The Effects of Glutathione on Clinically Essential Fertility Parameters in a Bleomycin Etoposide Cisplatin Chemotherapy Model.

Chemotherapeutic agents used in the treatment of testicular cancer cause damage to healthy tissues, including the testis. We investigated the effects of glutathione on sperm DNA integrity and testicular histomorphology in bleomycin etoposide cisplatin (BEP) treated rats. Twelve-week-old male rats of reproductive age (n = 24) were randomly divided into three groups, the (i) control group, (ii) BEP group, and (iii) BEP+ glutathione group. Weight gain increase and testes indices of the control group were found to be higher than that of the BEP group and BEP+ glutathione group. While the BEP treatment increased sperm DNA fragmentation and morphological abnormalities when compared to the control group, GSH treatment resulted in a marked decrease for both parameters. Moreover, BEP treatment significantly decreased serum testosterone levels and sperm counts in comparison to the control group, yet this reduction was recovered in the BEP+ glutathione treated group. Similarly, seminiferous tubule epithelial thicknesses and Johnsen scores in testicles were higher in the control and BEP+ glutathione groups than in the BEP-treated group. In conclusion, exogenous glutathione might prevent the deterioration of male reproductive functions by alleviating the detrimental effects of BEP treatment on sperm quality and testicular histomorphology.

Morphological and biomechanical effects of vitamin K2 on fracture healing: An animal study on the rat tibia fracture model.

OBJECTIVE: The aim of this study was to evaluate the effects of vitamin K2 on fracture healing. METHODS: Twenty-four 6-week-old male Wistar albino rats that had open tibia fractures induced were included in this study. They were divided into 2 groups of 12, a group that had vitamin K2 administered over 30 consecutive days and a control group. After 30 days, the rats were sacrificed, and from each group, 6 tibiae were selected for biomechanical testing to examine the mechanical strength of the callus tissue using the Instron 3-point bending test and 6 tibiae were selected for histological analysis to examine the density and organization of callus tissue using Allen's grading system and Huo et al's grading system. Furthermore, weekly x-rays were taken to evaluate bone union described by Lane and Sandhu, and osteocalcin, procollagen I N-terminal propeptide, and procollagen I C-terminal propeptide were examined in blood samples taken by intracardiac puncture during sacrification. RESULTS: Breaking force (P = .047), breaking time (P = .019), stiffness (P = .039), fracture strength (P = .041), and Young's modulus (P = .032) showed a statistically significant increase in the K2 group. Procollagen I C-terminal propeptide (P = .024), procollagen I N-terminal propeptide (.047), and osteocalcin (.048) levels were significantly higher in the K2 group compared to the control group. Furthermore, 3rd-week x-rays showed higher bone union scores according to the Lane and Sandhu method in the K2 group (P = .014). However, the histological grading systems of Allen and Huo et al did not show statistically significant differences between groups (P = .086, P = .07, respectively). CONCLUSION: In light of these findings, it could be concluded that vitamin K2 has a significant positive effect on fracture healing.

Rescue IVM of Denuded GV- and MI-Stage Oocytes of Premenopausal Rats with Oncostatin M, Insulin-like Growth Factor I, and Growth Hormone.

Immature oocytes are retrieved and matured through in vitro maturation (IVM). Maturation, fertilization rates, and embryo development via IVM are all lower than those found in vitro fertilization (IVF) cycles. We investigated the effects of oncostatin M (OSM), insulin-like growth factor-1 (IGF-I), and growth hormone (GH) in rescue IVM. A total of 111 germinal vesicle (GV) and 17 metaphase I (MI) oocytes were obtained after conventional IVF from 28 female Wistar albino rats. Denuded immature oocytes were cultured in maturation medium supplemented with OSM, IGF-1, or GH. The quantities of metaphase II (MII) oocytes matured from the GV stage were 17 of 30 (56.6%), 15 of 28 (53.5%), 10 of 30 (33.3%), and 7 of 23 (30.3%), in control, OSM, IGF-I, and GH groups, respectively. Maturation rates in control and OSM groups were higher than those in IGF-I and GH groups (p = 0.001). The quantities of MII oocytes matured from MI stage were 7 of 7 (100%), 4 of 4 (100%), 1 of 1 (100%), and 1 of 5 (20%) in control, OSM, IGF-I, and GH groups, respectively. Maturation rates from MI to MII stages in control, OSM, and IGF-I groups were higher than those in the GH group (p = 0.004). Acceptable maturation rates are observed with OSM in rat oocytes in rescue IVM.

