The neuroprotective and anti-inflammatory effects of Annona muricata (Graviola) on radiation-induced rat sciatic nerve injury

Associations of the fatty acids with the concentration of antioxidant enzymes in the blood in men with coronary heart disease

Background/Objectives: This study aims to investigate the effects of betanin, which possesses antioxidant and anti-inflammatory properties, against colitis, a disease in which inflammation and oxidative stress play a role in its pathophysiology, during the acute and subacute period. Methods: Thirty-two rats were included in the study and divided into four groups: control, colitis, 3-day betanin supplementation + colitis (bet3+colitis), and 15-day betanin supplementation + colitis (bet15+colitis). Experimental colitis was induced with trinitrobenzene sulfonic acid. Results: In the colitis group, malondialdehyde, myeloperoxidase, superoxide dismutase (SOD) inhibition rate, tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6, mucosal damage, and cell infiltration scores were higher than in the control group, while catalase and glutathione peroxidase (GPx) levels were lower. In the betanin supplementation groups, malondialdehyde, myeloperoxidase, TNF-α, IL-1β, mucosal damage, and cell infiltration scores were lower than in the colitis group, while GPx levels were higher. In addition, the SOD inhibition rate and interleukin-6 levels were lower in the bet15+colitis group than in the colitis group. TNF-α, IL-1β, interleukin-6, and GPx levels in the betanin groups were similar to the control group. Conclusions: Betanin supplementation demonstrated a significant anti-inflammatory effect by reducing inflammatory parameters and histopathological scores in both periods. Additionally, it exhibited a glutathione-related antioxidant effect by increasing GPx levels in both periods. However, although SOD inhibition rates decreased in the subacute period, no significant change in catalase levels was observed in either period. This indicates that it did not provide complete protection in terms of antioxidant effects in either period.

The effect of clotrimazole was examined using a spinal cord ischemia/reperfusion model. Twenty albino Wistar rats weighing 234 +/- 12.3 g were used in this study. Rats were anesthetized intraperitoneally with 50 mg/kg ketamine HCl. All animals underwent laparotomy under aseptic conditions. Abdominal aortas of the animals in all but the sham group were exposed. After opening the retroperitoneum, the infrarenal abdominal aorta was clipped for 45 minutes to produce ischemia/reperfusion injury. Polyethylene glycol (PEG, 1 mL) was administrated to the vehicle group. PEG (1 mL) and clotrimazole (30 mg/kg) were administered intraperitoneally in the clotrimazole group. Total laminectomy of T8-T12 was performed on all rats under a microscope. Spinal cords were excised for a length of 2-cm rostrally and 1-cm caudally to the injury site and deep frozen at -76 degrees C for biochemical studies. The levels of malondialdehyde, glutathione-peroxidase, superoxide dismutase, and catalase were measured as an indicator of ischemia level. The most cranial part of the specimens was evaluated morphologically. Treatment with clotrimazole significantly decreased malondialdehyde, glutathione-peroxidase, superoxide dismutase, and catalase levels in comparison with other groups (P = 0.008). Morphologic evaluation revealed that clotrimazole protected the axons and their myelin sheaths from ischemic damage. This study showed the neuroprotective effects of clotrimazole on spinal cord ischemia/reperfusion injury.

The cerebral epiphysis (pineal gland) secrets melatonin and number of other proteins and peptides. It was thus hypothesized that antioxidant properties of epiphyseal proteins and melatonin could potentially benefit from exogenous therapies. In view of the therapeutic potential of these proteins, the present experiment was conducted to investigate the effect of buffalo epiphyseal proteins (BEP, at 100 μg/kg BW, i.p.) and melatonin (MEL, at 10 mg/kg BW, i.p) on changes in hepatic and renal antioxidant enzymes of adult female Wistar rats. Buffalo epiphyseal proteins significantly (P < .05) increased hepatic lipid peroxidation (LPO), superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), reduced glutathione (GSH), and renal LPO, catalase (CAT), GR, GSH, GPx levels as compared to control animals. Similarly, MEL treatment significantly (P < .05) up-regulated hepatic SOD and GPx activity, whereas CAT, GR, GPx, and GSH levels in renal tissues were increased while SOD and LPO remained unaffected. Buffalo epiphyseal protein treatment produced greater effects on hepatic GPx and renal CAT and GSH levels than did MEL. These findings support the conclusion that buffalo epiphyseal proteins and melatonin activate a number of antioxidant mechanisms in hepatic and renal tissues.

