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Aims Caloric restriction (CR) is an experimental approach proposed to alleviate age-related oxidative damage. In the present study, we investigated the consequences of CR on renal redox homeostasis in rats at a specific time frame in early-adulthood.. Methods Three groups of male Sprague-Dawley rats; young control at 6-month-old, 2-year-old subjected to 40% CR between 18th-24th months of age, and their non-CR controls were sacrificed, and numerous redox status biomarkers including protein oxidation, glycation, lipid peroxidation, glycation end products, thiol groups, and superoxide dismutase were assayed. It was also ensured that CR rats and their non-CR corresponding rats had similar body weights at the end of the study to decrease the confounding effects of different body weights on redox homeostasis and caloric restriction. Results After CR, the detrimental effects of the protein oxidation, glycation, and lipid peroxidation were significantly improved in the renal tissue CR rats when compared to their non-CR control group. However, there were no significant difference in thiol fractions between younger controls and both of the elderly groups. Conclusion Detrimental consequences of renal senescence on redox homeostasis are significantly improved via CR especially applied in early-adulthood.

Evidence indicates that maintenance of redox homeostasis is fundamental for cellular longevity. Caloric-restriction (CR) is said to decrease the formation of oxidatively modified cellular macromolecules and improve health. On the other hand, some studies indicate that many CR studies are flawed, because ad libitum fed rats are not well-controlled. Thus, it is claimed that purported beneficial effects of CR could be not due to real CR effect, but due to control animals going obese. Also, it remains to be elucidated whether effects of CR could be observed even when CR is started in mid-adulthood. Male Sprague-Dawley rats were grouped as: non-CR 6-month-old rats (n=7), 24-month-old rats subjected to 40% CR for 6months between 18th and 24thmonths (n=8), and non-CR 24-month-old animals (n=8). We investigated 16 previously validated biomarkers of macromolecular redox homeostasis, ranging from protein and lipid oxidation to glycation and antioxidative capacity. In the present study, the protein, lipid and antioxidant capacity redox homeostasis biomarkers overwhelmingly indicate that, CR, even though not started very early in adulthood, could still offer potential therapeutic effects and it could significantly improve various redox homeostasis biomarkers associated with disease reliably in the heart tissue of aging male Sprague-Dawley rats. Therefore, the effects of CR likely operate through similar mechanisms throughout adulthood and CR seems to have real ameliorative effects on organisms that are not due to confounding factors that come from ad libitum fed rats. Bezmiâlem Vakıf Üniversitesi

While the deterioration of insulin-glucose metabolism (IGM), impaired redox homeostasis (IRH), β-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. β-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 β-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.

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.

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.

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.

The present study was undertaken to evaluate the place of oxidative stress on breast cancer. Lipid peroxidation as evidenced by malondialdehyde (MDA) and the status of the antioxidants superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were estimated in tissues of 10 fibroadenoma and 40 breast cancer patients. Lipid peroxidation in breast cancer tissues was enhanced compared to nonmalignant tissues (p

