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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.

Background: Ischemia/reperfusion (I/R) injury results from the onset of re-circulation following a perfusion deterioration period in the tissues, resulting in more damage than that caused by perfusion deterioration. This study aimed to determine the effects of pycnogenol on I/R injury in rat brain tissues., Methods: Eighteen albino Wistar rats were divided into three groups: I/R injury (IR, n = 6) group; I/R injury + pycnogenol (IR + P, n = 6) group; and sham group (SG, n = 6). After 30 min of transient ischemia, 24 h of reperfusion was achieved in the IR and IR + P groups. Surgical dissection, except for transient ischemia, was performed in SG. Next, histopathological and biochemical investigations were performed on brain tissues. Malondialdehyde (MDA), reduced glutathione (GSH), and glutathione peroxidase (GPO) were analyzed as oxidative stress markers; IL-1β and TNF-α were analyzed as inflammatory stress markers in biochemical tests., Results: Histopathological examination revealed normal morphology in SG and diffuse cortex damage with edema, vasopathology, and inflammatory cell infiltration in the IR group. The IR + P group showed less cortex damage, edema, and vasopathology than the IR group. The MDA, IL-1β, and TNF-α levels were significantly higher in the IR group than those in the SG group. The values of same markers for the IR + P group were significantly lower than the IR group. The GSH and GPO levels were significantly decreased with IR damage, but PYC treatment showed significant improvement in the levels., Conclusion: This study showed that the administration of pycnogenol ameliorated brain damage after I/R injury by reducing oxidative and inflammatory damage in the rat brain., (Copyright © 2019 Elsevier B.V. All rights reserved.)

The purpose of this study was to investigate the effects of a high fat and a high sucrosediet in wild type and BDNF (+/-) mice on oxidative stress in epididymal and subcutaneousadipose tissues by measuring different markers of oxidative stress and antioxidant enzymes. Wild type (WT) and BDNF (+/-) male mice were divided into six groups receiving fed control diet (CD), high sucrose diet (HSD), or high fat diet (HFD) for four months. Levels of 3-nitrotyrosine (3-NT) increased in the HFD-fed BDNF (+/-) mice, while 4-hydroxynonenal (4-HNE) levels increased in the CD and HFD-fed BDNF (+/-) groups. Malondialdehyde (MDA) levels decreased in subcutaneous tissue compared to epididymal adipose tissue, independently of diet type. Superoxide dismutase (SOD) activity was reduced by HFD (p < 0.05), butglutathione peroxidase (GSH-Px) activity was increased by HSD in epididymal adipose tissuein BDNF (+/-) mice (p < 0.05). GSH-Px activities was increased by CD and HFD in subcutaneous adipose tissue of BDNF (+/-) (p < 0.05). SOD2 and GSH-Px3 expressions were only decreased by HSD in epididymal and subcutaneous adipose tissues of BDNF (+/-) mice (p < 0.05). In conclusion, reduced BDNF may increase OS in epididymal adipose tissue, but not in subcutaneous adipose tissue following HSD and HFD., (Copyright © 2019. Published by Elsevier Inc.)

In this study we aimed to investigate whether reduced BDNF levels aggravate the susceptibility of the brain to hazardous effects of high fat diet. For this purpose, we fed BDNF heterozygous mice and wild type littermates with normal and high fat diet for 16 weeks. Concentrations of two synaptic proteins (SNAP-25 and PSD-95) and oxidative stress parameters (MDA, SOD, CAT) were evaluated in the cortex after diet period. Interestingly, body weights of BDNF heterozygous groups fed with control diet were higher than their littermates and heterozygous mice fed with HFD were the heaviest in all experimental groups. MDA levels were significantly elevated in both HFD groups (wild type and BDNF(+/-)). Synaptic markers PSD-95 and SNAP-25 markedly decreased in BDNF(+/-) group fed with HFD compared to other groups. In conclusion, we suggest that endogenous BDNF has an important and possibly protective role in diet-induced changes in the cortex.

Background: Paliurus spina-christi Mill. (PS) fruits are widely used for different medical purposes in Turkey. Like in many medicinal herbs the studies concerning their activity, the activities of PS are also not well clarified. The aim of this study is to evaluate the antigenotoxicity of the compounds isolated and identified from the extracts of PS fruits., Methods: The active compounds were separated, isolated, and determined by chromatographic methods and their structural elucidation was performed by Nuclear Magnetic Resonance (NMR) methods. The compounds were obtained from either ethyl acetate (EA) or n-butanol extracts. The cytotoxicities of the compounds using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and the antigenotoxic activities of the compounds using the alkaline single cell gel electrophoresis techniques (comet assay) were evaluated in Chinese hamster lung fibroblast (V79) cell lines., Results: The isolated major compounds were identified as (+/-) catechins and gallocatechin from EA fraction and rutin from n-butanol fraction of PS fruits. Their chemical structures were identified by 1 H-NMR, 13 C-NMR, HMBC, and HMQC techniques. Half-maximal inhibitory concentration of catechins, gallocatechin, and rutin were found to be 734 μg/mL, 220 μg/mL, and 1004 μg/mL, respectively. The methanolic extract of PS (1-100 μg/mL) alone did not induce DNA single-strand breaks while catechins (1-100 μg/mL), gallocatechin (1-50 μg/mL), and rutin (1-50 μg/mL) significantly reduced H 2 O 2 -induced DNA damage., Conclusion: It has been suggested that PS fruits and their compounds catechins, gallocatechin and rutin may have beneficial effects in oxidative DNA damage. It seems that PS fruits may be used in protection of the disorders related to DNA damage.

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.

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., (Copyright© 2015 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.)

