Objective. The purpose of this study is to determine the changes in oxidative damage and antioxidant parameters in open heart surgeries with cardiopulmonary bypass (CPB) in preoperative and early postoperative periods. Methods. A total of three consecutive arterial blood samples were obtained from the patients in the study group, in preoperative, early postoperative, and postoperative periods, respectively. Oxidative damage indicator (MDA) and antioxidant indicators (GPx, GSH, CAT, and SOD) were examined. Results. A statistically significant increase was observed in MDA level in postoperative period compared to preoperative and early postoperative periods. GSH levels and CAT activities increased significantly in early postoperative and postoperative periods. Analyses revealed an increase in GPx and SOD enzyme activities only in the postoperative period. Conclusion. Even though the increase in MDA level was suppressed by the increased GSH level and CAT activity like in early postoperative period, efficiency can be brought for the increases in insufficient significant antioxidant parameters in postoperative period by administering antioxidant supplements to the patients and thus the increase in MDA in postoperative period can be significantly suppressed.

In this study, the anti-oxidant and anti-inflammatory efficacy of ozone oxidative preconditioning (OOP) were investigated on hydrogen peroxide (HO)-induced human lung alveolar cells. In MTT and trypan blue viability tests, while 100 μmol/L HO caused a 17.3% and 21.9% decrease in the number of living cells, respectively, ozone at 20 μmol/L regenerated cell proliferation and prevented 9.6% and 11.0% of cell loss, respectively. In addition, HO decreased the transcription levels of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) 5.43-, 2.89-, and 5.33-fold, respectively, while it increased Bax, NF-κβ, TNF-α, and iNOS expression 1.57-, 1.32-, 1.40-, and 1.41-fold, respectively. Ozone pretreatment, however, increased CAT, GPx, and SOD transcription levels 7.08-, 5.17-, and 6.49-fold and decreased Bax, NF-κβ, TNF-α, and iNOS transcriptions by 1.25-, 0.76-, 3.63-, and 7.91-fold, respectively. Moreover, intracellular glutathione (GSH) level and SOD activity were decreased by 46.2% and 45.0% in the HO treatment group, and OOP recovered 58.5% and 20.1% of the decreases caused by HO. HO also increased nitrite levels 7.84-fold, and OOP reduced this increase by half. Consequently, OOP demonstrated potent anti-oxidant and anti-inflammatory effects on in vitro model of oxidative stress-induced lung injury.

Graphical abstract

Fructose corn syrup is cheap sweetener and prolongs the shelf life of products, but fructose intake causes hyperinsulinemia, hypertriglyceridemia, and hypertension. All of them are referred to as metabolic syndrome and they are risk factors for cardiovascular diseases. Hence, the harmful effects of increased fructose intake on health and their prevention should take greater consideration. Caffeic Acid Phenethyl Ester (CAPE) has beneficial effects on metabolic syndrome and vascular function which is important in the prevention of cardiovascular disease. However, there are no known studies about the effect of CAPE on fructose-induced vascular dysfunction. In this study, we examined the effect of CAPE on vascular dysfunction due to high fructose corn syrup (HFCS). HFCS (6 weeks, 30% fed with drinking water) caused vascular dysfunction, but treatment with CAPE (50 micromol/kg i.p. for the last two weeks) effectively restored this problem. Additionally, hypertension in HFCS-fed rats was also decreased in CAPE supplemented rats. CAPE supplements lowered HFCS consumption-induced raise in blood glucose, homocysteine, and cholesterol levels. The aorta tissue endothelial nitric oxide synthase (eNOS) production was decreased in rats given HFCS and in contrast CAPE supplementation efficiently increased its production. The presented results showed that HFCS-induced cardiovascular abnormalities could be prevented by CAPE treatment.