Background. The secondary injury process following spinal cord trauma has been shown to involve different mechanisms such as excessive release of excitatory amino-acids, and induction of free radical induced lipid peroxidation. In this experimental study, the time-level relationship of the nitric oxide and the neuroprotective effects of aminoguanidine were investigated in a rat spinal cord trauma model. Methods. The experiments were performed on 63 Wistar albino rats divided into three groups; sham-operated control (Group 1), trauma created control (Group 2) and aminoguanidine group (Group 3). In groups 2 and 3, spinal cord trauma was produced at thoracic level by using weight the drop technique (at a severity of 50 gr-cm). After the trauma, the rats in Group 3, received an intraperitoneal injection of 100 mg/kg aminoquanidine twice a day for 3 days. The effects of the injury and the efficacy of aminoguanidine were determined based on biochemical parameters (lipid peroxidation and nitric oxide levels in tissue), and on light microscopy findings in cord tissue collected at different times post-injury. Biochemical parameters were performed one hour, three and five days after injury. Functional recovery was assessed at 3, and 5 days after cord trauma with the inclined-plane technique and Tarlov’s motor grading scale. Findings. Although there was no statistically significant difference at the 1st hour, the values of the tissue nitric oxide in trauma created controls were 42% higher on the 3rd day and 40% higher on the 5th day when compared with those in sham controls. The levels of the tissue lipid peroxidation in trauma created controls were 88% higher at the 1st hour and 52.8% higher on the 5th day when compared with shame controls, but there was no meaningful difference on the 3rd day. In the trauma created control group, the mean motor function scores decreased to 1.16 ± 0.40 and to 1 ± 0 on the 3rd and 5th day, respectively. In this group the mean values of the inclined plane were 39.16 ± 2.04 on the 3rd day and 37.91 ± 1.02 on the 5th day. No statistically significant difference was observed in both tissue lipid peroxidation and nitric oxide levels for all time points between the aminoguanidine group and the sham-operated controls (p>0.01). The motor function scores were observed as 2.16 ± 0.40 on the 3rd day and as 3 ± 0 on the 5th day in aminoguanidine group. These values were significantly higher than the trauma created controls (p

Object. The toxic effects of glutamate in the central nervous system are well known. This neurotoxicity occurs through metabotropic and ionotropic receptors, the latter group composed of N-methyl-d-aspartate, α-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA), and kainate receptors. The authors investigated the neuroprotective effects of GYKI 52466, a 2,3-benzodiazepine that is a selective and potent AMPA receptor antagonist, in a rat spinal cord trauma model. Methods. Sixty Wistar albino rats were studied in three groups of 20 animals each: sham-operated controls (Group 1); spinal cord—injured rats (Group 2); and spinal cord—injured plus GYKI 52466—treated rats (Group 3). In Groups 2 and 3, spinal cord injury (SCI) was induced at the thoracic level by applying an aneurysm clip to the cord for 1 minute. One minute after the clip was removed, the rats in Group 3 received an intraperitoneal injection of 15 mg/kg GYKI 52466. Responses to injury and treatment were evaluated based on biochemical parameters (lipid peroxidation and adenosine 5′-triphosphate [ATP] levels in tissue), and on light and transmission electron microscopy findings in cord tissue collected at different times post-SCI. Five rats from each group underwent assessment of functional recovery at 1, 3, and 5 days after SCI; evaluation was performed using the inclined-plane technique and Tarlov motor grading scale. The mean lipid peroxidation levels in Groups 1 and 2 were 21.73 ± 4.35 and 35.53 ± 2.99 nmol/g of wet tissue, respectively. The level in Group 3 was 27.98 ± 3.93 nmol/g of wet tissue, which was significantly lower than that in Group 2 (p < 0.01). The mean ATP levels in Groups 1 and 2 were 166.21 ± 25.57 and 41.72 ± 12.28 nmol/g of wet tissue, respectively. The ATP level in Group 3 was 85.82 ± 13.92 nmol/g of wet tissue, which was significantly higher than that in Group 2 (p < 0.01). Light microscopic examination of Group 2 tissues showed hemorrhage, necrosis, polymorphonuclear leukocyte infiltration, and vascular thrombi. In contrast, the examination of Group 3 tissues showed limited hemorrhage and no necrosis or vascular thrombi. The most prominent findings in Group 2 were hemorrhage and necrosis, whereas the most prominent findings in Group 3 were focal hemorrhage and leukocyte infiltration. Electron microscopy demonstrated that GYKI 52466 protected the neurons, myelin, axons, and intracellular organelles. The mean inclined-plane angles in Groups 1, 2, and 3 were 65°, 40 to 45°, and 55°, respectively. Motor scale results in all groups showed a similar trend. Conclusions. The findings in this rat model suggest that GYKI 52466 may provide significant therapeutic protection from secondary damage after acute SCI. This agent may be a viable alternative treatment for SCI.