The main objective of the study has been to show whether carnosine has positive effects on liver and lung tissues of rats exposed to a range of formaldehyde concentrations, and to explore how irisin expression and antioxidant capacity are altered in these tissues by carnosine supplementation. Sprague-Dawley type male rats were divided into 8 groups with 6 animals in each: (I) Control; no chemical supplementation); (II) sham (100mg/kg/day carnosine); (III) low dose formaldehyde (LDFA) for 5 days/week; (IV) LDFA for 5 days/week and carnosine); (V) moderate dose formaldehyde (MDFA) for 5 days/week); (VI) MDFA for 5 days/week and carnosine; (VII) high dose formaldehyde (HDFA) for 5 days/week; (VIII) and HDFA for 5 days/week and carnosine. Sham and control groups were exposed to normal air. Irisin levels of the serum, liver and lung tissue supernatants were analyzed by ELISA, while the REL method was used to determine total oxidant/antioxidant capacity. Irisin production by the tissues was detected immunohistochemically. Increasing doses of FA decreased serum/tissue irisin and total antioxidant levels relative to the controls, as also to increases in TUNEL expressions, total oxidant level, oxidant and apoptosis index. Irisin expression was detected in hepatocyte and sinusoidal cells of the liver and parenchymal cells of the lung. In conclusion, while FA exposure reduces irisin and total oxidant in the serum, liver and lung tissues in a dose-dependent manner and increases the total antioxidant capacity, carnosine supplementation reduces the oxidative stress and restores the histopathological and biochemical signs., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background/aim: Lycopene, which is suggested to be a potent antioxidant, may play a protective role in diseases related to oxidative stress. In order to understand the effects of lycopene in the pathogenesis of cholestasis, we investigated the effects of lycopene on oxidative stress parameters and DNA damage induced by experimental biliary obstruction in the liver tissues and the lymphocytes of Wistar albino rats., Materials and Methods: The animals were randomized into 3 groups. The sham group was subjected to a sham operation, the BDL group was subjected to bile duct ligation (BDL), and the BDL+L group was subjected to BDL and treated with 10 mg/kg body weight of lycopene. After 7 days of treatment, the liver functions, oxidative stress parameters, and DNA damage were evaluated., Results: The lycopene treatment significantly ameliorated the liver function parameters in BDL rats. It significantly reduced malondialdehyde and nitric oxide levels and enhanced reduced glutathione levels and catalase, superoxide dismutase, and glutathione S transferase activities in the BDL rats. The lycopene treatment also decreased DNA damage as assessed by comet assay in the lymphocytes and hepatocytes of the BDL rats., Conclusion: These results suggest that lycopene might have protective effects on acute cholestasis.

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., (© 2014 Wiley Periodicals, Inc.)

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.

Objective: Oxidative stress and imbalance in the oxidant/antioxidant system have a critical role in carcinogenesis by affecting necrosis and apoptosis. The aim of this study is to evaluate the oxidant/antioxidant status and cell death modes in patients with oral squamous cell carcinoma (OSCC)., Materials and Methods: Twenty-nine patients with OSCC and 29 control subjects were included in the study. The levels of malondialdehyde (MDA), advanced oxidation protein products (AOPP) and ferric reducing antioxidant power (FRAP) were determined in plasma samples of all subjects. The necrotic and apoptotic cell death modes were evaluated with M65 ELISA and M30 ELISA, respectively., Results: MDA and AOPP values as oxidative stress markers were higher in patients with OSCC than in the control group. FRAP values evaluating plasma antioxidant status increased in OSCC patients. M65 and M30 levels indicating necrosis and apoptosis were significantly higher in OSCC patients compared to controls. There were significant correlations between MDA, AOPP and FRAP; M65 and M30 values., Conclusions: The elevated levels of oxidative stress markers together with the increase of antioxidant capacity and the presence of a strong correlation between MDA, AOPP and FRAP suggest an activation of antioxidant defense against accentuated oxidative stress determined in OSCC. Enhanced oxidation of lipids and proteins may cause decomposition of cell membranes with subsequent leakage of cytoskeletal cytokeratins as CK18 and caspase-cleaved CK18 (evaluated as M65 and M30, respectively) in the circulation, suggesting that both cell death modes are affected in OSCC.

Background/objective: Clinoptilolite is a natural zeolite crystal. Cytoprotective effects of clinoptilolite have been reported. However, so far there are no data about the effects of clinoptilolite treatment on oxidative stress after partial hepatectomy. In this experimental study, the effects of clinoptilolite treatment after partial hepatectomy on oxidative stress were evaluated., Methods: There were four experimental groups (n=8): Group S, the sham group; Group H, the hepatectomy group; Group HC, the clinoptilolite treatment after partial hepatectomy group; and Group CS, the clinoptilolite-treated sham group. A 70% partial hepatectomy was performed for Group H and HC. Clinoptilolite (5mg/kg) was given to the rats orally (via gavage tube) twice a day for 10 days after hepatectomy. Malondialdehyde (MDA), Cu-Zn super oxide dismutase (SOD), and glutathione (GSH) levels were assessed to evaluate oxidative stress., Results: Plasma and liver tissue MDA levels of Group HC were significantly lower than the H group (p=0.018 and p=0.000, respectively). Liver tissue Cu-Zn SOD activity and GSH levels of Group HC were significantly higher than Group H (p=0.003, p=0.007, respectively)., Conclusion: Clinoptilolite administration reduces oxidant activity and supports antioxidant response after partial hepatectomy., (Copyright © 2011. Published by Elsevier B.V.)