Tobacco has a time dependent effect on the antioxidant system of the body. This study was designed to determine and compare alteration in levels of erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) in blood subgroups of tobacco smokers and chewers with controls. Blood samples were collected from 30 tobacco smokers (> 20 cigarettes daily), 30 tobacco chewers (> 10 packets gutka daily) and 30 controls. These groups were further divided into three subgroups (n=10) based on duration of habit (<5 yrs, 5-10 yrs, >10 yrs). The level of erythrocyte SOD, GPx and CAT were measured using standard procedures. The SOD and CAT levels were significantly decreased in all subgroups of smokers and chewers whereas GPx level was significantly increased. Positive correlation was observed between SOD, GPx and CAT levels with change in duration of habit in all subgroups. No significant difference observed in SOD and CAT activity between tobacco smokers and chewers. The findings suggested that antioxidative enzyme activities have significant correlation with change in the duration of tobacco use. Measurement of markers of free radical activity might be useful for estimating the level of oxidative stress caused by tobacco use.

Aim and Objective: Tobacco is a major etiological factor for oral cancer development, accounting 30–40% of all cancer cases in India. Tobacco consumption generates free radicals and causes oxidative damages. In order to counteract these lethal effects, normal living cells have multiple antioxidant defense systems in a cascade manner. Thus, it seems that studying biological parameters, like antioxidant enzyme system, may be helpful in risk assessment and early diagnosis of oral cancer. Therefore, we analyzed erythrocytic and tissue antioxidant enzyme activities in terms of glutathione-S-transferase (GST), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and plasma thiol levels. Materials and Methods: Study included healthy controls with no habit of tobacco (NHT, n = 25), controls with habit of tobacco (WHT, n = 31) and oral cancer patients (n = 52). All the parameters were analyzed with highly sensitive and specific spectrophotometric methods. Results: Erythrocytic SOD and plasma thiol levels were significantly lower (p = 0.03), while GPx and CAT levels were higher (p = 0.017) in WHT as compared to NHT. No significant changes in GST and GR levels were observed between NHT and WHT. GST, GR, SOD and CAT activities were significantly higher (p = 0.05, p < 0.001, p = 0.003 and p < 0.001, respectively) while GPx and thiol levels were lower (p = 0.035 and p < 0.001, respectively) in oral cancer as compared to WHT. Odds ratio for erythrocytic GR, SOD, CAT and plasma thiol showed significantly higher risk of oral cancer development in WHT. Mean levels of SOD and CAT were increased, while GPx and thiol were decreased with the increase in habit duration in oral cancer. GST, GR and SOD activities were significantly higher (p = 0.0001, p = 0.005 and p = 0.005, respectively), while, CAT and thiol levels were lower (p = 0.0001 and p = 0.015, respectively) in malignant tissues as compared to adjacent normal tissues. Conclusion: The data revealed that evaluation of antioxidant enzyme activities and thiol levels in WHT can be helpful to identify individuals at a higher risk of oral cancer development

Background/objectiveFetal wound repair seems a relatively efficient process when compared to wound repair during adulthood, which may be explained by the effects of the fetal environment. This study examined the effects of an amnion cell culture medium (ACCM) on skin wound healing in a rat experimental model.MethodsSixteen adult female Wistar albino rats were used in this experimental animal study (treatment group, n = 8; control group, n = 8). Surgical wounds were formed on the dorsal skin of each rat. A commercially available ACCM was administered daily over each of the wound in the treatment group for 14 days and the control group did not receive any treatment. Wounds were evaluated for tissue perfusion with laser doppler, tissue superoxide dismutase (SOD), glutathione peroxidase (GPX), and malondialdehyde (MDA) levels as well as histopathological examination.ResultsControls had significantly higher tissue SOD levels when compared to the treatment group (10.0 ± 3.2 vs 6.7 ± 1.2, P = .005); however, the 2 groups did not differ in terms of tissue GPX and MDA levels. For open wounds, inflammation and neovascularization were more prominent in the ACCM group at day 14. However, at day 21 neovascularization and granulation were more prominent in controls. For closed wounds, neovascularization was more prominent in controls at days 14 and 21. The 2 groups did not differ in terms of tissue perfusion.ConclusionAlthough marginal difference was found between controls and ACCM group for several parameters, findings of this study do not support beneficial effect of ACCM on wound healing.