The aim of this study was to investigate the effect of vitamin E treatment on increased oxidative stress in rats exposed to a swimming exercise protocol. In order to examine the effects of physical swimming training on the antioxidant defences of tissues and on their susceptibility to damage induced by exercise, the levels of glutathione (GSH) and thiobarbituric acid reacting substances (TBARS) levels, on indicator of lipid peroxidation in various tissues, have been determined. In this study, four groups of female rats were used while the rats were trained to swim for 30 minutes a day and five days a week which lasted eight weeks and vitamin E (vit. E) supplementation (30 mg/kg/day) has been carried out for five days a week. TBARS levels are significantly found lower in both trained and sedentary vit. E supplemented groups, since vit. E is the most important antioxidant in an earlier line of defence in lipid peroxidation. Also, in vit. E supplemented trained rats, the glutathione response is observed to be significantly higher, supporting with the TBARS levels and in accordance with the literature. But in the sedentary group without vit. E supplementation, the GSH levels of the liver and the heart tissues were significantly lower than both vit. E supplemented sedentary and trained groups. These results evaluate that vit. E confers protection to GSH levels in these tissues where the GSH levels were found significantly lower in the groups not supplemented with vit. E.

In this study, we determined curcumin's anticancer and chemopreventive effects in mice bearing Ehrlich ascites tumor by evaluation of cancer biomarkers, sialic acid level and sialidase activity. Both plasma sialic acid level and sialidase activity increased significantly in the mice group with Ehrlich ascites tumor. When the tumor groups fed with curcumin and fed with sesame oil were compared, sialic acid level and sialidase activity in ascites fluid significantly reduced in the group fed with curcumin in addition to the increases of plasma sialic acid level and sialidase activity. The tumor group fed with curcumin lived twice longer than the one fed with sesame oil. Curcumin as a phenolic compound decreased all these parameters in Ehrlich ascites tumors and lengthened survival by 88% in the mice with tumor. We concluded that curcumin has anticancer activity.

BACKGROUND AND PURPOSE In the literature, there are few reports documenting intra-abdominal organ necrosis following laparoscopic procedures. This experimental study was planned to investigate whether intestinal ischemia develops during laparoscopic procedures and if laparoscopy could cause intestinal necrosis. MATERIAL AND METHODS Two experimental groups, each consisting of 10 adult New-Zealand rabbits, were used in this study. The first group comprised the study group which had pneumoperitoneum, the second group comprised the normal animals serving as the controls. A cervical tracheostomy was performed to achieve successful general anesthesia in both groups. In the study group, intraperitoneal CO2 insufflation was carried out and intraabdominal pressure (IAP) was adjusted so as not to exceed the arterial blood pressure. After 20 min high IAP period, the intraabdominal gas was aspirated. Five minutes later, samples of both small intestine and colon tissue were taken. In the control group, tissue samples were taken 25 min after anesthesia was achieved. Xanthine oxidase (XO) and malondialdehyde (MDA) levels were measured as indicators of intestinal ischemia and lipid peroxidation in the intestinal tissues. Statistical analysis was done to compare the XO and MDA levels of the small intestines and colons of both groups. RESULTS The mean colonic XO levels were 1.323+/-1.17 and 0.217+/-0.27 (U/mg protein) in study and control groups, respectively. This difference was statistically significant (t = 2.60, p

In this study, our aim was to determine whether or not type 1 diabetes mellitus affects salivary sialic acid level and SOD activity. For this purpose, unstimulated saliva specimen was collected. Saliva sialic acid level and SOD activity were measured by the methods of Warren and Sun, respectively. We found significantly decline in salivary sialic acid level and SOD activity. The decrease of salivary sialic acid level in type 1 diabetes may be due to changes in the activities of the enzymes taking part of in the synthesis and catabolism of sialic acid. The main reason for the decrease of salivary SOD activity may be increased glycation of the enzyme and/or deleterious effect of increased free oxygen radicals by glycated proteins on SOD activity in diabetes. We conclude the decline both in sialic acid and SOD in saliva may be a possible factor leading to oral complications of diabetes mellitus.

