Barbaros Balabanli

The effects of vitamin C supplementation on oxidative stress and antioxidant content in the brains of chronically exercised rats.

The purpose of this study was to ascertain whether vitamin C supplementation during chronic exercise training alters rat brain antioxidant content. Female Wistar albino rats were exercised on a treadmill for 30 min/day for 6.5 weeks and were administered daily intraperitoneal injections of vitamin C (20 mg/kg). After the training period, chronically exercised rats showed no significant changes in total brain thiobarbituric acid reactive substances (TBARS) levels. In contrast, rats supplemented with vitamin C during the training period showed significantly elevated brain TBARS levels. If such results were extrapolated to man, where vitamin supplementation is a common practice, this would indicate that vitamin C supplementation may not protect brain tissue against exercise-induced oxidative damage, in such circumstances, this water-soluble antioxidant behaves as a pro-oxidant. (Mol Cell Biochem xxx: 135–138, 2005)

The effects of EGb 761 on lipid peroxide levels and superoxide dismutase activity in sunburn

Background/Purpose: Free oxygen radicals are involved in inflammatory skin reactions induced by ultraviolet B (UVB). In this study, the effect of a herbal antioxidant Ginkgo biloba extract (EGb 761) was investigated in UVB irradiated mice skin.

Effects of Continuous and Intermittent Magnetic Fields on Oxidative Parameters In vivo

Continuous and intermittent 50 Hz, 1.5 mT magnetic field with the exposure period of 4 h/day for 4 days was used to investigate its possible effect on adult guinea pigs. Tissues and plasma specimens were assessed by biochemical parameters. Malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO) levels and myeloperoxidase activity (MPO) were examined in plasma, liver and brain tissues. All parameters were determined by spectrophotometer. While intermittent magnetic field was effective on plasma lipid peroxidation, continuous magnetic field was found to be effective on plasma MPO activity and NO levels. Augmentation of lipid peroxidation was also observed in liver tissue both intermittent and continuous magnetic field exposures. These results indicate that both the intermittent and continuous magnetic field exposures affect various tissues in a distinct manner because of having different tissue antioxidant status and responses.

Changes in zinc levels and superoxide dismutase activities in the skin of acute, ultraviolet-B-irradiated mice after treatment with ginkgo biloba extract.

Acute ultraviolet-B (UV-B) irradiation is known to act as an initiator in the formation of reactive oxygen species. These oxygen products are highly reactive and they are able to cause irreversible damage to cellular components. Oxygen free radicals are normally neutralized by very efficient systems in the body. These include antioxidant enzymes like superoxide dismutase (SOD). In a healthy subject, there is a balance between free radicals and the levels of antioxidants. In some pathological conditions such as oxidative stress, the level of antioxidants is significantly reduced. The skin contains relatively high levels of zinc (Zn), an essential element known to be a cofactor in some metabolic pathways. Zinc has also been reported to have antioxidant properties.In the present study, we investigated the effect of ginkgo biloba extract (Gbe), a potent free-radical scavenger, on UV-B-irradiated skin by measuring SOD activity and Zn levels in the skin, before and after treatment. The SOD activity was decreased after UV-B exposure, in comparison with the control group (p<0.05). After Gbe treatment, the SOD activity increased (p<0.05) as compared with the untreated UV-B irradiated group. The Zn levels changed in the same pattern as the SOD activity values.

Effects of Epidermal Growth Factor on Lipid Peroxidation and Nitric Oxide Levels in Oral Mucosal Ulcer Healing: A Time-Course Study

PurposeEpidermal growth factor (EGF) has been used as a vulnerary agent. Epidermal growth factor accelerates wound healing. Nitric oxide (NO) is considered to be an important factor which is involved in wound healing. The objective of this study was to examine the effects of interactions between exogenous EGF and NOx which may have either similar or quite opposed properties in the process of oral wound repair on different days. In addition, lipid peroxidation was found to be an indicator of free radical damage.MethodsFive-month-old New Zealand albino male rabbits were used for this study. A surgical incision was made in the right mandibula diestema region of the rabbits, which were then divided into controls and EGF implanted groups. All parameters were analyzed by spectrophotometry.ResultsIn the EGF-implanted groups, both the NOx and lipid peroxidation indicator levels significantly decreased in comparison to those of the control groups on the first day after wounding. However, on the 3rd and 5th days after wounding, the NOx levels of the tissue strips also decreased in both modalities, but there was no significant alteration between the 3rd and 5th day after wounding.ConclusionIt was concluded that EGF affects oral wound healing by downregulating both the lipid peroxidation and NOx levels, and it may thus be considered to be an oxygen radical scavenger.

Effect of transforming growth factor beta 1 (TGF-beta 1) on nitric oxide production and lipid peroxidation in oral mucosal wound healing

Wound healing is a highly orchestrated process including complex and coordinated interactions involving peptide growth factors of which transforming growth factor-beta (TGF-beta) is one of the most important modulators. Exogenous TGF-beta treatment has been shown to accelerate wound healing in normal and impaired animal models. Nitric oxide (NO) also plays a key role in wound healing. The objective of this study is to examine the effects of exogenous TGF-beta 1 treatment on NO and lipid peroxidation levels in the process of oral wound healing on different days. In this study, we used 5-month-old New Zealand albino male rabbits. After a standard surgical incision in the diestema region, the rabbits were divided into controls and TGF-beta 1 implanted groups. NO levels and malondialdeyhde (MDA) levels which are indicators of lipid peroxidation were determined by spectrophotometry. In the TGF-beta 1 implanted groups, both NO and MDA levels significantly increased only on the third day after wounding when compared to control groups. We found decreased MDA levels parallel to NO levels on the fifth day after wounding. These findings suggest that TGF-beta 1 affects mucosal wound healing by altering NO production on different days of wounding. TGF-beta 1 may regulate NO production by its dual effect in as both an activator and inhibitor an in oral mucosal healing.