The study was undertaken to check the effects of cyanocobalamin on antioxidant enzymes of male Wistar albino rats infected with T. b. brucei. Fifty-four (54) male Wistar albino rats were divided into six groups of three rats each which were replicated three times. The rats were marked and kept in stainless wire cages labeled A-F. Groups A, B, and C were normal, negative and standard control respectively. Groups D, E and F were infected with 1.0 x 106 trypanosomes and treated with 0.2mg/kg (low-dose), 0.3mg/kg (enriched-dose), and 0.4mg/kg (high-dose) body weight of vitamin B12 respectively. The experiment lasted for twenty-one days from the day T. b. brucei infection was established. A sample of heart tissue homogenate was collected weekly across the groups and subjected to biochemical determination of catalase, superoxide dismutase (SOD), glutathione reductase, and glutathione peroxidase concentrations. There were significant differences in the effect of cyanocobalamin on the concentrations of cardiac tissue antioxidant enzymes which were also dependent on the duration of the experiment. At post-treatment, catalase, superoxide dismutase, and glutathione reductase levels differed significantly (p<0.05) from the negative control. There were significant reductions in the levels of catalase, glutathione reductase, glutathione peroxidase, and rise in the SOD level as infections grow. The result, however, showed that cyanocobalamin caused a significant elevation in the catalase, glutathione reductase, reduction in the concentration of SOD and no change in the level of glutathione peroxidase following treatments with cyanocobalamin. In conclusion, there were significant reductions in the level of SOD, evidenced in an increase in the catalase and glutathione reductase levels, and no change in the glutathione peroxidase concentration following treatments with cyanocobalamin.

Active forms of oxygen are formed in the course of the organism's vital activity in biochemical reactions. These forms, when the pro/antioxidant balance is disturbed, trigger a cascade of lipid peroxidation, which can be the cause of the development of various pathological conditions. To prevent the negative influence of lipid peroxidation products in the body, a powerful antioxidant system is activated. This system consists of an enzymatic and a non-enzymatic link. An important aspect of the normal functioning of this system is the provision of the body with important trace elements. A number of minerals are included in the active center of antioxidant enzymes or have an effect on the reactions of non-enzymatic antioxidants. Research was conducted on fattening bulls of the Ukrainian meat breed. During the monitoring of microelements in feed, it was found that the vast majority of farm feed was deficient in copper, selenium and manganese and for this reason the animals consumed an insufficient amount of these minerals. These data were confirmed by the low content of these trace elements in blood serum. The addition of inorganic salts of microelements to the basic diet led to an increase in the concentration of copper, manganese and selenium in the blood serum by 20.5%, 37.3% and 23.9%. The study of the content of lipid peroxidation products showed that during the 30 days of the experiment, the level of lipid hydroperoxide increased by 25.5%, diene conjugates by 22.8%, and malonic dialdehyde by 22.0%. This indicates that against the background of increased age-related metabolism in the body of young animals, the oxidation-reduction reactions that are a predictor of the start of peroxidation processes increase. It was also noted that with a deficiency of certain trace elements, the activity of both the enzymatic and non-enzymatic links of the antioxidant system was reduced. Thus, in 30 days, the level of catalase, superoxide dismutase, and glutathione peroxidase decreased by 9.4%, 15.3%, and 13.0%, respectively. During this time, the content of tocopherol and ceruloplasmin decreased by 16.8% and 9.8%. Additives also had a positive effect on the activity of the antioxidant system by increasing its components. Additives of trace elements had different effects on the activity of antioxidant enzymes. The greatest effect on the level of catalase and superoxide dismutase was observed when copper salts were added, when the increase of these enzymes was noted by 1.11 and 1.23 times, respectively. Accordingly, the level of glutathione peroxidase was the highest in animals that received additional selenium – 1.21 times. The addition of copper also had the greatest biological effect on the important non-enzymatic component of antioxidant protection – ceruloplasmin. Its level increased by 1.24 times under the action of copper sulfate. The level of tocopherol was higher under the action of manganese, when its concentration was 1.11 times higher than the control. Against this background, there was a decrease in the products of lipid peroxidation: lipid hydroperoxides – 1.19 times under the action of selenium; diene conjugates – by 1.22 times and malonіс dialdehyde – by 1.11 times under the influence of copper and manganese compounds, respectively.

We investigate the protective and therapeutic effects of ozone therapy (OT) in radiotherapy (RT)-induced testicular damage. Thirty healthy adult male Wistar rats divided into five groups consisting of six animals each as follows: (1) Control (C), (2) RT, (3) OT, (4) OT + RT, and (5) RT + OT group. Histopathological findings, Johnsen scores, thiobarbituric acid-reactive substances (TBARS), glutathione (GSH), superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) levels were evaluated. RT caused a significant decrease in testicular weight and Johnsen score compared to the control group. In addition, TBARS level was significantly higher, whereas GSH, SOD, catalase, and GPx levels were significantly lower in the RT group when compared to the control group. Pre and postRT OT significantly increased GSH, SOD, catalase, and GPx levels and decreased TBARS level. Furthermore, testicular weight and Johnsen score were increased with OT. The present study showed that OT is protective and therapeutic in radiation-induced testicular damage. OT may be beneficial to the patients who underwent RT.