Thermal injury initiates systemic inflammatory reactions producing burn toxins, an inflammatory response, oxygen radicals and finally peroxidation. The relationship between the amount of products of oxidative metabolism and natural scavengers of free radicals determines the outcome of local and distant tissue damage, and further organ failure in burn injury. To determine the relationship between the level of total natural scavengers of the body, the place of superoxide dismutase in this capacity, and its relation with lipid peroxidation, malondialdehyde, superoxide dismutase levels and total antioxidant status were measured in plasma. Animals were subjected to 30 per cent full thickness body surface area burn, and their blood was collected at 24 h postburn. Plasma malondialdehyde levels were significantly elevated above the level of controls (P0.02). Burn injury caused a remarkable decrease in superoxide dismutase (45 per cent decrease, P0.0001) and total antioxidant status (14 per cent decrease, P0.01) when compared to control.

WOS:000231920000007 PubMed: 24672133 Background: The relationship between oxidative stress and osteoarthritis (OA) has been widely investigated. Serum malondialdehyde (MDA), nitric oxide (NO), and Cu/Zn superoxide dismutase (SOD) levels are useful markers of oxidative stress. Because of the importance of oxidative stress markers in the pathogenesis of OA, treatment might involve modification of these markers to control oxidative stress. Objective: The aim of this study was to compare the effects of 2 conventional NSAIDs on markers of oxidative stress in patients with OA of the knee. Methods: This 3-week, prospective, randomized, open-label, active- and placebo-controlled study was conducted at the Cerrahpasa Faculty of Medicine, Istanbul University, Istanbul, Turkey Adult patients with clinically and radiographically diagnosed moderate OA of the knee who were previously untreated were enrolled. Patients were randomly assigned to 1 of 3 treatment groups: flurbiprofen 100 mg PO (tablets) BID, tiaprofenic acid 300 mg PO (tablets) BID, or placebo tablets BID. Patients were evaluated using clinical assessment and laboratory testing before treatment (week 0; baseline) and at the end of week 3. The primary end points were the differences in serum MDA, NO, and SOD levels versus placebo. Clinical parameters-pain at rest and on motion-were evaluated using a 10-cm visual analog scale (0 = no pain to 10 = worst pain imaginable). The duration (in minutes) of morning stiffness was recorded by patients, using patient diaries. The differences between treatment groups were assessed using multivariate analysis. Results: Thirty-nine patients (20 women, 19 men; mean [SD] age, 59.0 [11.3] years) were included in the study Mean serum MDA and NO levels were significantly decreased at 3 weeks compared with baseline in the 2 active-treatment groups (all, P < 0.001); these values remained statistically similar to baseline in the placebo group. Serum SOD levels were increased significantly from baseline in the 2 active-treatment groups (both, P < 0.00 1), but not in the placebo group. No significant differences in serum MDA and NO levels were found between the group receiving flurbiprofen and that receiving tiaprofenic acid. Serum SOD levels were significantly higher in the flurbiprofen group compared with the tiaprofenic acid and placebo groups (both, P < 0.0 1). The mean (SD) score for pain at rest was significantly lower at 3 weeks compared with baseline with flurbiprofen and tiaprofenic acid (both, P < 0.00 1), but not with placebo. The mean score for pain on motion was significantly reduced from baseline values only with tiaprofenic acid (P < 0.001). The duration of morning stiffness was significantly shorter at 3 weeks compared with baseline in all 3 study groups (all, P < 0.001). The mean scores for pain on motion and duration of morning stiffness were significantly reduced with tiaprofenic acid compared with placebo (both, P < 0.05). The study had some limitations (ie, small sample size, no blinding, the short duration of the study, and the weak correlation between serum and synovial fluid levels of NO). Conclusions: In this comparison of the effects of 3 weeks of treatment with flurbiprofen 100 mg BID and tiaprofenic acid 300 mg BID in patients with knee OA, both treatments effectively reduced serum MDA and NO levels compared with placebo. Only tiaprofenic acid significantly improved pain at rest and on motion and duration of morning stiffness compared with placebo.