The identification and dissection of cellular stress mechanisms is fundamental to understanding the susceptibility of the kidney to chemicals and pharmaceuticals and for the development of renal biomarkers indicative of sub lethal injury. Here, we utilised whole genome DNA microarrays in an attempt to uncover molecular mechanisms of response to nephrotoxin exposure. Human renal proximal tubular cells (HK-2) were treated for 12h and 48 h with 5 μM Cadmium (Cd), 30 μM Diquat Dibromide (Diq), and 5 μM Cyclosporine A (CsA). Nephrotoxin treatment resulted in an alteration of a total of 4608 transcripts. Ingenuity Pathways Analysis™ revealed the anti-oxidant and detoxification Nrf2 pathway as the most significantly enriched signaling pathway in the selected dataset. Activation of this transcription factor was confirmed as nuclear translocation and paralleled the temporal alterations of compound induced H(2)O(2) production. Transcriptomics, western blot and immunofluorescence showed an induction of both HO-1 and NQO1 with Cd and Diq exposure, but not with CsA treatment. Knockdown of Nrf2 by siRNA, reduced compound induced NQO1 mRNA to basal levels and attenuated toxin induced HO-1 mRNA expression. siRNA knock down of HO-1, but not NQO1, enhanced Cd induced H(2)O(2) production and Cd induced toxicity. Using an un-biased transcriptomic approach we have identified the Nrf2 pathway as the most significant signaling response in renal epithelial cells challenged with nephrotoxin. This study highlights the importance of this pathway and particularly HO-1 in renal epithelial adaptation to oxidative stress., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

Objective: Obstructive jaundice develops after occlusion of the common bile duct. Direct hyperbilirubinaemia, which occurs secondary to the condition, causes various life-threatening pathologies. Cytoprotective effects of Ganoderma lucidum (GL) have previously been shown. In this study, the effects of GL on oxidative stress and oxidant DNA damage in experimental obstructive jaundice were evaluated., Methods: Sixty Wistar albino adult female rats were randomly divided into six weight-matched equal groups: sham group, bile duct ligated group (BDL); after sham operation 250 mg/kg/d of GL administered group, after sham operation 500 mg/kg/d of GL administered group, after bile duct ligation 250 mg/kg/d of GL administered (GL1BDL) group, and after bile duct ligation 500 mg/kg/d of GL administered (GL2BDL) group. GL polysaccharide was orally administered to the rats via gavage tube once a day for 14 days after bile duct ligation., Results: The plasma malondialdehyde levels of the GL1BDL and GL2BDL groups were significantly lower than those of the BDL group (p < 0.01). The plasma 8-hydroxy-2'-deoxyguanosine levels of the GL1BDL and GL2BDL groups were significantly lower than those of the BDL group (p < 0.001). The liver tissue Cu-Zn superoxide dismutase level of the GL2BDL group was significantly higher than that of the BDL group (p < 0.05)., Conclusion: GL protected against DNA and liver tissue damage by reducing oxidative stress in obstructive jaundice., (Copyright © 2010 Asian Surgical Association. Published by Elsevier B.V. All rights reserved.)

A shift from redox regulation to oxidative damage is known to contribute organ dysfunction and aging-related disorders. Exposure to reactive oxygen species throughout the life-span increases the incidence of several liver diseases. A redox basis of the loss of antioxidant capacity of aged livers has not been fully elucidated in both genders. In the current study, we investigated the gender-dependent relations between protein carbonyl (PCO), a commonly used marker of protein oxidation and other protein oxidation parameters such as advanced oxidation protein products (AOPP) and total thiol (T-SH). Our study also covered other oxidative stress markers, such as malondialdehyde (MDA), lipid hydroperoxides (LHP), and glutathione (GSH) in liver tissue of the male and female aged rats. PCO and AOPP levels in old male and female rats were significantly higher than those in the young control groups (P < 0.001 and P < 0.01, respectively for male rats; P < 0.001 for both parameters in female rats). On the other hand, T-SH levels were not found to be different between young and old rat groups. Plasma MDA levels of old male and female rats were significantly higher compared to those of the young control groups (P < 0.01 and P < 0.001, respectively). LHP levels were only found out to be significantly higher in old female rats when compared to those in young male rats. GSH levels in old male and female rats were significantly lower than in the corresponding young control groups (P < 0.01 for male rats; P < 0.05 for female rats). Our results demonstrated greater susceptibility to hepatic oxidative damage in females than in males. This appears to contradict the general assumption that females are less susceptible to oxidative injury than males are.

Introduction: The effect of aging on plasma-protein, lipid and DNA oxidation is well documented. However, none of the studies specify the effect of gender. The purpose of this study is to clarify the ambiguity raised in preliminary reports as to gender dependency of oxidative damage in plasma., Methods: In the current study, we investigated the relation between 8-hydroxy-2'-deoxyguanosine levels (8-OHdG), which is a measure of DNA oxidation and protein oxidation parameters such as protein carbonyl (PCO), total thiol (T-SH), and advanced oxidation protein products (AOPP). Our study also covered other oxidative stress parameters, such as lipid hydroperoxides (LHP), malondialdehyde (MDA), erythrocyte glutathione (GSH), superoxide dismutase (Cu-Zn SOD) and the catalase (CAT) activity in plasma of the male and female aged rats., Results: 8-OHdG and MDA levels in male rats were significantly higher than those in the female group (p < 0.01 for both parameters). T-SH levels were found to be higher in female rats than in the male (p < 0.05). Plasma Cu-Zn SOD activities of male rats were significantly higher compared with those of the female rats (p < 0.05). On the other hand, PCO, AOPP, LHP, GSH levels, and CAT activity were not found to be different between genders., Conclusions: We suggest that increased T-SH levels found in female rats may point to an adaptive reaction to oxidative damage, reflecting 8-OHdG and MDA overproduction. We are of the conviction that the increased 8-OHdG and MDA that we have determined in aged male rats may be a risk factor in the extent of oxidation in plasma.

Objective: To determine the effects of sudden intra-abdominal pressure (IAP) changes on the terminal ileum in a pneumoperitoneum model., Design: An experimental controlled study., Setting: University hospital in Turkey., Animal(s): Thirty-two adult female Sprague-Dawley rats., Intervention(s): The rats were divided into four groups. Group 1 was not subjected to IAP. In group 2, IAP insufflation was performed continuously to keep the IAP at 10 mmHg. Groups 3 and 4 underwent an insufflation-desufflation procedure: group 3 was fluctuated 5 times, and group 4 was fluctuated 10 times within the pneumoperitoneum period of 60 minutes. Thirty minutes after the desufflation, the terminal ileum was removed for the measurement of tissue malondialdehyde (MDA) values and histopathological examination., Main Outcome Measure(s): The tissue MDA values and histopathological damage scores., Result(s): The tissue MDA values in the IAP groups (groups 2, 3, and 4) were significantly increased when compared with those of the control group. The mean MDA value in group 4 was higher than that in groups 2 and 3. Histopathologic oxidative damage scores in the mucosa and submucosal layers were significantly higher in groups 2 and 3, compared with those of the control group. However, the highest histopathologic damage scores were observed in group 4., Conclusion(s): Unexpected desufflation-insufflation even at normal IAP levels during laparoscopy leads to significant oxidative stress-induced damage in the terminal ileum.