It has been suggested that the extract of gingko biloba (EGb) may enhance the efficiency of the classic antipsychotic haloperidol in patients with chronic schizophrenia, especially on positive symptoms, and reduce serum superoxide dismutase (SOD) levels. Therefore, we decided to evaluate the therapeutic effect of EGb and to examine the effect of it on the levels of antioxidant enzymes in schizophrenic patients on olanzapine treatment. We hypothesized that EGb would have the beneficial effects on schizophrenic symptoms and might cause reductions in antioxidant enzymes. The subjects were randomly assigned to the two groups: olanzapine plus EGb (group I) (n=15) and olanzapine alone (group II) (n=14). The patients were evaluated at baseline and at week 8 with respect to the Positive and Negative Syndrome Scale (PANSS), serum SOD, catalase (CAT), and glutathion peroxidase (GPX) levels. At baseline, no statistically significant difference regarding the mean total PANSS scores between treatment groups was found. At the evaluation of week 8, a significant difference in mean Scale for the Assessment of Postive Symptoms (SAPS) scores but not in Scale for the Assessment of Negative Symptoms scores between groups was found. Total patients had statistically significant higher serum SOD, CAT and GPX levels compared to control groups at baseline. At 8 weeks, there were significant differences in the mean decrease in SOD and CAT levels but not in GPX levels between treatment groups. The changes in SOD and CAT levels were correlated with the change in SAPS in group I, but not in the group II. The present study supported the findings of the previous study demonstrating that EGb might enhance the efficiency of antipsychotic in patients with schizophrenia, particularly on positive symptoms of the disorder.

Fundamentals of marine acoustics

Evaluation of softwood and hardwood sawmill wastes impact on the common carp "Cyprinus carpio" and its aquatic environment: An oxidative stress study

AIM: One of the problems in treating anemia of CRD is iron deficiency, and intravenous (IV) iron supplementation has become an accepted therapy of iron deficiency in CRD patients. However, it is known that free iron is prooxidant and causes oxidative stress by generation of hydroxyl radicals through the fenton reaction.The purpose of this study was to determine the relationship between IV iron treatment and oxidative stress, and to determine the effect of N-acetylcysteine (NAC), which is an antioxidant, on this possible oxidative stress. MATERIAL and METHOD: 30 patients with iron deficiency anemia and CRD (stage3-5 according to K/DOQI) scheduled to receive IV iron treatment were separated into two groups. One group received only IV iron, and the other group received NAC orally beside IV iron treatment. Malondialdehyde (MDA), glutathione peroxidase (GPx),catalase (CAT) and superoxide dismutase (SOD) levels were measured to determine oxidative stress in each group. RESULTS: The antioxidant enzyme levels of erythrocyte Glutathion peroxidase (GPx) and catalase (CAT) decreased significantly but erythrocyte superoxide dismutase (SOD) activity did not change in the IV iron treatment group. The decrease in CAT levels was prevented with NAC pre-treatment but GPx levels decreased significantly and SOD levels also did not change from the baseline. CONCLUSION: Our study shows that IV iron therapy in CRD changes some oxidative stress parameters.600 mg/d NAC pre-treatment dose not increase the antioxidant effect of IV iron therapy significantly.

To investigate the anti-apoptotic and anti-oxidant effects of systemic uridine treatment in a rat model of sciatic nerve injury. Thirty-two adult male rats were equally randomized to Sham, Control, U100, and U500 groups. Sham rats received a sham operation by exposing the right sciatic nerve without transection, while those in the Control, U100, and U500 groups underwent right sciatic nerve transection followed by immediate primary anostomosis. Sham and Control groups received saline (0.9% NaCl) injections intraperitoneally (i.p.), while U100 and U500 groups received 100 mg/kg and 500 mg/kg uridine injections (i.p.), respectively, once a day for 7 days after the surgery. Rats in all the groups were sacrificed on the eighth day; sciatic nerve samples were analyzed for apoptosis by Western Blotting and for oxidation parameters including myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) by Enzyme-Linked Immunosorbent Assay (ELISA). Uridine treatment at the dose of 500 mg/kg significantly decreased as apoptosis determined by Caspase-3/Actin ratio and exhibited significant anti-oxidant effects as determined by decreased levels of MPO and MDA as well as increased levels of SOD, GPx, and CAT compared to controls. Uridine at 100 mg/kg was only found to decrease the Caspase-3/Actin ratio, although it significantly decreased MDA and increased CAT levels compared to controls. Treatment with uridine reduces apoptosis and oxidation in a rat model of sciatic nerve injury dose-dependently. Thus, uridine may be beneficial in peripheral nerve regeneration by exhibiting anti-apoptotic and anti-oxidant effects.