Morphological and biochemical effects of carnosic acid on human hepatocellular carcinoma HepG2 cells / Efectos Morfológicos y Bioquímicos del ácido Carnósico en Células de Carcinoma Hepatocelular Humano HepG2

Background/aim: Autophagic cell death and apoptosis of tumor cells has become one of the main objectives in cancer treatment, whereas tumor cell lines are mainly used in studies for providing important data for the evaluation of potential anti cancer substances. In this study, our objective was to evaluate morphological and biochemical changes including rate of apoptosis and Alpha Fetoprotein (AFP) levels at different concentrations of Carnosic Acid (CA) on Human Hepatocellular Carcinoma HepG2 Cells.Materials and methods: Human Hepatocellular Carcinoma (7th passage HepG2 cells) Cell lines were cultured on 11 µM D263M schott glass coverslips placed in 12-well plates and were treated with DMSO, 1, 2.5, 5 and 10 µM concentrations of CA for 24, 48 and 72 hours. Morphological and biochemical data were recorded daily including apoptosis rates demonstrated by Caspase 3, Annexin V expressions under inverted light and Immunofluorescence microscopy, then data were analyzed for statistical significance. AFP, albumin and total protein levels were analyzed spectrophotometricaly for biochemical evaluation.Results: Our results showed that CA significantly inhibited HepG2 cell proliferation in a dose and time dependant manner and significantly caused the formation of autophagic vacuoles starting from 5µM and reaching significance at 10 µM concentrations. Significant decrease was observed in AFP when 48 and 72 hours expressions were examined, with the lowest level reached at 72 hours in the 10 µM CA group. Additionally, increase in albumin levels reached significance only in the 48 h group whereas non-significant increases were also observed in 24 h and 72 h groups.Conclusion: Our current study demonstrates significant increase in apoptosis rates by Carnosic Acid mainly at 10µM concentrations, supporting its anticancer effect on HepG2 cells. These findings are also supported by changes in biochemical analyses of Albumin and AFP levels at 10 µM concentrations.

Antecedentes / objetivos: La muerte celular autofágica y la apoptosis de células tumorales se ha convertido en uno de los principales objetivos en el tratamiento del cáncer, mientras que las líneas celulares tumorales se utilizan principalmente en estudios para proporcionar datos importantes para la evaluación de posibles sustancias anticancerígenas. En este estudio, nuestro objetivo fue evaluar los cambios morfológicos y bioquímicos, incluida la tasa de apoptosis y los niveles de alfa fetoproteína (AFP) a diferentes concentraciones de ácido carnósico (CA) en células de carcinoma hepatocelular humano HepG2.Materiales y métodos: Carcinoma hepatocelular humano (HepG2).Las líneas celulares se cultivaron en cubreobjetos de vidrio Schott D263M de 11 µM colocados en placas de 12 pocillos y se trataron con DMSO, concentraciones de CA 1, 2,5, 5 y 10 µM durante 24, 48 y 72 horas. Los datos morfológicos y bioquímicos se registraron diariamente, incluidas las tasas de apoptosis demostradas por Caspasa 3, las expresiones de Anexina V bajo luz invertida y microscopía de inmunofluorescencia, luego se analizaron los datos para determinar la significación estadística. Los niveles de AFP, albúmina y proteínas totales se analizaron espectrofotométricamente para evaluación bioquímica.Resultados: Nuestros resultados mostraron que CA inhibió significativamente la proliferación de células HepG2 de una manera dependiente de la dosis y el tiempo y causó significativamente la formación de vacuolas autofágicas comenzando desde 5 µM y alcanzando significancia a concentraciones de 10 µM. Se observó una disminución significativa en la AFP cuando se examinaron las expresiones de 48 y 72 horas, alcanzando el nivel más bajo a las 72 horas en el grupo de CA 10 µM. Además, el aumento en los niveles de albúmina alcanzó significación solo en el grupo de 48 h, mientras que también se observaron aumentos no significativos en los grupos de 24 hy 72 h.Conclusión: Nuestro estudio demuestra un aumento significativo en las tasas de apoptosis por el ácido carnósico principalmente a concentraciones de 10 µM, lo que respalda su efecto anticancerígeno en las células HepG2. Estos hallazgos también están respaldados por cambios en los análisis bioquímicos de los niveles de albúmina y AFP a concentraciones de 10 µM.

