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Summary The current study included fifty-six young male albino rats (4 months old and weighted 280 –290 gm), and twenty-four senescent male albino rats (24 months old and weighted 420 – 450 gm). The study was conducted in Biology Department of the College of Science, University of Mosul, and in the Medical Research Center of Hawler Medical University. Animals' treatment and assessing biomarkers of the experiment lasted a period between January- 2013 and December - 2014. The present study aimed to investigate the antiaging properties of grape seed extract (GSE), green tea extract (GTE), pomegranate seed extract (PSE), ginkgo biloba extract (GBE), α- lipoic acid (LA) and centrophenoxine (CPH) in normal and D- galactose (D-gal) induced aged male albino rats, and their preventing and improving effects in some biomolecular and physiological biomarkers of aging resulted from oxidative damage to cells in natural and D-gal Induced aged rats. Young male rats of four months age were divided randomly into eight groups (7 rats in each group), group I (control), group II (D-gal.), group III (D-gal. +CPH), group IV (D-gal. + GSE), group V (D- gal. + GTE), group VI (D-gal.+ LA), group VII (D-gal. + PSE) and Group VIII (D- gal. +GBE). Senescent male rats of 24 month old were divided randomly into four groups (7 rats in each group), group I (control), group II (CPH), group III (GSE) and group IV (GTE). At the end of the nine weeks experimental treatment period, blood samples were collected and the obtained serum were stored at-80 °C then used for biochemical assay. The dissected liver and brain of each animal in the all groups had been homogenized and liver and brain supernatant was collected and stored at -80 °C then used for oxidative stress biomarkers assay, also small pieces were taken from the liver and the brain of each animal to be used in the biomolecular studies. The results showed that mitochondrial Deoxyribonucleic acid (mtDNA) deletion4834 bp, 8-hydroxy-2'-deoxy guanosine (8-OHdG), Malondialdehyde
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(MDA) and isoprostane (IsoP) significantly (P< 0.01) increased in the liver and
brain of natural aged and D-gal. induced aging rats. Cellular mtDNA copy
number is significantly (P< 0.01) increased also in liver and brain of natural
aged and D-galactose induced aging rats in response to oxidative stress with the
aging. Administration of antiaging biocompounds; GSE, GTE, PSE, GBE, LA
and CPH significantly (P< 0.01) decreased mtDNA deletion4834 bp and 8-
OHdG, mtDNA copy number, MDA and IsoP in liver and brain of normal aged
rats and D-Galactose induced aging groups.
The data of this study showed a significant (P< 0.01) decrease in total
antioxidant capacity (TCA), total glutathione (T.GSH), superoxide dismutase
(SOD) and catalase (CAT) of the liver and brain of rats and indicates that this
decrease may be involved in the mechanisms of free radical induced damage to
lipids, proteins and DNA during normal aging and chronic administration of Dgalactose.
Administration of antiaging biocompounds; GSE, GTE, PSE, GBE,
LA and CPH significantly (P< 0.01) increased TCA, T.GSH, SOD, CAT of the
liver and brain in natural and D-gal. induced aging rats.
Total non-heme iron and ferritin concentration of liver and brain were
significantly (P<0.01) increased in natural and induced aged rats. Treatment
with GSE, GTE, PSE, GBE, LA and CPH significantly (P< 0.01) caused
decrease of the non-heme iron in liver and brain of normal and induced ageing
rats.
Significant (P<0.05) elevation in serum aspartate aminotransferase (AST),
alanine aminotransferase (ALT), alkaline phosphate (ALP), gamma-glutamyl
transferase (GGT) and significant (P<0.05) reduced of albumin (ALB) and total
bilirubin (TBI) as a liver function biomarkers was shown in natural and D-gal.
induced aging rats. Rats treated with GSE, GTE, PSE, GBE, LA and CPH
showed a protective role in decreasing significantly (P<0.05) the serum levels of
AST ALT, ALP, GGT with significant (P<0.05) increasing in the serum ALB
and TBI as a liver function biomarkers in natural and D-gal. induced aging rats.
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The levels of serum lactate dehydrogenase (LDH) and creatine phosphokinase
(CPK) as a hepatic function biomarkers significantly (P<0.05) increased in
natural and D-gal. induced aging rats. The treatment with GSE, GTE, GSE,
GBE, LA and CPH showed a protective role in significantly decreasing the
serum levels of LDH and CPK in natural and D-gal. induced aging rats.
The levels of serum urea, creatinine and uric acid as a renal function biomarkers
significantly (P<0.05) increased in natural and D-gal. induced aging rats. The
rats treated with GSE, GTE, GPE, GBE, LA and CPH showed a protective role
in decreasing significantly (P< 0.05) the serum levels of uric acid, urea and
creatinine in natural and D-gal. induced aging rats.
Body weight and organs weight (liver, heart and brain) were slightly
decreased in D-gal. induced model rats but antioxidants administration improves
them.
In conclusion, this study demonstrates that aging induces a significant
mtDNA oxidative damage and oxidative stress biomarkers in rats. Chronic
administration of D-gal. accelerates aging via enhancing production of reactive
oxygen species and advanced glycation ends products (AGE), this sequence of
events results an oxidative stress and cellular damage. 9-week supplementation
of GSE, GTE, PSE, GBE, LA and CPH supplementation suppresses senescence
biomarkers and down regulates oxidative stress damage in the liver, heart,
kidney and brain tissues of normal and D-gal.-induced aging rats.