Evaluation of oxidative stress and antioxidant parameters in children with carbon monoxide poisoning.

OBJECTIVE: In this study, we aimed to investigate oxidative stress and antioxidant parameter levels in patients with carbon monoxide (CO) poisoning. METHODS: The study was conducted prospectively between March 1, 2015 and April 30, 2016 in the pediatric emergency department. Eligible patients included children aged 0-18 years old with a diagnosis of CO poisoning. To determination of oxidative stress and antioxidant parameter levels, venous blood with heparinized and urine samples were drawn during the admission and after normobaric oxygen (NBO) and hyperbaric oxygen (HBO) treatment. RESULTS: Forty-seven children with CO poisoning for study group and 29 patients as control group were included to the study. Sixteen patients treated with HBO. Basal plasma malondialdehyde levels were found to be significantly higher in the CO poisoning group when compared with the control group (p = 0.019). There is no significant difference in oxidative stress and antioxidant parameter levels except erythrocyte catalase enzyme levels in patients treated with NBO when comparing before and after NBO treatment (p > 0.05). Decreasing of basal erythrocyte catalase enzyme levels were found statistically significant after NBO treatment (p = 0.04). There was no significant difference in oxidative stress and antioxidant parameter levels in patients treated with HBO before and after therapy (p > 0.05). CONCLUSIONS: CO poisoning is associated with increased lipid peroxidation in children immediately after the poisoning. However, both treatment modalities including NBO or HBO do not have a significant effect on oxidative stress or antioxidant parameter levels.

Evaluation of oxidative and antioxidative parameters in pediatric hematopoietic SCT patients.

Conditioning regimens preceding hematopoietic SCT (HSCT) usually consist of high-dose chemotherapy. Chemotherapy and radiation therapy are associated with increased formation of free radicals and depletion of critical plasma and tissue antioxidants. Oxidative stress and antioxidant depletion have been described during the transplantation period in HSCT patients. In a limited number of studies, it was observed that the conditioning regimen resulted in oxidative stress and antioxidant depletion in HSCT patients. The objective of this study was to look for further evidence of oxidative stress and antioxidant status in pediatric HSCT patients. In this study, blood samples were collected from 21 pediatric allo-HSCT patients before and after conditioning therapy. Erythrocyte and plasma malondialdehyde (MDA) levels, erythrocyte reduced and oxidized glutathione (GSH) levels, erythrocyte antioxidant enzymes activities, plasma α-tocopherol and ß-carotene levels were determined. After high-dose chemotherapy, erythrocyte and plasma MDA levels increased. Reduced GSH levels decreased whereas oxidized GSH levels increased first and then decreased significantly compared with the values before the chemotherapy regimen. It was also observed that catalase, superoxide dismutase and GSH-S-transferase activities decreased, but there was no change in GSH peroxidase activity. On the other hand, plasma α-tocopherol levels increased, but ß-carotene levels did not change.

Hypocholesterolemia is associated negatively with hemolysate lipid peroxidation in sickle cell anemia patients.

The oxidative stress levels in plasma and hemolysate and cholesterol levels in plasma of sickle cell anemia patients, carriers and controls were evaluated. A total of 40 cases-17 patients, 13 carriers and 10 controls-were involved in the study. Plasma and hemolysate malondialdehyde (MDA) were detected via thiobarbituric acid reaction with a fluorimetric detector by high-performance liquid chromatography system. Plasma cholesterol was determined by enzymatic colorimetric method. Mean MDA levels of SCA patients were higher than those of the carriers' and healthy children's both in plasma and in hemolysate (P < 0.005). The mean plasma and hemolysate MDA levels were 25.3 ± 1.6 nmol/l and 86.7 ± 19.3 nmol/l in patients, 19.1 ± 0.8 nmol/l and 54.1 ± 10.8 nmol/l in carriers and 19.6 ± 0.8 nmol/l and 56.8 ± 9.3 nmol/l in healthy children. Mean plasma total cholesterol levels were 92.1 ± 19.1 mg/dl in patients, 116.2 ± 23.3 mg/dl in carriers and 126.6 ± 16.4 mg/dl in controls (P < 0.005). There was a significant negative correlation of -0.520 between hemolysate MDA and plasma cholesterol levels in patients (P < 0.05). The degree of correlation increased up to -0.782 (P = 0.008) in the patients with HbSS phenotype. This negative correlation between MDA and cholesterol may imply a potential association between oxidative stress and hypocholesterolemia in sickle cell anemia.

