Significance of Intercellular adhesion molecule-1 Lys496Glu gene polimorphism on plasma redox status regulation in laryngeal carcinoma.

BACKGROUND: Intercellular adhesion molecule-1 (ICAM-1) is a surface glycoprotein important for tumor invasion and angiogenesis. The present research is conducted to investigate whether specific gene polymorphism of ICAM-1 K469E (rs5498) and plasma redox status could be associated with laryngeal cancer (LC) development. Since there is no clear evidence which investigates the relationship between ICAM-1 polymorphism and ROS-mediated plasma protein oxidation in LC, our study is the first significant contribution for investigating the relationship. METHODS: The study covered patients with primary LC and their age-matched healthy control subjects. Evaluation of ICAM-1 K469E (rs5498) gene polymorphism was performed by polymerase chain reaction-restriction fragment length polymorphism. Plasma redox status was assessed with spectrophotometric methods. RESULTS: In the current paper, we found that LC patients with GG genotype had a decreasing trend for the plasma oxidative damage biomarker levels when compared with all allele genotypes (AA and AG). CONCLUSION: We concluded that G allele of the ICAM-1 K469E gene plays a significant role in the optimal regulation of plasma redox homeostasis in patients with LC.

Potential therapeutic effects of ethyl pyruvate in an experimental rat appendicitis model.

BACKGROUND: Pathophysiology of appendicitis is associated with the underlying inflammatory processes. Ethyl pyruvate (EP) has potent antioxidant and anti inflammatory properties. In this study, we aimed to investigate the effects of EP on the treatment of appendicitis and to examine whether adding EP to the antibiotic treatment could increases the effectiveness of the treatment in a rat appendicitis model. METHOD: Thirty two Wistar rats, which had previously created appendicitis, were randomly divided into 4 groups: Group 1 (0.1 ml saline solution), Group 2 (15 mg/kg ceftriaxone), Group 3 (50 mg/kg EP), Group 4 (EP 50 mg/kg + ceftriaxone 15 mg/kg). In all groups, saline solution, ceftriaxone and EP were administered intraperitoneally and the same procedure was repeated twice a day for the following five days. On day 6, the rats underwent relaparotomy and then intraabdominal findings were recorded. Histopathological examination and interleukin 6 (IL 6) level were performed on appendiceal specimens. RESULTS: Intra abdominal adhesion score was significantly lower in Group 4 than in Group 1. Total inflammation score was significantly lower in Group 2 than in Group 1 and was significantly lower in Group 4 than in Group 3 and 1. IL 6 level was significantly lower in Group 4 than in Group 3 and 1. CONCLUSION: We found that adding EP to the antibiotic therapy increased the efficacy of the treatment in the rat appendicitis model. Further studies are required to apply our findings to the clinical setting.

Caloric restriction and redox homeostasis in various regions of aging male rat brain: Is caloric restriction still worth trying even after early-adulthood?: Redox homeostasis and caloric restriction in brain.

Despite recent studies have shown that caloric restriction (CR) could improve some functional loss associated with brain aging, the biochemical effects of CR on brain aging are still not well understood on a quantifiable biochemical basis, including whether CR could be protective when started around middle adulthood, when age-related neurodegenerative diseases are thought to set in. Therefore, in the light of more than ever aging societies and increasing neurodegenerative diseases, we aimed to test the biochemical effects of CR on redox homeostasis in different parts of male Sprague-Dawley rat brain by using the biomarkers we consistently validated in our previous work (TOS, PCO, AOPP, AGEs, sRAGE, P-SH, LHPs, 4-HNE, TAS, Cu, Zn-SOD). Our results indicate that oxidative stress biomarkers are lower in CR group, implying a more favorable redox status that has been previously shown to be correlated with better neural function. PRACTICAL APPLICATIONS: We report that the beneficial effects of caloric restriction (CR) on various brain tissues result in significant improvements in biochemical markers, even though CR is not started in early adulthood. Hence, our select age group provides a sound redox status-related neurochemical understanding for many recent CR studies, where a functional loss was detected at this age.