Role of serum adropin measurement in the assessment of insulin resistance in obesity.

Obesity has recently been mentioned as a metabolic pandemic in developed and developing countries and is an important known risk factor for type 2 diabetes and cardiovascular diseases. The main mechanism responsible for obesity is insulin resistance. Adropin is a peptide-structured regulatory hormone that is suggested to play a role in insulin resistance and metabolic regulation. We aimed to evaluate the associations of serum adropin with insulin resistance and clarify the factors affecting serum adropin concentrations. The study included 50 obese patients and 22 healthy controls. Patients with chronic disease and drug use history were excluded. Serum adropin and other metabolic parameters were obtained after overnight fasting. ELISA was used to measure serum adropin concentrations. The homeostatic model assessment-insulin resistance (HOMA-IR) index was used to calculate insulin resistance. Insulin resistance was defined as HOMA-IR >2.5. Serum adropin values were found to be low in the obese otherwise healthy patient group (p<0.001). Linear regression analysis revealed that age, body mass index (BMI), waist circumference (WC), high-density lipoprotein cholesterol, fasting glucose, and HOMA-IR affect serum adropin level. In multiple regression analysis, age is the most significant factor affecting serum adropin concentration. Serum adropin concentrations were negatively correlated with BMI, WC, diastolic blood pressure, fasting glucose, and insulin. Serum adropin concentrations were low in obese patients and the optimum cut-off point for adropin to indicate HOMA-IR at 2.5 is 216.7 ng/L. The findings suggest that serum adropin may contribute to the regulation of glycolipid metabolism and insulin resistance in obese patients.

The Effects of Initial Procalcitonin Levels on Mortality Rates in Geriatric Patients Undergoing Surgery.

Introduction The aim of the current study is to investigate the relationship between mortality rate in geriatric patients undergoing surgery with preoperative serum levels of procalcitonin, C-reactive protein, and erythrocyte sedimentation rate. Methods This was a single-center retrospective study, including three groups with 101 patients, who are older than 65 years of age. A retrospective investigation was carried out from the laboratory information system for all groups from January to December 2018. Group 1 included patients who had surgery and then mortality within 30 days after surgery. Group 2 included hospitalized patients who had surgery and no mortality within 30 days after surgery. Group 3 included outpatient patients, who had suspicion for a bacterial infection and then no surgery or no mortality within 30 days. Results When three group comparisons were made for procalcitonin, C-reactive protein, and erythrocyte sedimentation rate values, the p-value of one-way analysis of variance (ANOVA) was higher than 0.05 for procalcitonin and lower than 0.05 for C-reactive protein and erythrocyte sedimentation rate, suggesting that one or more groups were significantly different. When post-hoc multiple comparison methods were applied, there were statistically significant differences between Groups 1 and 3 for C-reactive protein and erythrocyte sedimentation rate. Conclusions Procalcitonin levels do not predict mortality following surgery. C-reactive protein and erythrocyte sedimentation rate are more useful biomarkers predicting mortality in geriatric patients undergoing surgery.

Intercellular Adhesion Molecule-1 Lys469Glu Polymorphism, Systemic Redox Homeostasis and Gestational Diabetes Mellitus in Pregnant Women.

OBJECTIVES: Intercellular adhesion molecule-1 (ICAM-1) plays an important role in endothelial function. Hyperglycemia-induced impaired redox status is 1 of the well-known pathophysiologic characteristics of gestational diabetes mellitus (GDM), and it plays a crucial role in the causes of disease. Our aim was to clarify any possible relationship between the ICAM-1 Lys469Glu polymorphism and systemic redox status in women with and without GDM. Also, we investigated whether this polymorphism could be associated with a change for better or worse as evidenced by clinical and redox biomarkers. METHODS: The ICAM-1 polymorphism statuses of 89 pregnant women without GDM and 53 pregnant women with GDM were found. Stratifying patients based on GDM and polymorphism status, we investigated various redox homeostasis markers. The independent t test was used. RESULTS: Significantly higher systemic oxidative damage and diminished antioxidant defense were found in pregnant women with GDM. Also, results showed that whether pregnant women were carrying the Lys469Glu polymorphism or not did not seem to be associated with significant differences, as evidenced by comparable systemic oxidative damage. CONCLUSIONS: Although no significant difference was observed between genotypes, the oxidative damage observed in patients with GDM warrants earlier screening and management in the light of new evidence.

