Effects of sodium arsenite on the some laboratory signs and therapeutic role of thymoquinone in the rats.

OBJECTIVE: Serious health problems in humans are caused by arsenic (As) exposure, which is wide spread in the environment. Sodium arsenite (SAs), capable of inducing macromolecular damage is evaluated for its damaging effect in the blood vessels, liver and kidneys of Wistar rats. This study was undertaken to investigate the ameliorative effects of thymoquinone on SAs-induced oxidative and inflammatory damages in the serum of male Wistar rats. MATERIALS AND METHODS: Wistar Albino rats divided into three groups of nine rats each were administered to controls saline (10 mg/kg), SAs (10 mg/kg), and SAs plus thymoquinone (10 mg/kg/day) for two weeks orally. Biochemical tests were analyzed by a otoanalyzer; nitric oxide levels specthrophometrically, and cytokines were measured by ELISA method in the rat serum samples. RESULTS: Inflammatory cytokines and some biochemical variables were found to be increased in the SAs group compared to control group. On the other hand, thymoquinone supressed these laboratory signs, which are thought to be the characteristic signs of SAs toxicity, most probably by its ameliorative effects including anti-inflammatory and antioxidant properties. CONCLUSIONS: From the results obtained, thymoquinone mitigates SAs-induced adverse effects in the serum of rats, which suggest that it may attenuate inflammation implicated in endotelial dysfunction.

Oxidative stress in acne vulgaris.

BACKGROUND: Acne vulgaris is one of the common dermatological diseases and its pathogenesis is multifactorial. In this study, we aimed to determine the effects of oxidative stress in acne vulgaris. MATERIALS AND METHODS: The study involved 32 patients with acne vulgaris in the patient group and 34 healthy adults in the control group. The parameters of oxidative stress such as catalase (CAT), superoxide dismutase (SOD), xanthine oxidase (XO), nitric oxide (NO) and malondialdehyde (MDA) in the venous blood of patients were measured spectrophotometrically. The values were compared with those of the control group. RESULTS: The serum levels of MDA and XO activity in the patients with acne vulgaris were significantly higher than those of the controls. A significantly lower SOD and CAT activity was found in the patient group than in the control group. Although the patient group had higher serum levels of NO than the control group, the difference was not statistically significant. CONCLUSION: These results suggest that oxidative damage may play a role in the pathogenesis of acne; therefore, significant alterations may occur in the antioxidant defence system.

Purine catabolic enzymes and nitric oxide in patients with recurrent aphthous ulceration.

OBJECTIVES: Recurrent aphthous ulceration (RAU) is one of the most common oral mucosal disorders found in humans. Although the exact etiology of RAU is unkown, local and systemic conditions, and genetic, immunologic, and infectious factors all have been identified as potential etiopathogenic agents. The aim of our study was to compare serum xanthine oxidase (XO) and adenosine deaminase (AD) activities, and malondialdehyde (MDA), nitric oxide (NO) and uric acid (UA) levels in a group of patients affected by RAU and in a group of healthy controls. SUBJECTS AND METHODS: A total of 26 patients with minor RAU were included in the study. Twenty-six healthy volunteers were selected to form the control group. AD and XO activities, and UA, NO, and MDA levels were studied in the serum samples of all patients and controls. RESULTS: Serum XO and AD activities, and MDA, NO, and UA levels were significantly higher in RAU patients than in controls. CONCLUSION: Increased XO and AD activities, NO and UA levels and lipid peroxidation were thought to take part in the pathogenesis of RAU. Hence the effects of XO inhibitors in the treatment of RAU should be evaluated in future studies.

Effects of whole-body hypoxic preconditioning on hypoxia/reoxygenation-induced intestinal injury in newborn rats.