The effects of delta-9-tetrahydrocannabinol on Krüppel-like factor-4 expression, redox homeostasis, and inflammation in the kidney of diabetic rat.

Diabetes mellitus is a complex, multifactorial disorder that is attributed to pancreatic ß cell dysfunction. Pancreatic ß cell dysfunction results in declining utilization of glucose by peripheral tissues as kidney and it leads to nephropathy. Excessive production and accumulation of free radicals and incapable antioxidant defense system lead to impaired redox status. Macromolecular damage may occur due to impaired redox status and also immune imbalance. Δ9-Tetrahydrocannabinol (THC) is the main active ingredient in cannabis. THC acts as an immunomodulator and an antioxidant agent. Our aim was to evaluate the effects of THC in the diabetic kidney. We analyzed macromolecular damage biomarkers as protein carbonyl (PCO), lipid hydroperoxide (LHP), malondialdehyde (MDA), 8-hydroxy-2'-deoxyguanosine (8-OHdG), and antioxidant defense system biomarkers as thiol fractions (T-SH, NP-SH, P-SH) and Cu/Zn-superoxide dismutase activity for the antioxidative effects of THC. Furthermore, mRNA expression of Krüppel-like factor-4, secreted immunopositive cell number changes of interleukin-6, nuclear factor κß (NF-κß), and peroxisome proliferator-activated receptor-γ and tumor necrosis factor α (TNF-α) levels were analyzed for the immunomodulatory activity of THC. Diabetic rats showed significantly increased levels of PCO, LHP, MDA, and 8-OHdG when compared with controls (P < 0.05 for each parameter). THC significantly reduced the elevated levels of PCO and 8-OHdG (P < 0.05 for both parameters) and also LHP and MDA levels were insignificantly reduced by THC. Also, thiol fractions insignificantly increased in THC administered diabetic kidney when compared with diabetic rats. The NF-κß cell number significantly decreased in the diabetic rats treated with THC compared with the diabetic group. According to our data, THC has ameliorative effects on the impaired redox status of diabetic kidney and also it acts as an immunomodulator. Therefore, THC might be used as a therapeutic agent for diabetic kidneys but its usage in the healthy kidney may show adverse effects.

Is D-Galactose a Useful Agent for Accelerated Aging Model of Gastrocnemius and Soleus Muscle of Sprague-Dawley Rats?

Elderly population and age-related diseases are on the rise. On the contrary, aging studies are technically hard to conduct, because they require elderly animals, the maintenance of which requires ample effort and is expensive. To tackle this problem, D-galactose is used to hasten the aging process in various tissues in rodent models and it has been shown to successfully mimic the oxidative alterations that take place in the natural aging process in various tissues both by our group and others. In the present study, the validity of D-galactose aging model in skeletal muscles was tested both on predominantly slow-twitch (soleus) and rather fast-twitch (gastrocnemius) muscle in male Sprague-Dawley rats and the results are compared with young littermate controls and naturally aged rats. Redox-related modifications in soleus and gastrocnemius were assessed by measurement of protein carbonyl groups, advanced oxidation protein products, lipid hydroperoxides, total thiol, and Cu, Zn-superoxide dismutase activities. In the present study, we provide biochemical evidence demonstrating that D-galactose-induced mimetic aging does result in oxidative stress-related redox alterations that are comparable with the alterations that occur in natural aging in soleus. On the contrary, in the D-galactose-induced mimetic aging of gastrocnemius, even though the oxidative stress markers were significantly increased, the endpoint redox homeostasis markers were not statistically comparable with the redox status of naturally aged group.

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.

The Effects on Obesity Related Peptides of Laparoscopic Gastric Band Applications in Morbidly Obese Patients.