Objectives: Reactive oxygen species generated after brain trauma trigger a cascade of events resulting in neuronal death. Despite numerous defenses, the brain is vulnerable to oxidative damage, mainly because of its high content of unsaturated fatty acids. The goal in this experimental study was to demonstrate the activities of antioxidant enzymes, namely, superoxide dismutase, catalase, and guanase, in plasma and brain tissue at 30 minutes and 60 minutes after brain trauma. Methods: Forty adult male Sprague-Dawley rats were used as subjects. Rats in group 1 were subjected to moderate head injury, whereas rats in group 2 were subjected to severe head injury. Eight rats served as a sham operated (control) group. Results: The results of this study showed that there is, in general, an increase in the activities of these 3 enzymes in plasma; however, in the brain tissue, we observed that guanase activities were decreased during the posttraumatic period. Conclusion: These alterations in enzyme activities suggest that lipid peroxidation ensues in the early period of trauma and that treatment strategies aimed to increase antioxidant enzyme activities may prevent the secondary mechanisms resulting in neuronal death.

In this study, solitary and combined effects of vitamin E and the calcium-channel blocker diltiazem were investigated in streptozotocin (STZ)-induced diabetic rats. Thirty male Wistar albino rats, weighing approximately 200 g were used. Diabetes mellitus was induced by a single intravenous injection of STZ at a dose of 65 mg/kg body weight. Five experimental groups were established as STZ-diabetic, STZ-diabetic + vitamin E, STZ-diabetic + diltiazem and STZ-diabetic + vitamin E + diltiazem. Vitamin E was injected intraperitoneally three times a week at a dose of 500 mg/kg body weight. Diltiazem was given orally every day at a dose of 25 mg/kg body weight. At the end of the study (10 weeks) blood glucose levels of diabetic rats, which had received vitamin E and diltiazem, had significantly decreased when compared with untreated diabetic rats (P < 0.02). Similarly, HbA1c levels had significantly decreased in diabetic rats which had received vitamin E (P < 0.05), diltiazem (P < 0.01) and vitamin E + diltiazem (P < 0.02) when compared with untreated diabetic rats. Liver glutathione levels of diabetic rats, which had received vitamin E (P < 0.01) and vitamin E + diltiazem (P < 0.05) had significantly increased when compared with untreated diabetic rats. Liver lipid peroxide levels had significantly decreased in diabetic rats, which had received vitamin E (P < 0.001) and diltiazem (P < 0.01). With respect to their metabolic and antioxidant effects, vitamin E proved superior to diltiazem.

Hydrocephalus causes damage to periventricular white matter at least in part through chronic ischemia. Emphasizing the periventricular ischemia/hypoxia in hydrocephalus, various authors indicated the secondary biochemical impairment and oxidative damage in experimentally induced and congenital hydrocephalic rat brain. (-)-Epigallocatechin gallate (EGCG), the main constituent of green tea polyphenols, has been shown to be of some protective value in various models of neurological injury as a free oxygen radical scavenger. In the present study the effects of EGCG were examined on the periventricular oxidative damage in experimental childhood-onset hydrocephalus. Hydrocephalus was induced in 3 weeks-old rat pups by kaolin injection into the cisterna magna. A single daily dose of 50 mg/kg of EGCG injected into the peritoneum of the rats for 15 days significantly reduced periventricular white matter malondialdehyde levels when compared to non-treated hydrocephalic animals. Our results indicate that EGCG may have a protective effect against periventricular white matter oxidative damage in hydrocephalus induced infantile rats.