Galactose-induced Aging Model in Rat Testicular Tissue.

OBJECTIVE: To examine whether the D-galactose induced aging model is an appropriate model for further aging research. STUDY DESIGN: Experimental study. PLACE AND DURATION OF STUDY: Aziz Sancar Institute of Experimental Medicine, Istanbul University, Turkey, June 2015- June 2017. METHODOLOGY: The study comprises 3 groups of rats. Group I is young control (YC) 5-month-old rats. Group II is 5-month- old rats, which were mimetically aged (MA) for 6 weeks via intraperitoneal D-galactose (60 mg/kg body weight/day, 0.5 mL) administration. Group III is naturally aged (NA) 24-month-old rats. Group I and III received intraperitoneal saline (0.9% 0.5 mL) for 6 weeks as vehicle. Group I and Group II received injections at 21 weeks age and Group III rats 6 weeks before 24 months age. Tissues were harvested when rats became 6.5-month-old (Group I and Group II) and 24-month-old (Group III). Quantitative biochemical analyses of proteins, lipids, DNA biomarkers and Cu, Zn-SOD were conducted. Statistical analysis of the data was conducted using ANOVA, followed by post-hoc Bonferroni test. RESULTS: Higher magnitude of oxidative damage and diminished antioxidant defence capacity were found in both mimetically aged and naturally aged testicular tissues. It is observed that D-galactose aging model group shares significant similarities in terms of impaired redox homeostasis with the naturally aged rats. CONCLUSION: D-galactose induced testicular aging model successfully mimics aging process. Therefore, D-galactose induced aging model may be used as an accelerated aging model to study the age related alterations and interventions.

Hyperoxic oxidative stress during abdominal surgery: a randomized trial.

PURPOSE: The hypothesis of our study is that during anesthesia, administration of 80 % oxygen concentration increases oxidative stress more than 40 % oxygen. METHODS: Forty ASA I-II patients were included in a randomized, single-blind study. Expiratory tidal volumes (ETV) were measured before induction and after extubation. After ventilation with 0.8 FiO2 and intubation, mini-bronchoalveolar lavage (mini-BAL), arterial blood gas (ABG), and blood samples were taken. Patients were randomly assigned to receive 0.8 (group I) or 0.4 (group II) FiO2 during management. Before extubation, mini-BAL, ABG, blood samples were taken. PaO2/FiO2, lactate, malondialdehyde (MDA), protein carbonyl (PCO), superoxide dismutase (SOD), total sulfhydryl (T-SH), non-protein sulfhydryl (NPSH), and protein sulfhydryl (PSH) were measured. In both groups, mean arterial pressure and heart rate values were recorded with 30-min intervals. RESULTS: ETV values were higher in group II after extubation. PaO2/FiO2 values were higher in group II after extubation compared to group I. In both groups, plasma PCO, SOD, and T-SH levels increased significantly before extubation, whereas the increase in MDA was not significant between groups. Plasma PCO, T-SH, and lactate levels were higher in group I, and plasma SOD, and PSH were higher in group I before extubation. In both groups, MDA, SOD, T-SH, and NPSH levels in mini-BAL increased significantly before extubation. Between-group comparisons, PCO, T-SH, PSH, and NPSH were significantly higher in the BAL samples of group II, and MDA levels were higher in group I. CONCLUSIONS: We found that 80 % FiO2 decreased ETV and PaO2/FiO2 and increased lactate levels and oxidative stress more, inhibiting antioxidant response compared to 40 % FiO2.

Asymmetric dimethylarginine (ADMA) in human blood: effects of extended haemodialysis in the critically ill patient with acute kidney injury, protein binding to human serum albumin and proteolysis by thermolysin.