Purpose: To assess estrogen-related changes in the redox status of the brain and liver proteins as well as the systemic oxidative stress in ovarectomised (OVX) rats, Methods: Twelve-week-old, sexually mature female Sprague-Dawley rats (200-250g) were randomly divided into four groups: The following treatment combinations were administrated daily to all in 0.05 ml 96% ethanol solution by gastric gavage. (1) Sham operation (2) OVX rats (3) OVX rats [0.02 mg/kg/day of 17beta-estradiol (E2) and 0.01 mg/kg/day of norethisterone acetate] (4) OVX rats [E2 (0.01 mg/kg/day) and drospirenon (0.02 mg/kg/day)]. Estrogen levels were determined using routine clinical-chemistry methods. We also measured protein oxidation parameters such as protein carbonyl (PCO), total thiol (T-SH) and the other oxidative stress markers malondialdehyde (MDA) and glutathione (GSH)., Results: Ovariectomy resulted in abnormal elevation of plasma and tissue oxidative stress markers and changes in redox status of the proteins in tissue dependent manner. Supplementation of various estrogens combinations partially alleviated these abnormalities and restored redox homeostasis of proteins after the ovariectomy. Among the studied protein oxidation parameters, plasma and tissue PCO levels of the OVX rats were higher than those of the control groups (P < 0.01). Hormone replacement therapies (HRT) caused a decrease in PCO and MDA in both plasma and tissue of the OVX rats (P < 0.01). HRT in OVX rats decreased plasma MDA and increased liver and brain GSH (P < 0.01). Liver MDA levels of the Drospirenon-treated rats were lower than in the norethisterone acetate group (P < 0.01). On the other hand, Drospirenon increases brain GSH s more effectively than norethisterone acetate (P < 0.01). After bilateral oopherectomy, plasma and tissue T-SH levels decreased in the OVX group compared with control (P < 0.01). Norethisterone acetate increased plasma T-SH more effectively than Drospirenon (P < 0.05), Conclusions: The study showed the extent of oxidative protein damage (OPD) in this model of estrogen deficiency. The protective effect of estrogens against tissue specific OPD suggests that estrogens play an important role within the antioxidant defense systems in plasma, liver and brain. The exact molecular mechanisms leading to these findings are not yet completely known. Meanwhile, hormone replacement therapy for the prevention of OPD in a tissue specific manner may be required.

Objective: Our aim was to clarify the effects of hypercholesterolemic diet and administeration of atorvastatin on lipid peroxidation, protein oxidation and oxidative DNA damage in male New Zealand white rabbits., Methods: We determined malondialdehyde (MDA), protein carbonyl (PCO) and total thiol (T-SH) levels in plasma and liver tissue, glutathione (GSH) levels in erythrocyte and liver tissue, and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels in plasma. Twenty rabbits were randomly divided into two groups and fed with a high-cholesterol diet (fortified with 1% cholesterol) for 4 weeks. Such rabbits were subjected to either (Group 1) a high-cholesterol diet non-supplemented with atorvastatin (n=10) or (Group 2) a high-cholesterol diet supplemented with atorvastatin (0.3mg atorvastatin per day/kg body weight) for 4 weeks (n=10). A control group (n=5) (Group 3) was fed a cholesterol free diet for 4 weeks. Colorimetric methods were used to determine the level of the oxidative stress markers, except 8-OHdG, which was measured by ELISA., Results: Rabbits were fed with the high-cholesterol diet alone (Group 1) showed higher levels of lipid profile and oxidative protein and DNA damage than compared with dose of the control group (Group 3). Atorvastatin therapy has substantially beneficial effects on oxidative protein and DNA damage in hypercholesterolemic rabbits., Conclusions: The current findings will, we hope, lead to a new insight into the pathogenesis of atherosclerosis. On the other hand inhibition of protein oxidation and DNA oxidation in the plasma by atorvastatin may be one of the pleiotropic effects of statins, and thus the underlying mechanism needs to be further clarifications.

Background and Aim: Reactive oxygen radicals that cause remote organ injury are increased after the one-lung ventilation frequently used in thoracic surgery. The aim of this study was to examine the effects of one-lung ventilation on the liver and ileum., Materials and Methods: Thirty rats were divided into five groups: a sham group; 3- and 4-h mechanical ventilation groups; and 1- and 2-h left lung collapse/2-h re-expansion groups (n = 6 for each group). In the collapse groups, the left lung was collapsed by bronchial occlusion for 1 and 2 h and then re-expanded and ventilated for an additional 2 h. At the end of the study, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were determined to assess liver functions. Myeloperoxidase (MPO) and malondialdehyde (MDA) activity were determined in the liver and ileum tissues. The tissues were also examined by light and electron microscope. Apoptosis was assessed using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL) assay., Results: Plasma ALT and AST, tissue MDA, and MPO activities in both tissues were significantly higher in the 2-h collapse/2-h re-expansion group than in the 4-h mechanical ventilation group (P < 0.05). Moreover, the levels were significantly higher in the 2-h collapse group compared to the 1-h collapse group (P < 0.016). Tissue damage and apoptotic index were most prominent in the 2-h collapse/2-h re-expansion group., Conclusion: Our findings showed that one-lung ventilation causes tissue damage in the liver and ileum and that this damage increases as occlusion duration rises.