Physical activity is known to induce oxidative stress in individuals subjected to intense exercise. Contrarily, there are enzymatic and nonenzymatic defence systems against oxygen radicals in aerobic organisms. Sulphydryl groups such as thiol and glutathione (GSH) can be given as an example to non-enzymatic low molecular weight antioxidants. Carnitine may be related to the performance enhancement in high intensity intermittent exercises and might probably improve the aerobic capacity by stimulating lipid oxidation in muscle cells during long term exercise. But, the effects caused by this supplement during physical activity have not been fully described in the literature. The aim of the study was to compare plasma thiols (PSH), malondialdehyde (MDA) and carnitine levels and maximal oxygen uptake (VO2(max)) of the soccers under regular training with the values of the healthy controls. Our results demonstrates that soccers seem to be under less oxidative stress, as their MDA levels were significantly lower (P0.001) when compared with the control group while their PSH levels were significantly elevated (P0.001), during resting condition. In addition, the plasma carnitine concentrations of the soccer group yields lower values while the VO2(max) yields a higher value when compared with the control group. The differences between the soccer and the control groups are significant (for both, P0.001). The present research reveals the fact that regular soccer training shows beneficial effect on decreasing of lipid peroxidation levels. Furthermore; the sportsmen who are under intense training programs have low plasma carnitine values which do not cause negative effect on their sportive performance.

Besides mechanical damage done by the enlarging ventricles, biochemical impairment in the periventricular tissue represents an important factor resulting from or contributing to the pathogenesis of hydrocephalus. In this study the changes in periventricular region total sialic acid levels in the early stage of experimentally induced hydrocephalus were evaluated.Hydrocephalus was induced in 3-week-old rat pups by kaolin injection into the cisterna magna. Ten days after hydrocephalus induction rats were sacrificed and total sialic acid levels in the periventricular area were determined by the thiobarbituric acid method.Sialic acid, a vital component of brain gangliosides, which play an essential role in the transmission and storage of information in the brain, was found to be significantly decreased in the periventricular area of hydrocephalic infantile rats.

Chronic ethanol administration is able to induce an oxidative stress in the central nervous system. N-Acetylcysteine (NAC) has antioxidant properties; as a sulphydryl donor, it contributes to the regeneration of glutathione and it acts through a direct reaction with hydroxyl radicals. In this study we investigated a possible beneficial effect of NAC on some of the free radical related parameters. Twenty four male Wistar rats were divided in to three groups and were given ethanol (Group 1), ethanol and NAC (Group 2) and isocaloric dextrose (Group 3). Ethanol and NAC were given intragastrically at doses of 6 g/kg/day and 1 g/kg/day, respectively. Our results show that chronic ethanol intake elicits statistically significant increase in MDA and NO levels and decrease in SOD and GSH levels in both plasma and brain (p < 0.001). GPx levels decreased in erythrocytes (p < 0.001). CAT activity showed significant decrease only in brain samples (p < 0.001). NAC administration effectively restores the above results to nearly normal levels. Therefore we suggest that reactive free radicals are, at least partly, involved in the ethanol-induced injury of brain cells and NAC mitigate the toxic effects of ethanol on the oxidant-antioxidant system of rat plasma and brain.

Significant elevations of serum sialic acid level have been documented in various diseases including in a variety of central nervous system disorders. But, in head injury, there is no any study on the serum and brain tissue sialic acid levels. So, we planned an experimental study to evaluate serum and brain tissue sialic acid levels in head injury.Marmarou's impact-acceleration model was used in rats to produce diffuse brain injury. Rats were divided into equal three groups. In Group I, 450 g weight was fell from 1 m height to heads of subjects, and from 2 m in Group II. Group III was control group. Sialic acid levels were measured in both sera and brain tissue supernatants after trauma.It was observed that serum sialic acid level was decreased according to the severity and period of trauma increased; and there was no change in brain tissue sialic acid levels.Serum sialic acid level might be used as a marker to show the degree of diffuse brain injury.

