Tamer Cebe1, Pınar Atukeren2, Karolin Yanar2, Aylin Irmak Kuruç1, Tuna Ozan1, Ahmad Kunbaz1, Mustafa Erinç Sitar2, Reza Mirmaroufizibandeh3, Seval Aydın2, Ufuk Çakatay4. 1. Cerrahpaşa Faculty of Medicine, Istanbul University, Turkey. 2. Department of Medical Biochemistry, Cerrahpaşa Faculty of Medicine, Istanbul University, Turkey. 3. Institute of Health Sciences, Cerrahpaşa Faculty of Medicine, Istanbul University, Turkey. 4. Department of Medical Biochemistry, Cerrahpaşa Faculty of Medicine, Istanbul University, Turkey. Electronic address: cakatay@yahoo.com.
Abstract
BACKGROUND: The effect of the natural aging process on systemic redox homeostasis is previously documented. However, none of the studies specify the effect of experimental aging on systemic redox homeostasis. The purpose of this study is to clarify the ambiguity raised in preliminary reports as to mimetic aging dependency of the type and magnitude of oxidative damage on constituents of plasma. METHODS: In the current study, we investigated the interrelationship among various groups of the systemic oxidative damage markers such as protein oxidation products (protein carbonyl groups, protein hydroperoxides, advanced oxidation protein products, protein thiol groups), lipid peroxidation products (malondialdehyde, lipid hydroperoxides, conjugated dienes), glycoxidation adducts (advanced glycation end products), and antioxidant capacity (ferric reducing/antioxidant power, Cu,Zn-superoxide dismutase, total thiol, non-protein thiol). All these markers were measured in plasma of mimetically aged (MA) rats (5-month-old rats subjected to d-galactose-induced experimental aging), naturally aged (NA) rats (24-month-old), and their corresponding young controls (YC) (5months old). RESULTS AND CONCLUSIONS: Our current results show that systemic oxidation markers of the MA group share significant similarities in terms of impaired redox homeostasis with the NA rats and may be considered as a reliable experimental aging model for intravascular aging. Additional methodological studies including d-galactose dosage and application time are warranted to clarify the potential involvement of all these systemic redox variations as mechanistic factors in the development of mimetic aging related intravascular deterioration. Reversing or preventing systemic oxidative damage in experimental and natural aging should therefore be considered the primary target for the development of effective therapeutic strategies to prevent or treat age-related vascular disorders.
BACKGROUND: The effect of the natural aging process on systemic redox homeostasis is previously documented. However, none of the studies specify the effect of experimental aging on systemic redox homeostasis. The purpose of this study is to clarify the ambiguity raised in preliminary reports as to mimetic aging dependency of the type and magnitude of oxidative damage on constituents of plasma. METHODS: In the current study, we investigated the interrelationship among various groups of the systemic oxidative damage markers such as protein oxidation products (protein carbonyl groups, protein hydroperoxides, advanced oxidation protein products, protein thiol groups), lipid peroxidation products (malondialdehyde, lipid hydroperoxides, conjugated dienes), glycoxidation adducts (advanced glycation end products), and antioxidant capacity (ferric reducing/antioxidant power, Cu,Zn-superoxide dismutase, total thiol, non-protein thiol). All these markers were measured in plasma of mimetically aged (MA) rats (5-month-old rats subjected to d-galactose-induced experimental aging), naturally aged (NA) rats (24-month-old), and their corresponding young controls (YC) (5months old). RESULTS AND CONCLUSIONS: Our current results show that systemic oxidation markers of the MA group share significant similarities in terms of impaired redox homeostasis with the NA rats and may be considered as a reliable experimental aging model for intravascular aging. Additional methodological studies including d-galactose dosage and application time are warranted to clarify the potential involvement of all these systemic redox variations as mechanistic factors in the development of mimetic aging related intravascular deterioration. Reversing or preventing systemic oxidative damage in experimental and natural aging should therefore be considered the primary target for the development of effective therapeutic strategies to prevent or treat age-related vascular disorders.
Authors: K Yanar; U Çakatay; S Aydın; A Verim; P Atukeren; N E Özkan; K Karatoprak; T Cebe; S Turan; E Ozkök; G Korkmaz; C Cacına; O Küçükhüseyin; İ Yaylım Journal: Oxid Med Cell Longev Date: 2015-11-22 Impact factor: 6.543
Authors: M Knaś; M Maciejczyk; I Daniszewska; A Klimiuk; J Matczuk; U Kołodziej; D Waszkiel; J R Ładny; M Żendzian-Piotrowska; A Zalewska Journal: J Diabetes Res Date: 2016-07-13 Impact factor: 4.011