Background: We hypothesized that prophylaxis with an anti-oxidant should prevent potential adverse outcomes of laparoscopy related to increased oxidative stress in splanchnic organs, including small intestine, liver, and kidneys, and melatonin is the most appropriate agent for this purpose., Methods: Twenty-four Sprague-Dawley rats weighing 300 to 350 g were allocated randomly into three groups consisting of eight in each as follows: Group I: gasless (control); group II: 15 mmHg intraabdominal pressure (IAP) with CO2 pneumoperitoneum for 60 min; group III: 15 mmHg IAP with CO2 pneumoperitoneum for 60 min, and melatonin (10 mg/kg) was administered at two occasions, 5 min before insufflation and immediately before the desufflation. In group II and III, rats left resting for 30 min after abdominal deflation, the small intestine (terminal ileum), liver and kidney examples were excised from same locations. The specimens were also obtained using the same time points in group I rats, comprising the control group. The specimens were immediately placed at -80 degrees C for the malondialdehyde (MDA) measurements. In addition, segments of terminal ileum were taken from the similar places in all of the animals for the histological examinations., Results: Comparisons among the groups revealed that highest mean MDA levels in liver, small intestine and kidney were in the group II, followed by the group III and control group. There was significant difference between mean MDA levels in small intestine, liver and kidney of group II and III (P < 0.0005). However, no significant difference was found between mean MDA levels in small intestine, liver, and kidney of the group III and control group. Mucosa and submucosa were affected significantly in 15 mmHg IAP group (no prophylaxis) when compared with the control and melatonin prophylaxis groups (P = 0.002). However, there was not a significant difference in mean damage score of mucosa, submucosa, and muscular layers in control group when compared to melatonin prophylaxis group., Conclusions: This experimental study indicated that melatonin prophylaxis, with anti-oxidant and anti-inflammatory actions, may have an important role in the prevention of potential complications related to oxidative stress injury on splanchnic organs induced by laparoscopy.

Background: This study was carried out to evaluate the effects of increased intraabdominal pressure (IAP) on testicular blood flow (TBF), oxidative stress markers, and morphology., Methods: Twenty-four Sprague-Dawley rats weighing 300 to 350 g were allocated randomly into 3 groups consisting of 8 animals each: A, gasless (control); B, 10 mm Hg IAP with CO(2) pneumoperitoneum for 60 minutes; and C, 20 mm Hg IAP with CO(2) pneumoperitoneum for 60 minutes. Testicular blood flow was studied using the Doppler technique. In the 10 and 20 mm Hg IAP groups, time points of TBF measurements were defined as follows: TBF(baseline), 10 minutes before insufflation; TBF(10min), 10 minutes after pneumoperitoneum; TBF(50min), 50 minutes after pneumoperitoneum; and TBF(reperfusion), 10 minutes after pneumoperitoneum deflation. To evaluate the changes in oxidative stress, we assayed the malondialdehyde (MDA) levels of testicular tissues. A 4-level grading scale was used to quantify histologic injury., Results: For both testes of each rat, TBF(10min), TBF(50min), and TBF(reperfusion) values of each group were separately evaluated according to their TBF(baseline) value percentages. The results revealed no significant differences for each time point of TBF measurements between the right and left testes in any group. Pneumoperitoneum caused a significant decrease in TBF at the 10th and 50th minutes of pneumoperitoneum, both in the 10 and 20 mm Hg IAP groups, compared with their baseline values. TBF(reperfusion) values in both groups were also lower than their baseline values. We determined that mean TBF(10min) and TBF(50min) values decreased significantly in the 20 mm Hg IAP group compared with the 10 mm Hg IAP group, despite there being no significant difference in their mean TBF(reperfusion) values. Mean MDA levels were significantly increased in both the 10 and 20 mm Hg IAP groups compared with those of the control group for the right and left testes. However, there was no significant difference between the mean MDA levels in these first 2 groups. The histologic injury score was significantly increased in both the 10 and 20 mm Hg IAP groups compared with the control group; however, there was no difference in the scores between these first 2 groups., Conclusions: We demonstrated in an animal model that abdominal deflation after IAP of 10 and 20 mm Hg for 60 minutes causes testicular hypoperfusion, free radical production, and subsequent testicular damage.

Objectives: To investigate possible protective effects of vitamin E and Ham's F-10 medium (HF-10) on lipid peroxidation, apoptosis, motility, and vitality of spermatozoa., Methods: Normozoospermic semen samples were obtained from 35 volunteers. Normal saline solution, HF-10 only, or HF-10 with vitamin E were added to split semen samples (control, group 1, and group 2, respectively). Sperm motility and vitality were evaluated at the end of 1, 2, and 24 hours. Superoxide dismutase, catalase, and malondialdehyde levels were assessed at the end of the first hour. Flow cytometric DNA analysis was performed at the end of 24 hours., Results: Superoxide dismutase, sperm motility, and vitality were not different among the groups. The catalase values decreased in group 1, but not in group 2. Malondialdehyde values in supernatants decreased in group 2 and apoptosis of spermatozoa decreased in groups 1 and 2., Conclusions: Our data suggest that vitamin E and HF-10 protect against the reactive oxygen species-mediated damage on spermatozoa.