PURPOSE: The precise cause of necrotizing enterocolitis (NEC) is elusive. Ischemia and reperfusion injury of the intestine has been considered to be a major contributing factor for NEC. Ischemic preconditioning is defined as one or more brief periods of ischemia with intermittent reperfusion that protects tissues against a sustained period of subsequent ischemia. Contribution of preconditioning to hypoxia/reoxygenation-induced intestinal injury in newborn rats has not been evaluated previously. METHODS: The study was carried out on 1-day-old Wistar albino rat pups. Whole-body hypoxia and reoxygenation (H/R) was achieved by 10 min hypoxia using 95 % N (2) + 5 % CO (2) followed by 10 min reoxygenation with 100 % oxygen. Whole body hypoxic preconditioning (HP) cycles were performed with 3 min hypoxia and 5 min reoxygenation. Thirty-three pups were randomly allocated into 4 groups. Group 1 served as untreated controls. The pups in group 2 were subjected to H/R only. In groups 3 and 4, 1 cycle and 3 cycles of HP were performed prior to H/R, respectively. Animals were killed at the end of the protocols. Intestine specimens were obtained to determine the histological changes, as well as to measure the tissue malondialdehyde (MDA) and nitric oxide (NO) levels, and xanthine oxidase (XO) and myeloperoxidase (MPO) activities. RESULTS: The microscopic lesions in H/R rat pups were virtually the same as those seen in neonatal NEC, with severe destruction of villi and crypts, in some cases extending to the muscularis. In both HP groups, the lesions were found to be milder. H/R resulted in a marked elevation in MDA and NO levels, and XO and MPO activities compared to the untreated controls. Both 1 cycle and 3 cycles of HP prior to H/R resulted in an obvious decrease in all biochemical parameters. Differences of the biochemical results between both HP groups were not statistically significant. CONCLUSION: This study revealed that whole-body hypoxic preconditioning is beneficial for hypoxia/reoxygenation-induced intestinal injury in newborn rats.

Vitamin E protects against acetone-induced oxidative stress in rat red blood cells.

Acetone may induce oxidative stress leading to disturbance of the biochemical and physiological functions of red blood cells (RBCs) thereby affecting membrane integrity. Vitamin E (vit E) is believed to function as an antioxidant in vivo protecting membranes from lipid peroxidation. The aim of the present study was the evaluation of possible protective effects of vit E treatment against acetone-induced oxidative stress in rat RBCs. Thirty healthy male Wistar albino rats, weighing 200-230 g and averaging 12 weeks old were randomly allotted into one of three experimental groups: Control (A), acetone-treated (B) and acetone + vit E-treated groups (C), each containing ten animals. Group A received only drinking water. Acetone, 5% (v/v), was given with drinking water to B and C groups. In addition, C group received vit E dose of 200 mg/kg/day i.m. The experiment continued for 10 days. At the end of the 10th day, the blood samples were obtained for biochemical and morphological investigation. Acetone treatment resulted in RBC membrane destruction and hemolysis, increased thiobarbituric acid reactive substance (TBARS) levels in plasma and RBC, and decreased RBC vit E levels. Vit E treatment decreased elevated TBARS levels in plasma and RBC and also increased reduced RBC vit E levels, and prevented RBC membrane destruction and hemolysis. In conclusion, vit E treatment appears to be beneficial in preventing acetone-induced oxidative RBC damage, and therefore, it can improve RBC rheology.

Caffeic acid phenethyl ester improves oxidative organ damage in rat model of thermal trauma.

Severe burn injuries cause functional impairment in distant internal organs. Although this mechanism is not clear, it is possible that free radical toxicity plays an important role. Research in animals and clinical studies have shown that there is a close relationship between a lipid peroxidative reaction and secondary pathological changes following thermal injury. It has been demonstrated that antioxidant treatment prevents oxidative tissue damage associated with thermal trauma. This study was designed to determine the possible protective effect of caffeic acid phenethyl ester (CAPE) treatment against oxidative damage in the kidney and lung induced by thermal injury. Rats were decapitated either 1, 3 or 7 days after burn injury. CAPE was administered intraperitoneally immediately after thermal injury. Kidney and lung tissues were taken for the determination of malondialdehyde (MDA) level, myeloperoxidase (MPO), catalase (CAT), superoxide dismutase (SOD) and xanthine oxidase (XO) activities. Severe skin thermal injury caused a significant decrease in SOD and CAT activities, as well as significant increases in MDA level, XO and MPO activities in tissues during the postburn period. Treatment of rats with CAPE (10 micromol/kg) significantly elevated the decreased SOD and CAT activities, while it decreased MDA levels and MPO as well as XO activity.