Preventive effect of aminoguanidine compared to vitamin E and C on cisplatin-induced nephrotoxicity in rats.

In this study, the antioxidant effect of aminoguanidine on nephrotoxicity of a single dose of cisplatin is investigated and compared with the effects of well-known antioxidants vitamin C and E combination. Tubular damage and perivascular inflammation were observed in kidney samples of the cisplatin-administered groups. Aminoguanidine and vitamin C-E combination are found to be capable of preventing these effects of cisplatin. Liver tissues of all groups were intact. Cisplatin-induced oxidative stress was evidenced by significant decrease in glutathione and significant increase in malondialdehyde levels in kidney samples. Antioxidants with cisplatin decreased malondialdehyde levels. Antioxidants with cisplatin prevented the decrease in liver glutathione levels. The nephrotoxicity was confirmed biochemically by significant elevation of serum urea and creatinine levels. Both vitamin C-E combination and aminoguanidine prevented the increase in serum urea levels according to the cisplatin group.

Antioxidant effect of taurine against lead-induced oxidative stress.

Oxidative stress is proposed as a molecular mechanism in lead toxicity, which suggests that antioxidants might play a role in the treatment of lead poisoning. The present study was designed to investigate whether taurine has a beneficial effect both on Chinese hamster ovary (CHO) cells and on Fisher 344 (F344) rats following lead exposure. Therefore, oxidative stress parameters (glutathione, malondialdehyde levels, catalase, and glucose-6-phosphate dehydrogenase [G6PD] activities) of lead-exposed CHO cells and F344 rats were determined following taurine treatment. Taurine was found to be effective in (1) increasing glutathione levels that had been diminished by lead; (2) reducing malondialdehyde levels, an end-product of lipid peroxidation; (3) decreasing catalase and erythrocyte G6PD activity, which had been increased by lead exposure; and (4) improving cell survival of CHO cells. However, taurine had no effect on blood and tissue lead levels when 1.1 g/kg/day taurine was administered to F344 rats for 7 days, following 5 weeks of lead exposure (2,000 ppm lead acetate). As a result, taurine seems to be capable of fortifying cells against lead-induced oxidative attack without decreasing lead levels. Therefore, administration of taurine, accompanied by a chelating agent, might increase its effectiveness in the treatment of lead poisoning.

Antioxidant role of alpha-lipoic acid in lead toxicity.

The assumption of oxidative stress as a mechanism in lead toxicity suggests that antioxidants might play a role in the treatment of lead poisoning. The present study was designed to investigate the efficacy of lipoic acid (LA) in rebalancing the increased prooxidant/antioxidant ratio in lead-exposed Chinese hamster ovary (CHO) cells and Fischer 344 rats. Furthermore, LA's ability to decrease lead levels in the blood and tissues of lead-treated rats was examined. LA administration resulted in a significant improvement in the thiol capacity of cells via increasing glutathione levels and reducing malondialdehyde levels in the lead-exposed cells and animals, indicating a strong antioxidant shift on lead-induced oxidative stress. Furthermore, administration of LA after lead treatment significantly decreased catalase and red blood cell glucose-6-phosphate dehydrogenase activity. In vitro administration of LA to cultures of CHO cells significantly increased cell survival, that was inhibited by lead treatment in a concentration-dependent manner. Administration of LA was not effective in decreasing blood or tissue lead levels compared to a well-known chelator, succimer, that was able to reduce them to control levels. Hence, LA seems to be a good candidate for therapeutic intervention of lead poisoning, in combination with a chelator, rather than as a sole agent.

Antioxidant effects of N-acetylcysteine and succimer in red blood cells from lead-exposed rats.