Aim: Nitric oxide (NO) is a highly reactive oxidant synthesized from L-arginine by nitric oxide synthase (NOS). NO may cause injury through the generation of potent radicals. Nw- nitro-L-arginine methyl ester (L-NAME) is a non-selective inhibitor of NOS. We aimed to evaluate whether L-NAME treatment had protective effects against oxidative stress in rats intragastrically fed with ethanol during a 4 wk-period., Methods: Thirty-six male Wistar rats were divided into 3 equal groups: group 1 (control group-isocaloric dextrose was given), group 2 (6 g/kg.d ethanol-induced group) and group 3 (both ethanol 6 g/kg.d and L-NAME 500 mg/L in drinking water-given group). Animals were sacrificed at the end of 4 wk-experimental period, and intracardiac blood and liver tissues were obtained. Biochemical measurements were performed both in plasma and in homogenized liver tissues. Alanine amino transferase (ALT), aspartate amino transferase (AST), malondialdehyde (MDA), NO, superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) levels were measured by spectrophotometry., Results: ALT and AST in group 2 (62 U/L and 128 U/L, respectively) were higher than those in group 1 (24 U/L and 38 U/L) and group 3 (37 U/L and 81 U/L) (P<0.001 for both). Plasma and tissue levels of MDA in group 2 (4.66 micromol/L and 0.55 nmol/mg protein) were higher than in group 1 (2.65 micromol/L and 0.34 nmol/mg protein) and group 3 (3.43 micromol/L and 0.36 nmol/mg protein) (P<0.001 for both). Plasma and liver tissue levels of NO in group 2 (54.67 micromol/L and 586.50 nmol/mg protein) were higher than in group 1 (34.67 micromol/L and 435.33 nmol/mg protein) and group 3 (27.50 micromol/L and 412.75 nmol/mg protein) (P<0.001 for both). Plasma and liver tissue SOD activities in group 2 (15.25 U/mL and 5.38 U/ mg protein, respectively) were lower than in group 1 (20.00 U/mL and 8.13 U/ mg protein) and group 3 (19.00 U/mL and 6.93 U/ mg protein) (P<0.001 for both). Plasma and liver tissue CAT activities in group 2 (145 U/mL and 37 U/ mg protein, respectively) were lower than in group 1 (176 U/mL and 73 U/mg protein) and group 3 (167 U/mL and 61 U/mg protein) (P<0.001 for both). Meanwhile, erythrocytes and liver tissue levels of GSH in group 2 (4.12 mg/g Hb and 5.38 nmol/mg protein, respectively) were lower than in group 1 (5.52 mg/g Hb and 4.49 nmol/mg protein) and group 3 (5.64 mg/g Hb and 4.18 nmol/mg protein) (P<0.001 for both)., Conclusion: Our findings show that L-NAME may produce a restorative effect on ethanol-induced liver damage via decreasing oxidative stress and increasing antioxidant status.

Background: The aim of this study was to investigate the correlation between plasma and tissue oxidative stress and the antioxidative response, by measuring malon dialdehyde (MDA) and glutathione (GSH) in late sepsis induced by cecal ligation and perforation., Materials and Methods: A prospective, randomized, controlled experimental study in rats was done. Forty rats, weighing 200-250 g, were randomly divided into two groups (n = 20). In group 1, laparotomy was performed under aseptic conditions, and the cecum ligated and perforated. The abdomen was closed. In group 2, sham control, there was only laparotomy. Twenty-four hours later, blood samples were taken by cardiac puncture for plasma MDA and GSH, followed by harvesting of samples from lung, liver, kidney, and heart in both groups., Results: In the liver, lung, plasma, heart, and kidney, MDA concentrations were increased in the sepsis group after 24 h (P < 0.001 for all organ samples). In the same organs, GSH concentrations were decreased by sepsis (P < 0.001 for all organ samples). In both groups, plasma MDA was positively correlated to MDA in heart (r = 0.82, P < 0.001), liver (r = 0.76, P < 0.001), lung (r = 0.78, P < 0.001), and kidney (r = 0.73, P < 0.001). Similarly, plasma GSH was positively correlated to GSH in liver (r = 0.93, P < 0.001), heart (r = 0.86, P < 0.001), lung (r = 0.91, P < 0.001), and kidney (r = 0.79, P < 0.001)., Conclusions: Plasma MDA and GSH were positively correlated with tissue MDA and GSH in intra-abdominal sepsis in a rat model.

Ischemia due to transient splanchnic vasoconstriction following major burns causes oxidative and/or nitrosative damage in intestinal tissue followed by reperfusion injury. Thus, burn injury leads to breakdown in the intestinal mucosal barrier which can induce bacterial translocation (BT). As an antioxidant and anti-inflammatory agent the protective effects of N-acetylcysteine (NAC) are documented in several studies. This study was designed to determine the effect of NAC treatment on the oxidative stress in the intestine and BT after burn injury. To evaluate this, 32 Wistar rats were randomly divided into four groups as sham (n = 8), burn (n = 8), pre-burn, NAC injection (150 mgkg(-1), intraperitoneally) 15 min before thermal injury (n = 8), post-burn, NAC injection (150 mgkg(-1), intraperitoneally) 2h after thermal injury. Under anesthesia, the shaved dorsal skin of rats was exposed to boiling water for 12s to induce burn injury in a standardized manner. Twenty-four hours later, tissue samples from mesenteric lymph nodes (MLN), spleen, and liver were obtained under sterile conditions for microbiological analysis and ileum samples were harvested for biochemical analysis. In the burn group, the incidence of isolating bacteria in MLN, spleen, and liver specimens was significantly higher than other groups. NAC treatment prevented burn-induced BT in both pre- and post-burn groups. Thermal injury caused a significant decrease in glutathione (GSH) level, significant increases in malondialdehyde (MDA) and myeloperoxidase (MPO) activity at post-burn 24th hour. Treatment of rats with NAC significantly elevated the reduced GSH levels while decreasing MDA levels and MPO activity. These data suggested that NAC has a crucial cytoprotective role in intestinal mucosal barrier and preventive effects against burn injury-induced BT.

Oxidative stress in sustained hypertension was shown with several biochemical parameters. Oxidized low-density lipoprotein (oxLDL) plays an important role during the atherosclerosis process and paraoxonase (PON1) can significantly inhibit lipid peroxidation. Serum PON1 activity, oxLDL and malondialdehyde (MDA) concentrations and their relationship with serum lipid parameters and systolic and diastolic blood pressures (SBP and DBP) were determined in subjects with white coat hypertension (WCH), sustained hypertension (HT) and normotension (NT). The study group consisted of a total of 86 subjects, 30 with WCH (14 male, 16 female subjects), 30 with HT (13 male, 17 female subjects) and 26 with NT (12 male, 14 female subjects). Both white coat hypertensive and hypertensive subjects had significantly higher levels of MDA than normotensives (P<0.026 and P<0.001, respectively). The oxLDL level of the HT group was significantly higher than the NT group (P<0.023). The WCH group had an oxLDL level similar to both hypertensive and normotensive groups. HT and WCH groups had significantly lower PON1 levels than the normotensive group (P<0.001). oxLDL correlated with MDA positively (P=0.008), and PON1 negatively (P=0.008). A negative correlation between MDA and PON1 (P=0.014) was detected. MDA correlated positively with both SBP and DBP (P=0.001), while PON1 correlated with both of them negatively (P=0.01 and P=0.008, respectively). OxLDL correlated with diastolic blood pressure positively (P=0.008). Our data demonstrate that oxidative stress increase in WCH is associated with a decrease in PON1 activity. The reduction in PON1 activity may be one of the factors leading to an increase in oxidative status in WCH.