The effectiveness of nimodipine and N-acetylcysteine in experimental spinal cord injury was evaluated by measuring tissue lipid peroxidation levels of the damaged spinal cords 1 hour after the injury We used the clip compression method to produce acute spinal cord injury in 40 female Sprague-Dawley rats were used. The rats were divided into four groups of 10 each. Lipid peroxidation was assessed by measuring the tissue content of malonil dialdehyde (MDA). In group 3, nimodipine, and in group 4, N-acetylcysteine, was administered i.p. as a single dose immediately after the injury. The rats were sacrificed 1 hour after clip application. The tissue mean MDA content was 3,992 micromol MDA/gww in group 1 (sham operated), 10,192 micromol MDA/gww in group 2 (trauma), 10,449 micromol MDA/gww in group 3 (nimodipine treatment) and 9,009 micromol MDA/gww in group 4 (N-acetylcysteine treatment). These results demonstrated that a single dose of nimodipine and N-acetylcysteine had no effect on peroxidation of lipid membranes in the early period of experimental spinal cord injury.

Xanthine oxidase is most recognized for its role as the rate-limiting enzyme in nucleic acid degradation through which all purines are channelled for terminal oxidation. The enzyme serves as a source of oxygen-derived free radicals which induce both cellular injury and edema as well as changes in vascular permeability. In the study we compared xanthine oxidase levels of human brain tumors with normal brain tissues. Statistical evaluation of our results shows significantly higher xanthine oxidase levels in tumoral brain tissues. However, xanthine oxidase has not any significance for the differentiation of tumor types among each others. The oncotypes studied were meningioma and astrocytoma.

Study Design: The effect of epidural space perfusion with chilled saline solution (% 0.9 NaCl) on lipid peroxidation after experimental spinal cord injury in rats was evaluated. Objectives: The extent of lipid peroxidation is a useful parameter for evaluating the cellular disturbance caused by spinal cord trauma in experimental conditions. The protective effects of hypothermia against neurological injury resulting from trauma or ischemia both in experimental and clinical situations have been demonstrated. Setting: Departments of Neurosurgery and Biochemistry, Cerrahpasa Medical School, Istanbul, Turkey. Methods: Twenty-five female Wistar Albino rats were used. There were five rats in group I (sham-operated), seven rats in group II (trauma), and eight rats in group III (epidural cooling). The remaining five rats were used for the pilot study to determine the spinal cord and body temperature. A clip compression method was used to produce acute spinal cord injury. In group III, 30 min after the trauma the injured spinal cord was cooled by perfusion of the epidural space with chilled saline solution (% 0.9 NaCl) with a flow rate of 5 ml/min for 30 min. At 2 h after trauma, all rats other than the ones used in the pilot study, were sacrificed and the spinal cords were excised. The extent of lipid peroxidation in the spinal cord was assessed by measuring the tissue content of malonil dialdehyde (MDA). Results: The tissue MDA contents were 1.58 micromol MDA/gram wet weight (gww) in group 1 (sham-operated), 2.58 micromol MDA/gww in group 2 (trauma), and 1.77 micromol/ gww in group 3 (epidural cooling), the differences being statistically significant. Conclusion: The results indicated that epidural cooling of traumatized spinal cord is effective in preventing secondary damage due to the peroxidation of lipid membranes.

Superoxide dismutase “SOD” enzyme levels in leucocytes of patients with acute and chronic leukemia, were measured by using Misra and Fridovich's epinephrine method. In all types of leukemia, the SOD levels were found to be significantly higher than normals. However, these levels decreased to normal in remission. No relationship was found between the SOD level and types of leukemia. The absence of relationship between the increase in SOD level and various clinical parameters suggests that this increase is the result of a disturbed gene expression in the stem cells. Hence it is of interest to ascertain the effect of the chemotherapy leading to the normalization of the SOD levels.