TY - JOUR
T1 - Effect of natural exogenous antioxidants on aging and on neurodegenerative diseases
AU - Guerra-Araiza, Christian
AU - Álvarez-Mejía, Ana Laura
AU - Sánchez-Torres, Stephanie
AU - Farfan-García, Eunice
AU - Mondragón-Lozano, Rodrigo
AU - Pinto-Almazán, Rodolfo
AU - Salgado-Ceballos, Hermelinda
N1 - Funding Information:
We acknowledge support from FIS/IMSS projects No. FIS/IMSS/PROT/G11-2/1013 and FIS/IMSS/PROT552 as well as FP-2003/025 and 2005/1/I/061. Mondragó n-Lozano R.; Rodolfo Pinto received financial support from CONACYT; and Farfán-García E., Álvarez-Mejía A.L., and S á nchez-Torres S. received financial support from CONACYT and from IMSS.
PY - 2013/7
Y1 - 2013/7
N2 - Aging and neurodegenerative diseases share oxidative stress cell damage and depletion of endogenous antioxidants as mechanisms of injury, phenomena that are occurring at different rates in each process. Nevertheless, as the central nervous system (CNS) consists largely of lipids and has a poor catalase activity, a low amount of superoxide dismutase and is rich in iron, its cellular components are damaged easily by overproduction of free radicals in any of these physiological or pathological conditions. Thus, antioxidants are needed to prevent the formation and to oppose the free radicals damage to DNA, lipids, proteins, and other biomolecules. Due to endogenous antioxidant defenses are inadequate to prevent damage completely, different efforts have been undertaken in order to increase the use of natural antioxidants and to develop antioxidants that might ameliorate neural injury by oxidative stress. In this context, natural antioxidants like flavonoids (quercetin, curcumin, luteolin and catechins), magnolol and honokiol are showing to be the efficient inhibitors of the oxidative process and seem to be a better therapeutic option than the traditional ones (vitamins C and E, and β-carotene) in various models of aging and injury in vitro and in vivo conditions. Thus, the goal of the present review is to discuss the molecular basis, mechanisms of action, functions, and targets of flavonoids, magnolol, honokiol and traditional antioxidants with the aim of obtaining better results when they are prescribed on aging and neurodegenerative diseases.
AB - Aging and neurodegenerative diseases share oxidative stress cell damage and depletion of endogenous antioxidants as mechanisms of injury, phenomena that are occurring at different rates in each process. Nevertheless, as the central nervous system (CNS) consists largely of lipids and has a poor catalase activity, a low amount of superoxide dismutase and is rich in iron, its cellular components are damaged easily by overproduction of free radicals in any of these physiological or pathological conditions. Thus, antioxidants are needed to prevent the formation and to oppose the free radicals damage to DNA, lipids, proteins, and other biomolecules. Due to endogenous antioxidant defenses are inadequate to prevent damage completely, different efforts have been undertaken in order to increase the use of natural antioxidants and to develop antioxidants that might ameliorate neural injury by oxidative stress. In this context, natural antioxidants like flavonoids (quercetin, curcumin, luteolin and catechins), magnolol and honokiol are showing to be the efficient inhibitors of the oxidative process and seem to be a better therapeutic option than the traditional ones (vitamins C and E, and β-carotene) in various models of aging and injury in vitro and in vivo conditions. Thus, the goal of the present review is to discuss the molecular basis, mechanisms of action, functions, and targets of flavonoids, magnolol, honokiol and traditional antioxidants with the aim of obtaining better results when they are prescribed on aging and neurodegenerative diseases.
KW - Alzheimer's disease
KW - Flavonoid
KW - Honokiol
KW - Magnolol
KW - Neuronal injury
KW - Oxidative stress
KW - Parkinson's disease
KW - Quercetin
UR - http://www.scopus.com/inward/record.url?scp=84878821688&partnerID=8YFLogxK
U2 - 10.3109/10715762.2013.795649
DO - 10.3109/10715762.2013.795649
M3 - Artículo de revisión
SN - 1071-5762
VL - 47
SP - 451
EP - 462
JO - Free Radical Research
JF - Free Radical Research
IS - 6-7
ER -