The aim of this study was to investigate the effect of chronic restraint stress (RS) on spatial learning and memory. Fifty healthy male Wistar rats, aged three months were used. They were equally divided into five groups--C: Control, W: Water Maze, CS-1: Restrained for 21 days (1 h/day) + water maze protocol following stress period, CS-2: Restrained for 28 days (1 h/day) + water maze protocol during last 7 days of stress period, CS-3: Restrained for 21 days and allowed to recovery for 7 days (1 h/day). Corticosterone levels were higher in all stress groups than in C and W groups. Nitrite levels of frontal cortex and hippocampus were found to be elevated in chronic stress groups with respect to C and W groups. Thiobarbituric acid reactive substances (TBARS) of both tissues were increased significantly in CS1 and CS2 groups compared with C, W, and CS3 groups. Escape latencies of CS1 and CS2 groups were longer than those of the W group on each day of acquisition. In transfer test, CS1 and CS2 groups stayed significantly shorter in target quadrant according to the W group. Significant correlations between corticosterone and either nitrite or TBARS of hippocampus and frontal cortex were found. Both acquisition and memory performances were negatively correlated with plasma corticosterone level, nitrite, and TBARS levels of hippocampus and frontal cortex. The results of this study suggest that stress-induced lipid peroxidation may affect the acquisition and memory performances.

Background: Oxidative stress is increased in obesity, leading to endothelial dysfunction, atherogenesis, and platelet aggregation. The purpose of this study was to determine the effects of weight loss after bariatric surgery on serum lipids, malondialdehyde (MDA, a marker of oxidative stress), oxidized low-density lipoprotein (oxLDL, which is increased in obesity and causes endothelial dysfunction), paraoxonase (PON-1, which inhibits lipid peroxidation), leptin and plasminogen activator inhibitor type-1 (PAI-1, which contributes to a thrombotic state)., Methods: 40 morbidly obese patients had insertion of a Swedish adjustable gastric band (SAGB). A lipid profile, MDA, oxLDL, PON-1, leptin and PAI-1 levels were drawn before and 6 months after the operation. 20 patients underwent open (Group 1) and 20 laparoscopic (Group 2) SAGB, to compare the systemic inflammatory response of the two approaches., Results: Patient demographics, indications for surgery, and postoperative results were no different between the groups. Postoperative BMI and concentrations of lipid, MDA, oxLDL, leptin and PAI-1 decreased significantly in both groups. PON-1 activity increased and was negatively correlated with BMI (r=-0.618, P< 0.01), MDA (r=-0.735, P<0.001), oxLDL (r=-0.701, P< 0.01), leptin (r=-0.626, P<0.01) and PAI-1 (r=-0.461, P<0.05). There was a correlation between BMI and MDA (r=0.790, P <0.001), and also leptin (r=0.900, P<0.001) and PAI-1 (r=0.888, P=0.001). There was no correlation between BMI and oxLDL., Conclusion: These findings support the hypothesis that in morbid obesity, weight loss after surgery has positive effects on fibrinolytic function, oxidative stress and antioxidant activity. Both operative approaches had similar effects in this study.

Copper is an essential trace element with various biological functions. Excess copper, however, is extremely toxic, leading to many pathological conditions that are consistent with oxidative damage to membranes and molecules. Exposure to high levels of copper results in various changes in the tissues. In liver, hypertrophy of hepatocytes, hepatitis, hepatocellular necrosis, and hepatocellular death are the results. Lipid peroxidation causes dysfunction in the cell membrane, decreased fluidity, inactivation of receptors and enzymes, and changes ion permeability. In this study, we aimed to determine the effect of copper on oxidative and antioxidative substances in plasma and liver tissue in a rat model. Sixteen male Sprague-Dawley rats were divided into two groups: Group 1 rats included control rats given tap water. Group 2 rats were given water containing copper in a dose of 100 microg/mL. All rats were sacrificed at 4 wk under ether anesthesia. Plasma and liver superoxide dismutase (SOD) activities, plasma and liver MDA (malondialdehyde) levels, and liver glutathione (GSH) levels were studied. Plasma and liver SOD activities were found to be higher in group 2 than those in group 1. Although plasma MDA levels were higher in group 2, MDA levels in liver tissues were comparable. Liver tissue glutathione levels were lower in group 2. It was concluded that although copper is needed in trace amounts, an excess amount is toxic for the organism. It increases lipid peroxidation and depletes GSH reserves, which makes the organism more vulnerable to other oxidative challenges.