Free, non-protein bound asymmetrically guanidine-dimethylated arginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthesis. Human erythrocytic membrane comprises considerable amounts of large (>50 kDa) ADMA-containing proteins. Location in the erythrocyte membrane and identity and physiological functions of ADMA-containing proteins are unrevealed. In healthy subjects, the concentration of free ADMA in heparinised plasma is almost identical to that of serum. We hypothesised that the robustness of free ADMA concentration in human blood is due to a remarkable resistance of erythrocytic ADMA-containing proteins against proteases. In vivo, we investigated the course of the concentration of ADMA in serum and EDTA plasma of a critically ill patient with acute kidney injury during extended haemodialysis. In vitro, we studied the effects of thermolysin, a useful experimental proteolytic enzyme of erythrocyte membrane proteins, on erythrocytic ADMA. The protein binding (PB) of ADMA to human serum albumin (HSA) was also determined. In these studies, ADMA was measured by a previously reported, fully validated GC-MS/MS method. We measured almost identical ADMA concentrations in plasma and serum samples of the patient. During dialysis, the circulating ADMA concentration decreased slowly and moderately indicating removal of this substance, which was however much less than expected from its low molecular weight (202 Da) and high water solubility. After dialysis, circulating ADMA concentration increased again, a phenomenon called rebound, and ADMA reached higher levels compared to the baseline. The PB value of ADMA to HSA was about 30 %. This surprisingly high PB value of ADMA to HSA may be an explanation for the rather poor dialysance of ADMA. Washed human erythrocytes suspended in phosphate-buffered physiological saline were found not to release appreciable amounts of free and ADMA-containing proteins. The lack of effect of coagulation or anticoagulation on the concentration of circulating free ADMA in humans is likely to be due to a remarkable resistance of ADMA-containing proteins in the erythrocyte membrane against proteases in vivo in humans. Our study suggests that free ADMA is released in the circulating blood at relatively high rates. The considerable PB of ADMA to HSA is likely to add to the apparently poor dialysability of ADMA. Other contributing factors could be redistribution of free ADMA between plasma and erythrocytes in favour of plasma ADMA and parallel formation of free ADMA from erythrocytic ADMA-containing proteins during haemodialysis.

A comprehensive study of myocardial redox homeostasis in naturally and mimetically aged rats.

Age-related myocardial dysfunction has important implications with impaired redox homeostasis. Current study focused on investigation of redox homeostasis and histopathological changes in the myocardium of mimetically (MA), naturally aged (NA), and young control (YC) rats. Chronic D-galactose administration to young male Wistar rats (5 months old) was used to set up experimental aging models. We investigated 16 different oxidative damage biomarkers which have evaluated redox homeostasis of cellular macromolecules such as protein, lipid, and DNA. As a protein oxidation biomarker, advanced oxidation end products, protein carbonyl groups, protein-bound advanced glycation end products, dityrosine, kynurenine, and N-formylkynurenine concentrations in MA and NA rats were found to be significantly higher compared to those in YC rats. On the other hand, the levels of protein thiol groups were not significantly different between groups, whereas lipid peroxidation biomarkers such as conjugated diens, lipid hydroperoxides, and malondialdehyde in MA and NA rats were found to be significantly higher in comparison to those in YCs. For the assessment of oxidative DNA damage, we analyzed eight hydroxy-5'-deoxyguanosine concentrations of MA and NA groups which were higher than YCs. As an antioxidant status in the MA and NA groups, Cu-Zn superoxide dismutase, ferric reducing antioxidant power, and total thiol levels were lower than those in the YCs. Only nonprotein thiol levels were not significantly different. We also observed similar histopathological changes in MA and NA rats. We concluded that the mimetic aging model could be considered as a reliable experimental model for myocardial senescence.

Oxidation scrutiny in persuaded aging and chronological aging at systemic redox homeostasis level.

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.

Human serum albumin and its relation with oxidative stress.