Aim: Tobacco smoke negatively affects the male reproductive system. Ellagic acid (EA) has protective effects against oxidative damage. The aim of the study was to examine the protective effects of EA on testis of rats exposed to tobacco smoke. Material and Methods: Twenty-four male Spraque-Dawley rats were divided into 4 groups (n=6): Control, tobacco smoke (TS), tobacco smoke+corn oil (TS+C) and tobacco smoke+ EA (TS+EA). TS, TS+C and TS+EA groups were exposed to tobacco smoke 1 hour twice a day and EA was applied 12 mg/kg every other day. Testis tissues were removed. eNOS immunohistochemical stain and TUNEL methods were applied. Biochemical analyzes and sperm analyzes were performed. Results: Degeneration in germinative epithelium, cell debris in the seminiferous tubule lumen, seperation in basement membrane, atrophic tubules, vascular congestion and edema in interstitial area were observed in TS and TS+C groups. Increased apoptotic cells and eNOS immunreactivity were observed in TS and TS+C groups. EA administration caused a decrease in histological alterations, eNOS immunreactivity and apoptotic cells. Increased MDA levels, decreased CAT and GSH-Px activities were observed in TS and TS+C groups. MDA levels decreased, CAT and GSH-Px activities increased in TS+EA group. A significant increase in the amount of abnormal sperm was detected in TS and TS+C groups. The reduction in the amount of abnormal sperm was detected in TS+EA group. Conclusions: Exposure to TS led to marked alterations on testes tissue and treatment with EA might prevent these toxic effects.

Purpose:The aim of this study is to evalute the anti-inflammatory effects of morus migra on experimentally-induced periodontitis in rats.Materials and methods:Twenty-four Wistar-albino rats were randomly divided into three groups: control group (C, n=8), experimental periodontitis (PER, n=8), experimental periodontitis and treated with Morus nigra (MN+PER, n=8) (50 mg/kg per day for 21 days). After 21 days, the rats were sacrificed, and alveolar bones were evaluated histopathologically and histometrically analyzed to obtain level of alveolar bone loss. The detection of RANKL and OPG were immunohistochemically performed. Serum and tissue levels of MMP-8 and MMP-13 were also analyzed.Results:Morus nigra treatment decreased tissue MMP-8 and MMP-13 levels and there were significant differences in the case of tissue levels of MMP-8 and MMP-13 between groups PER and MN+PER (p=0.035, p=0.041). There were no significant differences among all the groups serum levels of MMP-8 and MMP-13 (p=0.067, p=0.082). In the histometric evaluation, alveolar bone loss was greater in the PER group compared to C and MN groups (p=0.035). Immuno-histochemical staining of RANKL activities were found significantly lower (p=0.037) and OPG activities were found significantly higher in MN+PER group when compared to PER group (p=0.021).Conclusion:The present study reveals that systemic administration of Morus nigra significantly inhibited the regional alveolar bone resorption and contributes to periodontal healing in the rat experimental-periodontitis models.

Objective: Metabolic syndrome (MetS), one of the common health problems seen with increasing frequency in today’s modern societies, is also a important risk factor for neurological disorders such as stroke, depression, Alzheimer’s disease. On the other hand, melatonin is a neurohormone, has potent antioxidant and neuroprotective activities. In the present study, we aimed to investigate the possible protective effects of melatonin administration on brain tissue in fructose-mediated MetS model.Methods: Male adult Sprague-Dawley rats were randomly divided into four groups (n=8); control, fructose, melatonin and fructose plus melatonin. MetS was induced by fructose solution 20% in tap water, and melatonin was administered at the dose of 20 mg/kg bw/day by oral gavage. Systolic blood pressures (SBP) were measured by tail-cuff method. After the experimental period of 8 weeks, serum triglyceride, glucose, insulin, and tissue ATP/ADP ratio, nitric oxide (NOx) and 3-nitrotyrosine (3-NT) levels were measured. Also tissue endothelial and inducible nitric oxide synthase (eNOS and iNOS) protein levels were determined.Results: Fructose consumption increased SBP, serum triglyceride, insulin levels and induced insulin resistance significantly compared to control group and MetS model was successfully demonstrated. In comparison with control group, fructose administration did not cause significant changes in tissue ATP/ADP ratio and 3-NT levels. NOx levels did not change significantly among groups, and iNOS-eNOS proteins were not detected in any groups. Interestingly, tissue 3-NT levels were elevated significantly while ATP/ADP ratio was diminished in fructose plus melatonin group compare with both control and fructose groups.Conclusion: These results indicate that high fructose diet for 8 weeks does not influence nitric oxide production, energy metabolism and protein nitration in brain. Nevertheless melatonin acted as a pro-oxidant at that dose when administered with fructose.