Uric acid and evolution

被引:290
作者
Alvarez-Lario, Bonifacio [1 ]
Macarron-Vicente, Jesus [2 ]
机构
[1] Dept Rheumatol, Burgos 09005, Spain
[2] Dept Neurol, Burgos, Spain
关键词
Uric acid; Gout; Uricase; Hyperuricaemia; Oxidative stress; Neuroprotection; Evolution; Neurodegenerative diseases; Antioxidants; Salt ingestion; MN SUPEROXIDE-DISMUTASE; NEW-ZEALAND MAORI; URATE OXIDASE; RISK-FACTOR; LIFE-SPAN; ALL-CAUSE; GOUT; HYPERURICEMIA; HYPERTENSION; PEROXYNITRITE;
D O I
10.1093/rheumatology/keq204
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Uric acid (UA) is the end product of purine metabolism in humans due to the loss of uricase activity by various mutations of its gene during the Miocene epoch, which led to humans having higher UA levels than other mammals. Furthermore, 90% of UA filtered by the kidneys is reabsorbed, instead of being excreted. These facts suggest that evolution and physiology have not treated UA as a harmful waste product, but as something beneficial that has to be kept. This has led various researchers to think about the possible evolutionary advantages of the loss of uricase and the subsequent increase in UA levels. It has been argued that due to the powerful antioxidant activity of UA, the evolutionary benefit could be the increased life expectancy of hominids. For other authors, the loss of uricase and the increase in UA could be a mechanism to maintain blood pressure in times of very low salt ingestion. The oldest hypothesis associates the increase in UA with higher intelligence in humans. Finally, UA has protective effects against several neurodegenerative diseases, suggesting it could have interesting actions on neuronal development and function. These hypotheses are discussed from an evolutionary perspective and their clinical significance. UA has some obvious harmful effects, and some, not so well-known, beneficial effects as an antioxidant and neuroprotector.
引用
收藏
页码:2010 / 2015
页数:6
相关论文
共 60 条
[1]   URIC-ACID PROVIDES AN ANTIOXIDANT DEFENSE IN HUMANS AGAINST OXIDANT-CAUSED AND RADICAL-CAUSED AGING AND CANCER - A HYPOTHESIS [J].
AMES, BN ;
CATHCART, R ;
SCHWIERS, E ;
HOCHSTEIN, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1981, 78 (11) :6858-6862
[2]   EVOLUTION AND ENVIRONMENT IN THE HOMINOIDEA [J].
ANDREWS, P .
NATURE, 1992, 360 (6405) :641-646
[3]   Gout in the UK and Germany: prevalence, comorbidities and management in general practice 2000-2005 [J].
Annemans, L. ;
Spaepen, E. ;
Gaskin, M. ;
Bonnemaire, M. ;
Malier, V. ;
Gilbert, T. ;
Nuki, G. .
ANNALS OF THE RHEUMATIC DISEASES, 2008, 67 (07) :960-966
[4]   HYPERURICEMIA AS A RISK FACTOR OF CORONARY HEART-DISEASE - THE FRAMINGHAM-STUDY [J].
BRAND, FN ;
MCGEE, DL ;
KANNEL, WB ;
STOKES, J ;
CASTELLI, WP .
AMERICAN JOURNAL OF EPIDEMIOLOGY, 1985, 121 (01) :11-18
[5]   URIC-ACID AND INTELLIGENCE [J].
CERVINI, C ;
ZAMPA, AM .
ANNALS OF THE RHEUMATIC DISEASES, 1982, 41 (04) :435-435
[6]   Independent impact of gout on mortality and risk for coronary heart disease [J].
Choi, Hyon K. ;
Curhan, Gary .
CIRCULATION, 2007, 116 (08) :894-900
[7]   URATE OXIDASE IN PRIMATE PHYLOGENESIS [J].
CHRISTEN, P ;
PEACOCK, WC ;
CHRISTEN, AE ;
WACKER, WEC .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1970, 12 (01) :3-&
[8]   New insights into the epidemiology of gout [J].
Doherty, Michael .
RHEUMATOLOGY, 2009, 48 :2-8
[9]   Astroglia-mediated effects of uric acid to protect spinal cord neurons from glutamate toxicity [J].
Du, Yangzhou ;
Chen, Christopher P. ;
Tseng, Chia-Yi ;
Eisenberg, Yuval ;
Firestein, Bonnie L. .
GLIA, 2007, 55 (05) :463-472
[10]   PALEOLITHIC NUTRITION - A CONSIDERATION OF ITS NATURE AND CURRENT IMPLICATIONS [J].
EATON, SB ;
KONNER, M .
NEW ENGLAND JOURNAL OF MEDICINE, 1985, 312 (05) :283-289