Human serum albumin, a negative acute phase reactant and marker of nutritive status, presents at high concentrations in plasma. Albumin has always been used in many clinical states especially to improve circulatory failure. It has been showed that albumin is involved in many bioactive functions such as regulation of plasma osmotic pressure, binding and transport of various endogenous or exogenous compounds, and finally extracellular antioxidant defenses. Molecules like transferrin, caeruloplasmin, haptoglobin, uric acid, bilirubin, alpha-tocopherol, glucose, and albumin constitute extracellular antioxidant defenses in blood plasma but albumin is the most potent one. Most of the antioxidant properties of albumin can be attributed to its unique biochemical structure. The protein possesses antioxidant properties such as binding copper tightly and iron weakly, scavenging free radicals, e.g., hypochlorous acid (HOCl) and Peroxynitrite (ONOOH) and providing thiol group (-SH). Whether it is chronic or acute, during many pathological conditions, biomarkers of oxidative protein damage increase and this observation continues with considerable oxidation of human serum albumin. There is an important necessity to specify its interactions with Reactive Oxygen Species. Generally, it may lower the availability of pro-oxidants and be preferentially oxidized to protect other macromolecules but all these findings make it necessary that researchers give a more detailed explanation of albumin and its relations with oxidative stress.

Oxidative damage parameters in renal tissues of aged and young rats based on gender.

PURPOSE: Aging is characterized by a gradual functional decrease of all systems including the kidneys. Growing evidence links altered lipid protein redox-homeostasis with renal dysfunction. The effect of sexual dimorphism on the lipid protein redox-homeostasis mechanisms in the aging kidney is obscure. In the current study, we aimed to investigate redox homeostasis as it related to sexual dimorphism on protein oxidation and lipid peroxidation parameters, as protein carbonyl (PCO), total thiol (T-SH), advanced oxidation protein products (AOPP), malondialdehyde, glutathione (GSH), and superoxide dismutase (SOD) activity, as potential aging biomarkers, which may contribute to an analysis of the free radical theory of aging. MATERIALS AND METHODS: The study was carried out with 16 naturally aged rats (24 months old; eight males and eight females) and their corresponding young rat groups as controls (6 months old; eight males and eight females). All of the aforementioned parameters (PCO, T-SH, AOPP, MDA, GSH, SOD) were measured manually instead of automated devices or ELISA kits. RESULTS: PCO, AOPP, and malondialdehyde levels in aged rats were significantly higher in the older rat group than in the younger rat group, whereas SOD activities were significantly lower in old rats. T-SH levels were not significantly different in male groups; however, T-SH levels were lower in the aged female group than in the young female control group. In addition, GSH levels were significantly different between the aged rat group and the corresponding young control group for both genders. CONCLUSION: With respect to PCO and AOPP, impaired redox homeostasis is substantially more prominent in males than females. The decrease of G-SH levels in male groups could be attributed to stabilizing the redox status of protein thiol groups by the depletion of the GSH groups. Considering the results, the renal tissue proteins and lipids in different genders may have different susceptibilities to oxidative damage.

Comparison of oxidative stress biomarkers in renal tissues of D-galactose induced, naturally aged and young rats.

Ageing of kidneys is a clinical health issue of the society. Age-related renal insufficiency has important implications due to impaired redox homeostasis. We examined protein, DNA and lipid oxidation biomarkers as well as protein-bound sialic acid (SA) in the kidney tissues of D-galactose induced ageing rats, naturally aged rats and their corresponding young control group. Intraperitoneal injection of D-galactose (60 mg/kg/day) for 6 weeks to young male Sprague-Dawley rats (20-week-old) was used to establish mimetic ageing model. In this study, we investigated the levels of protein carbonyl groups (PCO), various thiol fractions such as total thiol groups (T-SH), protein (P-SH) and non-protein thiol groups (NP-SH), lipid oxidation parameters such as lipid hydroperoxides (LHP) and malondialdehyde (MDA), SA and 8-hydroxy-2'deoxyguanosine (8-OHdG) parameters for comparison of naturally aged, induced aged and young rats. In D-galactose induced aged group, PCO, LHP, MDA, and 8-OHdG concentrations were significantly higher than young control group, whereas T-SH, P-SH levels were significantly lower than the young rats. In addition, NP-SH and SA concentrations were similar between the mimetic ageing and young control groups. In naturally ageing rats, PCO and MDA levels were significantly higher, whereas T-SH, P-SH, NP-SH concentrations were low compared to young controls. On the other hand, SA and 8-OHdG levels were not different between the naturally ageing group and the young control group. Our results demonstrated that the rats in the mimetic ageing group, have significant similarities with the naturally aged rats in terms of impaired redox homeostasis and can be used as a reliable animal model for renal ageing.