Erdosteine improves oxidative damage in a rat model of renal ischemia-reperfusion injury.

The aim of the present study was to determine the effects of erdosteine, a new antioxidant and anti-inflammatory agent, on lipid peroxidation, neutrophil infiltration, and antioxidant enzyme activities in a rat model of renal ischemia-reperfusion (I/R) injury. Twenty-eight rats were divided into three groups: sham operation, I/R, and I/R plus erdosteine groups. After the experimental procedure, rats were sacrificed and kidneys were removed and prepared for malondialdehyde (MDA) levels, myeloperoxidase (MPO), xanthine oxidase (XO), catalase (CAT) and superoxide dismutase (SOD) activities. MDA level, MPO and XO activities were significantly increased in the I/R group. On the other hand, SOD and CAT activities were found to be decreased in the I/R group compared to the sham group. Pretreatment with erdosteine significantly diminished tissue MDA level, MPO and XO activities. Our data support a role for erdosteine in attenuation in renal damage after I/R injury of the kidney, in part at least by inhibition of neutrophil sequestration and XO activity.

Oxidant-antioxidant enzymes and lipid peroxidation in generalized vitiligo.

Vitiligo is a common pigmentary disorder of the skin with selective destruction of melanocytes. The pathogenetic mechanisms in vitiligo have not been completely clarified. The aim of our investigation was to evaluate the oxidative stress in the pathogenesis of generalized vitiligo. Twenty-seven patients with generalized vitiligo and 24 phototype-, age-, and sex-matched healthy controls were included in this study. We analysed serum levels of malondialdehyde (MDA), nitric oxide (NO), and serum activities of superoxide dismutase (SOD) and xanthine oxidase (XO) in the patients with vitiligo and in the controls. We found significantly higher levels of MDA and XO activity (P < 0.001 and P < 0.05, respectively), and a significantly lower level of serum SOD activity (P < 0.05) in patients with vitiligo compared with the controls. However, the increase in the level of serum NO was insignificant (P > 0.05). These results suggest that lipid peroxidation of cellular membrane of melanocytes by free radicals may have a significant role in the pathogenesis of generalized vitiligo.

Alterations in plasma essential trace elements selenium, manganese, zinc, copper, and iron concentrations and the possible role of these elements on oxidative status in patients with childhood asthma.

The aim of the present study is to evaluate the status of plasma essential trace element selenium (Se), manganese (Mn), copper (Cu), zinc (Zn), and iron (Fe) concentrations and the effect of these elements on oxidative status in patients with childhood asthma. Plasma Se, Mn, Cu, and Zn concentrations were determined by atomic absorption spectrophotometry (AAS) and Fe concentrations, malondialdehyde (MDA), and total antioxidant capacity (TAC) were determined by the colorimetric method. The plasma MDA/TAC ratio was calculated as an index of oxidative status. Plasma albumin levels were measured to determine nutritional status. Plasma Fe concentrations, MDA levels and the MDA/TAC ratio were significantly higher (p<0.001, p<0.001, and p<0.01, respectively) and Se and Mn concentrations and TAC were lower (p<0.01, p<0.05, and p<0.01, respectively) in patients when compared to the healthy subjects. Plasma Zn, Cu, and albumin levels were not found to be significantly different in patients and controls (p>0.05). There were positive relationships between plasma MDA and Fe (r=0.545, p<0.001) and TAC and Se (r= 0.485, p<0.021), and a negative correlation between TAC and MDA values (r= -0.337, p<0.031) in patients with childhood asthma. However, there was no correlation between these trace elements and albumin content in patient groups. These observations suggest that increased Fe and decreased Se concentrations in patients with childhood asthma may be responsible for the oxidant/antioxidant imbalance.