This study examined whether lead-induced alterations in selected parameters that are indicative of oxidative stress accompany the toxic effects of lead in red blood cells (RBCs) in vivo. It also explored the possibility that treatment with N-acetylcysteine (NAC) or succimer (meso-2,3-dimercaptosuccinic acid) was capable of reversing parameters indicative of lead-induced oxidative stress. Fisher 344 rats were given 2000 ppm lead acetate in their drinking water for 5 weeks. The lead was then removed and the animals were given NAC (800 mg/kg/day) or succimer (90 mg/kg/day) in their drinking water for 1 week, after which the RBCs were harvested. Animals not given lead and those given lead, but not NAC or succimer, served as negative and positive controls, respectively. At the end of the experiment, blood-lead levels were 35 +/- 4 microg/dl in lead-treated animals, which were reduced to 2.5 +/- 1 microg/dl by treatment with succimer and to 25 +/- 3 microg/dl by treatment with NAC. Lead-exposed animals demonstrated signs of anemia as evidenced by anisocytosis, poikilocytosis, and alterations in hemoglobin, hematocrit, and mean corpuscular volume. Lipid peroxidation, as evidenced by increased malondialdehyde (MDA) content, as well as decreases in reduced glutathione (GSH) and increases in catalase and glucose 6-phosphate dehydrogenase (G6PD) activity were noted in RBCs from lead-treated rats, suggesting that the lead induced oxidative stress. In addition, a significant reduction in blood delta-aminolevulinic acid dehydratase (ALAD) activity suggested that accumulation and autooxidation of delta-aminolevulinic acid might contribute to lead-induced oxidative stress. Treatment with either NAC or succimer reversed lead-induced alterations in MDA and GSH content, but only succimer appeared to partially restore ALAD activity. These results provide in vivo evidence supporting the hypothesis that lead induces oxidative stress in RBCs, which is reversible by treatment with a thiol antioxidant (NAC), as well as a chelating agent (succimer).

Serum protein and zinc levels in patients with thoracic empyema.

The element Zn is the metal component or activator of many important enzymes. The tissue concentrations and activities of Zn metalloenzymes direct the rate of protein and nucleic acid syntheses, thereby influencing tissue growth and reperative processes. Most of the serum Zn is normally bound to circulating proteins. Low serum Zn concentrations might result from depletion of Zn-binding proteins. Serum protein and Zn concentrations have been reported to be depressed in patients with acute and chronic diseases. We compare the serum protein and Zn values of patients with thoracic empyema (n = 20) with those of a control group (n = 20). The values obtained in the empyema group were significantly lower than those in the control group before the study. Test group administered 220 mg zinc sulfate (ZnSO4.7H2O) over 20 d and there was a significant increase in the values for serum protein and Zn after the oral administration of the zinc sulfate.

Serum and parotid saliva testosterone, calcium, magnesium, and zinc levels in males, with and without periodontitis.

Fourteen male patients with periodontitis and 10 patients free of periodontitis were included in the study. The concentrations of testosterone (T), calcium (Ca), magnesium (Mg), and zinc (Zn) were measured in serum and parotid saliva. Patients with periodontitis had increased Ca and decreased Zn serum levels, and they had decreased Ca and increased T levels in parotid saliva. Furthermore, there was a low correlation between parotid saliva T and Mg levels in the patients with periodontitis (r = 0.61, n = 14, t = 2.663, p less than 0.005), and there is an inverse relationship between serum and parotid saliva Mg levels (r = - 0.58, n = 14, t = 2.468, p less than 0.05).

Zinc in tears.

The tear and serum zinc (Zn) levels were determined simultaneously by atomic absorption spectrophotometry in 11 healthy subjects. The mean tear Zn level was found to be 1.537 +/- 0.146 (SEM) ppm while the mean serum Zn level was found to be 1.03 +/- 0.046 (SEM) ppm.

Instant effect of induced abortion on serum ceruloplasmin activity, copper and zinc levels.

Serum ceruloplasmin activity, serum copper and zinc levels were determined in 20 patients aged 19-43 with normal pregnancies of first trimester (5-9 weeks) admitted to hospital for legal abortion. Blood samples were taken from each patient 30 min before and 3 h after induced abortion. Significantly reduced ceruloplasmin activity (P less than 0.01) and serum copper level (P less than 0.05) were observed following induced abortion while zinc level didn't demonstrate any significant change (P greater than 0.05). A high degree of correlation was observed between the ceruloplasmin activity and the serum copper level (r = 0.87). Ceruloplasmin activity and serum copper values seem to be an index of feto-placental function in early pregnancy.