BACKGROUND: The aim of this study was to examine the relationship between weight loss and resistin, apelin, chemerin, and visfatin after laparoscopic adjustable gastric banding (LAGB). METHODS: The study group consisted of 19 patients who were operated on for morbid obesity (BMI: 48.7 ± 6.6 kg/m2), and 22 healthy, normal-weight (BMI: 22.9 ± 2.5 kg/m2) subjects formed the control group. We obtained blood samples from the study subjects at three different times: before undergoing surgery and at one month and 6 months after surgery. Blood was obtained once from the control group. RESULTS: Significant weight loss was achieved at one and 6 months after surgery. Plasma levels of apelin, resistin, chemerin, and visfatin were higher in morbidly obese patients compared with the control group. Obesity-related peptides decreased one month and 6 months after surgery. CONCLUSIONS: Elevated plasma resistin, apelin, chemerin, and visfatin levels in morbidly obese patients are gradually reduced after weight loss. According to these findings, LAGB surgery is found to be an important and efficient means for morbidly obese patients both to lose weight and to develop a better metabolic risk profile in a short time period.

The effects of lipoic acid on redox status in brain regions and systemic circulation in streptozotocin-induced sporadic Alzheimer's disease model.

While the deterioration of insulin-glucose metabolism (IGM), impaired redox homeostasis (IRH), ß-amyloid accumulation was reported in Sporadic Alzheimer's Disease (SAD) model, aforementioned factors related to lipoic acid administration and anthropometric indexes (AIs) are not yet studied with integrative approach. ß-amyloid accumulation, redox homeostasis biomarkers and AIs are investigated in SAD model. Streptozotocin-induced inhibition of insulin-signaling cascade but not GLUT-2 and GLUT-3 transporters takes a role in ß-amyloid accumulation. Inhibition types are related to IRH in cortex, hippocampus and systemic circulation. Lipoic acid (LA) shows both antioxidant and prooxidant effect according to the anatomical location. LA administration also leads to improved AIs during GLUT-2 inhibition and cortical redox status in GLUT-3 inhibited group. Optimal LA action could be possible if its redox behavior is balanced to antioxidant effect. Diagnostic usage of systemic IRH parameters as biomarkers and their possible correlations with deteriorated IGM should be investigated. Graphical abstract ᅟ.

Crucial Roles of Systemic and Tissue Lipid Peroxidation Levels and Anti-Oxidant Defences Following Contrast Agent Application.

BACKGROUND: One of the most important side effects of contrast pharmaceutical agents, which are used very common in routine radiology practice, is contrast induced nephropathy. Even ischemia, oxidative stress and osmolality related cytotoxic effects are considered, the molecular mechanisms underlying this pathology have not been identified completely yet. OBJECTIVES: The aim of the current study was to reveal the role of oxidative stress and antioxidant enzymatic defence mechanisms in the aetiopathogenesis of contrast-induced nephropathy. We also studied possible alleviating effects of N-acetylcysteine (NAC), a potent antioxidant, to obtain extra information regarding the molecular mechanisms underlying this pathology. MATERIALS AND METHODS: This is an clinical-experimental study, This study was conducted of Istanbul/Turkey between September 15, 2012 and April 15, 2013. Three groups of male rats were randomly set up as a control group (C), a 100 mg/kg intraperitoneal NAC + 7 mL/kg contrast agent group (N + CIN) and a 7 mL/kg intraperitoneal contrast agent group (CIN). They were placed in individual metabolic cages 48 hours after agent administration to obtain 24-hour urine samples. Renal function tests (albumin, urea, creatinine, total protein) were conducted, oxidative stress parameters (Cu, Zn superoxide dismutase activity - Cu, Zn-SOD; advanced oxidation protein products - AOPP; protein carbonyls - PCO; total thiol groups - T-SH; and lipid hydroperoxides -LHP) were measured and tissues were analysed histopathologically. RESULTS: Compared with the control group, groups CIN and N + CIN had significantly higher urea and LHP levels (P < 0.05 and P < 0.001, respectively) and significantly lower Cu, Zn-SOD activity and creatinine clearance (P < 0.05). There was no statistically significant difference between the groups in PCO or AOPP levels despite differences in descriptive statistics. CONCLUSIONS: Contrast-agent-induced nephropathic changes are more closely related to the magnitude of lipid peroxidation than protein oxidation.

