.膳食锌对大鼠COX-2表达及舌和食管癌发生的调节作用。
J Natl Cancer Inst. 2005 Jan 5;97(1):40-50. doi: 10.1093/jnci/dji006.
3
A role for heme in Alzheimer's disease: heme binds amyloid beta and has altered metabolism.血红素在阿尔茨海默病中的作用:血红素与β淀粉样蛋白结合并代谢发生改变。
Proc Natl Acad Sci U S A. 2004 Jul 27;101(30):11153-8. doi: 10.1073/pnas.0404349101. Epub 2004 Jul 19.
4
Lipoic acid as a potential therapy for chronic diseases associated with oxidative stress.硫辛酸作为一种针对与氧化应激相关的慢性疾病的潜在疗法。
Curr Med Chem. 2004 May;11(9):1135-46. doi: 10.2174/0929867043365387.
5
Decline in transcriptional activity of Nrf2 causes age-related loss of glutathione synthesis, which is reversible with lipoic acid.Nrf2转录活性的下降会导致与年龄相关的谷胱甘肽合成减少,而硫辛酸可使其逆转。
Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3381-6. doi: 10.1073/pnas.0400282101. Epub 2004 Feb 25.
6
(R)-alpha-lipoic acid reverses the age-related loss in GSH redox status in post-mitotic tissues: evidence for increased cysteine requirement for GSH synthesis.(R)-α-硫辛酸可逆转有丝分裂后组织中与年龄相关的谷胱甘肽(GSH)氧化还原状态的丧失:GSH合成对半胱氨酸需求增加的证据。
Arch Biochem Biophys. 2004 Mar 1;423(1):126-35. doi: 10.1016/j.abb.2003.12.020.
7
Zinc deficiency induces oxidative DNA damage and increases p53 expression in human lung fibroblasts.锌缺乏会诱导人肺成纤维细胞发生氧化性DNA损伤并增加p53表达。
J Nutr. 2003 Aug;133(8):2543-8. doi: 10.1093/jn/133.8.2543.
8
Meta-analysis of double blind randomized controlled clinical trials of acetyl-L-carnitine versus placebo in the treatment of mild cognitive impairment and mild Alzheimer's disease.乙酰左旋肉碱与安慰剂治疗轻度认知障碍和轻度阿尔茨海默病的双盲随机对照临床试验的荟萃分析。
Int Clin Psychopharmacol. 2003 Mar;18(2):61-71. doi: 10.1097/00004850-200303000-00001.
9
Low intracellular zinc induces oxidative DNA damage, disrupts p53, NFkappa B, and AP1 DNA binding, and affects DNA repair in a rat glioma cell line.细胞内低锌水平会诱导氧化性DNA损伤,破坏p53、核因子κB和活化蛋白1与DNA的结合,并影响大鼠胶质瘤细胞系中的DNA修复。
Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):16770-5. doi: 10.1073/pnas.222679399. Epub 2002 Dec 12.
10
Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging.血红素缺乏可能是衰老过程中线粒体和神经元衰退的一个因素。
Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):14807-12. doi: 10.1073/pnas.192585799. Epub 2002 Nov 4.

通过调节新陈代谢来延长寿命。为了使人类健康和寿命最大化,科学家们必须摒弃过时的微量营养素模型。

Increasing longevity by tuning up metabolism. To maximize human health and lifespan, scientists must abandon outdated models of micronutrients.

作者信息

Ames Bruce N

机构信息

The Children's Hospital Oakland Research Institute, Oakland, CA, USA.

出版信息

EMBO Rep. 2005 Jul;6 Spec No(Suppl 1):S20-4. doi: 10.1038/sj.embor.7400426.

DOI:10.1038/sj.embor.7400426
PMID:15995656
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1369274/
Abstract

To maximize human health and lifespan, scientists must abandon outdated models of micronutrients

摘要

为了最大化人类健康和寿命,科学家们必须摒弃过时的微量营养素模型。