In our experimental study, we investigated the protective effect of 3-aminobenzamide (3-AB), the poly (ADP-ribose) synthetase (PARS inhibitor), on the ileal histopathology and the apoptosis in lipopolysaccharide (LPS)-induced inflammation in rats with obstructive jaundice (OJ). We randomized 40 rats into five groups. Group 1: sham group; Group 2: OJ group; Group 3: OJ+LPS; Group 4: OJ+3-AB+LPS; Group 5: OJ+LPS+3-AB. At the fifth day; the rats were jaundiced. In Group 3; 10 mg kg(-1) LPS was injected intraperitoneally at the fifth day and then after 6h the rats were sacrificed. In Group 4; 10 mg kg(-1) 3-AB was administrated intraperitoneally at the fifth day and repeated daily for 3 days and at the eighth day, 10 mg kg(-1) LPS was injected intraperitoneally. In Group 5, 10 mg kg(-1) LPS was injected intraperitoneally at the fifth day and after 6h 10 mg kg(-1) 3-AB was administrated intraperitoneally and repeated daily for 3 days. At the eighth day, rats were sacrificed. Blood samples were taken for detection of serum MDA levels. Ileum samples were taken after relaparotomy for histopathological examination to evaluate the endotoxin-related intestinal injury and Caspase-3 apoptosis and for detection of tissue MDA and ATPase activities. There was marked destruction of villous and crypt epithelial cells and extensive apoptosis in Groups 3 and 5 in histopathological examination. In Group 4, the scores of intestinal mucosal damage and apoptotic cells were reduced significantly (P<0.05). On the other hand, the scores of intestinal mucosal damage and apoptotic cells were not improved in Group 5. After the administration of 3-AB (Group 4), serum and ileal MDA levels decreased, ileal ATPase increased as compared to Groups 1 and 2. Our study showed that 3-AB prevented the mucosal damage and apoptotic loss of intestinal epithelial cells significantly if it was administrated before LPS. However, 3-AB failed to prevent the mucosal damage and apoptotic loss of intestinal epithelial cells significantly if there was established endotoxemia in OJ.

Aim: To investigate free-radical scavenger effect of n-acetylcysteine in rats intragastrically fed with ethanol., Methods: Twenty-four rats divided into three groups were fed with ethanol (6 g/kg/day, Group 1), ethanol and n-acetylcysteine (1 g/kg, Group 2), or isocaloric dextrose (control group, Group 3) for 4 weeks. Then animals were sacrificed under ether anesthesia, and intracardiac blood and liver tissues were obtained. Measurements were made in both serum and homogenized liver tissues. Malondialdehyde (MDA) level was measured by TBARS method. Glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) levels were studied by commercial kits. Kruskal-Wallis test was used for statistical analysis., Results: ALT and AST in Group 1 (154 U/L and 302 U/L, respectively) were higher than those in Group 2 (94 U/L and 155 U/L) and Group 3 (99 U/L and 168 U/L) (P=0.001 for both). Serum and tissue levels of MDA in Group 1 (1.84 nmol/mL and 96 nmol/100 mg-protein) were higher than that in Group 2 (0.91 nmol/mL and 64 nmol/100 mg protein) and Group 3 (0.94 nmol/mL and 49 nmol/100 mg-protein) (P<0.001 for both). On the other hand, serum GSH-Px level in Group 1 (8.21 U/g Hb) was lower than that in Group 2 (16 U/g Hb) and Group 3 (16 U/g-Hb) (P<0.001). Serum and liver tissue levels of SOD in Group 1 (11 U/mL and 26 U/100 mg-protein) were lower than that in Group 2 (18 U/mL and 60 U/100 mg protein) and Group 3 (20 U/mL and 60 U/100 mg-protein) (P<0.001 for both)., Conclusion: Ethanol-induced liver damage was associated with oxidative stress, and co-administration of n-acetylcysteine attenuates this damage effectively in rat model.

Aim: There is increasing evidence that alcohol-induced liver damage may be associated with increased oxidative stress. We aimed to investigate free-radical scavenger effect of n-acetylcysteine in rats intragastrically fed with ethanol., Methods: Twenty-four rats divided into three groups were fed with ethanol (6 g/kg/day, Group 1), ethanol and n-acetylcysteine (1 g/kg, Group 2), or isocaloric dextrose (control group, Group 3) for 4 weeks. Then animals were sacrificed under ether anesthesia, intracardiac blood and liver tissues were obtained. Measurements were performed both in serum and in homogenized liver tissues. Malondialdehyde (MDA) level was measured by TBARS method. Glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) levels were studied by commercial kits. Kruskal-Wallis test was used for statistical analysis., Results: ALT and AST in Group 1 (154 U/L and 302 U/L, respectively) were higher than those in Group 2 (94 U/L and 155 U/L) and Group 3 (99 U/L and 168 U/L) (P=0.001 for both). Serum and tissue levels of MDA in Group 1 (1.84 nmol/mL and 96 nmol/100 mg-protein) were higher than Group 2 (0.91 nmol/mL and 64 nmol/100 mg-protein) and Group 3 (0.94 nmol/mL and 49 nmol/100 mg-protein) (P<0.001 for both). On the other hand, serum GSH-Px level in Group 1 (8.21 U/g-Hb) was lower than Group 2 (16 U/g-Hb) and Group 3 (16 U/g-Hb) (P<0.001). Serum and liver tissue levels of SOD in Group 1 (11 U/mL and 26 U/100 mg-protein) were lower than Group 2 (18 U/mL and 60 U/100 mg-protein) and Group 3 (20 U/mL and 60 U/100 mg-protein) (P<0.001 for both)., Conclusion: This study demonstrated that ethanol-induced liver damage is associated with oxidative stress, and co-administration of n-acetylcysteine attenuates this damage effectively in rat model.

Purpose of investigation: Current infertility treatment strategies may result in ovarian hyperstimulation syndrome (OHSS), which can present with hemodynamic instability that involves hemoconcentration, hypoxia, and liver and renal dysfunction that may result from thrombosis. This study’s purpose was to measure the serum biochemical oxidative stress markers in women with severe OHSS. Material and methods: For this prospective controlled study, serum levels of ischemia modified albumin (IMA), total antioxidant capacity (TAC), total oxidative capacity (TOS), oxidative stress capacity (OSI), and serum malondialdehyde (MDA) were measured in women with (n = 25) and without (n = 27) OHSS. Results: In our study, we observed significant differences between the two groups in terms of IMA, TAC, TOS, OSI, and MDA levels. High oxidative stress parameter levels in the OHSS group may indicate that OHSS is an oxidative stress condition. A bivariate correlation analysis revealed a significant correlation between serum TOS level, OSI ratio, and embryo or oocyte quality scores. In addition, there was a negative, non-significant tendency among OHSS patients regarding high IMA, OSI, TOS, and MDA levels and low oocyte and embryo scores. Pregnancy results were not affected in a statistically significantly manner. Conclusion: These results might indicate that oxidative stress status and oxygen radicals may negatively affect ART cycle outcomes.