Gender and chronological age affect erythrocyte membrane oxidative indices in citrate phosphate dextrose adenine-formula 1 (CPDA-1) blood bank storage condition.

It is well known that in vitro storage lesions lead to membrane dysfunction and decreased number of functional erythrocytes. As erythrocytes get older, in storage media as well as in peripheral circulation, they undergo a variety of biochemical changes. In our study, the erythrocytes with different age groups in citrate phosphate dextrose adenine-formula 1 (CPDA-1) storage solution were used in order to investigate the possible effect of gender factor on oxidative damage. Oxidative damage biomarkers in erythrocyte membranes such as ferric reducing antioxidant power, pro-oxidant-antioxidant balance, protein-bound advance glycation end products, and sialic acid were analyzed. Current study reveals that change in membrane redox status during blood-bank storage condition also depends on both gender depended homeostatic factors and the presence of CPDA-1. During the storage period in CPDA-1, erythrocytes from the male donors are mostly affected by free radical-mediated oxidative stress but erythrocytes obtained from females are severely affected by glyoxidative stress.

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.

Individual and Combined Effects of CTLA4-CD28 Variants and Oxidant-Antioxidant Status on the Development of Colorectal Cancer.

BACKGROUND: Colorectal cancer (CRC) is the third most frequent cancer worldwide. Research has revealed the contributions of the immune system and anti-inflammatory pathways in the development of cancer. The balance between cluster of differentiation 28 (CD28) and cytotoxic T-lymphocyte-associated protein 4 (CTLA4) signaling is important for the regulation of immune responses. The oxidant-antioxidant balance by sustaining redox control via several defense mechanisms is also an important factor for the progression of cancer. The aim of the present study was to determine the distribution of CTLA4/CD28 variants and oxidant-antioxidant status in patients with CRC. MATERIALS AND METHODS: This study enrolled 80 patients with CRC and 115 healthy controls. We used a spectrophotometric assay to detect the levels of lipid peroxidation products malon dialdehyde (MDA) and lipid hydroperoxide (LHP), and measured the concentration of protein damage products, advanced oxidation protein products (AOPP) and protein carbonyl (PCO). Additionally, antioxidant levels were detected by measuring copper, zinc, superoxide dismutase (Zn-Cu SOD) and total thiol (T-SH) levels, and advanced glycation end-products (AGEs). The CTLA4 -318C>T, CTLA4 49A>G and CD28C>T genotypes were determined by using restriction enzymes. RESULTS: AOPP and PCO levels were increased in patients with CRC as well as those of LHP, MDA and AGE, while the levels of antioxidants such as Cu-Zn SOD and T-SH were lower. Lower serum levels of CTLA4 and higher serum levels of CD28 were detected in patients and, an association of the CTLA4 -318C/T polymorphism was found in patients with CRC. CONCLUSION: Our oxidative stress was increased in patients with CRC, suggesting the contribution of this disturbed oxidative status to serum CTLA4 and CD28 levels, and to the pathogenesis of CRC.

Ameliorative Effects of Testosterone Administration on Renal Redox Homeostasis in Naturally Aged Rats.