Application of platelet derived growth factor-BB and diabetic wound healing: the relationship with oxidative events

Abstract The reasons that cause delay in wound healing in diabetes are a decrease in the level of growth factors secretion, an increase in the destruction of growth factors and in oxidative stress. Platelet derived growth factor (PDGF) is one of the important growth factors that play a role in all phases of wound healing. This study investigates time-dependent effects of topically PDGF-BB administration on oxidative events on the healing of dorsolateral-excisional wounds in diabetic rats. Forty-two female Wistar-albino rats with streptozotocin-induced diabetes were divided into four groups: control group, untreated group, chitosan-treated group, chitosan + PDGF-BB-treated group. Two identical full-thickness excisional skin wounds were made under anaesthesia in all rats except for the control group. In the PDGF-BB-treated and chitosan-treated groups, the wounds were treated topically PDGF-BB (7 ng/mL, single daily dose) and blank chitosan gel (equal amount) after wounding, respectively. After these administrations, on day 3 and day 7 of wound healing, rats were sacrificed. Thiobarbituric acid reactive substances, glutathione, nitric oxide, ascorbic acid levels, and superoxide dismutase activity in wound tissues were spectrophotometrically measured. PDGF-BB administration significantly increased TBARS levels and non-enzymatic antioxidant levels in early phase of diabetic wound healing. PDGF-BB dramatically reduced NOx levels on day 3 and sharply increased NOx levels on day 7 of wound healing. Consequently, PDGF-BB administration can be effective on oxidative balance in the early phase of diabetic wound healing.

The effect of vitamin A pretreatment on radiation induced alteration in neutrophil functions.

The aim of this investigation was to determine whether pre-administration of vitamin A will be effective in preventing the radiation-induced decline in MPO-H2O2 system and the end product of reactive nitrogen species (NOx) in guinea pig. Animals were subjected to 612 cG of radiation and polimorfonuclear leukocytes were isolated and then NOx and myeloperoxidase activity were measured. In irradiated animals, a marked decrease in NOx level and myeloperoxidase activity have been found compared to control (p = 0.001 and p < 0.000 respectively). The application of vitamin A significantly improved the radiation-induced decrease (for both p < 0.00). In conclusion pre-treatment of vitamin A is efficient to protect against radiation induced alteration in polimorfonuclear leukocyte.

Role of free radicals on mechanism of radiation nephropathy

Purpose: In our study, after applying a single dose of 612 cGy irradiation, we aimed to observe the role of free radicals on tissue damage in the kidney caused by radiation by measuring NO level, Na/K-ATPase activity and TBARS amount which is an indicator of free radical damage. On the other hand we investigated whether the tissue damage can be prevented by vitamin A or not. Materials and methods: This study was performed on three groups: 1. Control group 2. The group to which irradiation was administrated 3. The group which was given radiation + vitamin A. The irradiation group of animals were given a single dose of gamma irradiation at a sublethal dose. In the group which was administrated both irradiation + vitamin A, vitamin A was given for two days prior to irradiation. The amount of NO was measured by ESR spectroscopy, Na/K-ATPase and TBARS were measured by spectrophotometry. Results and conclusions: As a result of radiation mediated tissue damage in the kidney, we observed a NO loss, a decrease in Na/K-ATPase activitiy and an increase in TBARS amount. Although the administration of vitamin A before radiation, did not have any effect on NO loss and decrease in Na/K-ATPase.

Exacerbative role of vitamın A on radiation damage in vivo

Purpose In our study, after applying a single dose of 612 cGy irradiation, we aimed to observe the role of free radicals on tissue damage in liver caused by irradiation, by measuring the nitric oxide (NO) level, superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzyme activities, and the amount of thiobarbituric acid reactive substance (TBARS), which is an indicator of free-radical damage. On the other hand we investigated whether tissue damage can be prevented by vitamin A or not. Materials and methods The study was performed on three groups: (1) the control group, (2) the group to which irradiation was administrated, and (3) the group which was given irradiation + vitamin A. The irradiation group of animals was given a single dose of gamma irradiation at a sublethal dose. In the group to which both irradiation and vitamin A were administered, vitamin A was given for 2 days prior to irradiation. The amount of NO was measured by electron spin resonance (ESR) spectroscopy, whereas SOD, GPx and TBARS were measured by spectrophotometry. Results and conclusion As a result of irradiation-mediated tissue damage in liver, we observed a NO loss and an increase in TBARS amount. Administration of vitamin A before irradiation resulted in an increase in both NO and TBARS and a decrease in SOD and GPx enzyme activities. Together, these data indicate that vitamin A may play an exacerbative role in free-radical-mediated tissue damage.