BACKGROUND: Testosterone biosynthesis gradually decreases with age. Impaired redox homeostasis-related oxidative damage in cellular macromolecules has a high risk for the development of renal insufficiency. Our aim was to study the effects of testosterone replacement therapy on redox homeostasis. METHODS: We investigated various oxidative damage biomarkers in kidney. Experimental animals were separated into three groups-naturally aged rats, testosterone-administered naturally aged rats (single dose of 25 mg/kg testosterone enanthate), and their respective young controls. RESULTS: Our results showed that the testosterone-administered naturally aged group shared significant similarities with the young rats with respect to their redox status. In testosterone-administered naturally aged rats, kynurenine, protein carbonyl, advanced oxidation protein products, lipid peroxidation markers, and xanthine oxidase activities were significantly lower and Cu-Zn superoxide dismutase activities and testosterone levels were higher than naturally aged rats. In testosterone-administered naturally aged rats, catalase activities, ferric reducing anti-oxidant power, and testosterone levels were significantly lower and dityrosine, N-formyl kynurenine, protein carbonyl, and protein hydroperoxides were significantly higher than in young rats. On the other hand, in naturally aged rats, Cu-Zn superoxide dismutase, catalase activities, ferric reducing anti-oxidant power, and testosterone levels were lower and dityrosine, kynurenine, protein carbonyl, protein hydroperoxide, advanced oxidation protein products, lipid peroxidation markers, advanced glycation end products, and xanthine oxidase activities were higher than controls. CONCLUSIONS: Our results showed that a single dose of testosterone administration has a positive effect on the redox status of the aged kidney. Future studies are needed to clarify the exact molecular mechanism(s) involved in the action of testosterone in maintaining kidney redox homeostasis.

Age-related changes in rat prostate tissue; perspective of protein oxidation.

BACKGROUND: Increased systemic oxidative stress is considered as an important risk factor for prostate cancer occurrence; however, the relationship between impaired redox homeostasis of prostate tissue and aging remains unclear. OBJECTIVE: In our study, we hypothesized that age-related deterioration of redox homeostasis in prostate tissue may be considered as a predisposing factor for prostate cancer occurrence. METHODS: Sprague-Dawley rats were divided into two groups as young control (5 months) and naturally aged (24 months). We investigated the levels of oxidant and antioxidant parameters in prostate tissue. RESULTS: Advanced oxidation protein products, protein carbonyl, non-protein thiol and lipid hydroperoxides levels of aged rats were significantly higher than in the young control rats (p < 0.01, p < 0.05, p < 0.001, p < 0.05, respectively). Additionally, antioxidant activity of Cu-Zn-superoxide dismutase in elderly group was significantly lower than young controls (p < 0.05). CONCLUSIONS: We suggest that increased non-protein thiol levels found in aged rats may prevent further dissemination of oxidative protein damage. We also propose that the increased levels of oxidative protein damage markers and decreased Cu-Zn superoxide dismutase activity in aged prostate may be considered as a predisposing factor for prostate cancer. Further studies are warranted to clarify all these oxidative changes as initiation factors for prostate cancer in the association of aging with prostate cancer.

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.

Effect of tempol on redox homeostasis and stress tolerance in mimetically aged Drosophila.

We aimed to test our hypothesis that scavenging reactive oxygen species (ROS) with tempol, a membrane permeable antioxidant, affects the type and magnitude of oxidative damage and stress tolerance through mimetic aging process in Drosophila. Drosophila colonies were randomly divided into three groups: (1) no D-galactose, no tempol; (2) D-galactose without tempol; (3) D-galactose, but with tempol. Mimetic aging was induced by d-galactose administration. The tempol-administered flies received tempol at the concentration of 0.2% in addition to d-galactose. Thiobarbituric acid reacting substance (TBARS) concentrations, advanced oxidation protein products (AOPPs), Cu,Zn-superoxide dismutase (Cu,Zn-SOD), sialic acid (SA) were determined. Additionally, stress tolerances were tested. Mimetically aged group without tempol led to a significant decrease in tolerance to heat, cold, and starvation (P < 0.05), but tempol was used for these parameters. The Cu,Zn-SOD activity and SA concentrations were lower in both mimetically aged and tempol-administered Drosophila groups compared to control (P < 0.05), whereas there were no significantly difference between mimetically aged and tempol-administered groups. Mimetically aged group without tempol led to a significant increase in tissue TBARS and AOPPs concentrations (P < 0.05). Coadministration of tempol could prevent these alterations. Scavenging ROS using tempol also restores redox homeostasis in mimetically aged group. Tempol partly restores age-related oxidative injury and increases stress tolerance.

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.