Decreased paraoxonase 1 activity and increased oxidative stress in low lead-exposed workers

Paraoxonase 1 (PON1) has been proposed as an antioxidant enzyme. Although lead-inhibited PON1 activity has been demonstrated mostly based on in vitro experiments, it is uncertain whether this phenomenon is relevant in pathogenesis of lead-induced oxidative stress in the lead exposure. We examined associations of blood lead levels (BLL) and PON1 activity along with oxidative stress parameters in lead exposure workers. We determined malondialdehyde (MDA), conjugated diene (CD), total peroxides (TP), total antioxidant status (TAS), the oxidative stress index (OSI), and PON1 activity in earthenware factory workers (n = 60) and control subjects (n = 65). The lead-exposed group significantly increased lipid peroxidation parameters and OSI compared to the control group (p < 0.001). The lead-exposed group had significantly decreased PON1 activity and TAS levels compared to the control group (p < 0.001). Multiple linear regression analysis revealed that BLL were significantly correlated with decreased TAS (r = -0.496) and PON1 activity (r = -0.434), but with increased CD (r = 0.694), TP (r = 0.614), MDA (r = 0.788), and OSI (r = 0.722). Interestingly, BLL at 10 μg/dL significantly decreased PON1 activity and increased oxidative stress parameters with insignificant changes in other biochemical and hematological parameters. Altogether, the reduction of PON1 activity may associate in an imbalance in pro-oxidants and antioxidants, leading to oxidative damage in lead-exposed workers even at low BLL.     

Status of lipid peroxidation and plasma iron level in bronchial asthmatic patients

Low antioxidant levels and oxidative stress due to airway inflammation may be determinant of asthma severity. The study was conducted to find the extent of lipid peroxidation and change in the levels of plasma iron in asthmatic patients with severity of disease. Study included 155 asthmatic and 156 healthy volunteers of the age groups 18-45 of either sex. Asthmatic patients were grouped into mild, moderate and severe groups on the basis of Forced Expiratory Volume in first second percent (FEV1%). Level of plasma malondialdhyde (MDA) was used as index of lipid peroxidation. A significant increase (P<0.01) in plasma MDA and plasma iron levels was found in asthmatic subjects as compared to controls. There was maximum increase in plasma MDA and iron levels in moderate asthmatic group. A positive correlation between plasma MDA and iron (r = +0.3) has been found in asthmatic patients. An increased plasma iron levels in asthmatics may contribute to aggravate lipid peroxidation.     

Lipid peroxidation and antioxidant protection in patients during acute depressive episodes and in remission after fluoxetine treatment

Increasing numbers of studies indicate that free radicals and their derivatives play a role in some neuropsychiatric disorders, such as depression. The aim of this study was to investigate the activities of antioxidant enzymes, lipid peroxidation and total antioxidant status (TAS) in patients suffering from major depressive disorder (MDD) as compared to healthy controls. Specifically,we wanted to estimate how fluoxetine influences antioxidant defense and lipid peroxidation.Fifty MDD patients and thirty healthy controls participated in the study. Antioxidant enzyme activities and lipid peroxidation levels were measured in erythrocytes, while TAS was measured in plasma. All measurements were taken during an acute depressive episode and then again during depression remission after a three-month fluoxetine treatment.During acute depressive episodes, patients had significantly higher activity levels of antioxidant enzymes, such as copper-zinc superoxide dismutase (SOD1) and catalase (CAT), as compared to healthy controls. Concentrations of malondialdehyde (MDA) were also significantly higher during depressive episodes. Activity levels of glutathione peroxidase (GPx) did not differ significantly between depressed patients and healthy control subjects. Moreover, the plasma total antioxidant status of the depressed patients was decreased in comparison to control subjects. After three months of fluoxetine treatment, the above parameters did not change significantly.Major depressive disorder is accompanied by disturbances in the balance between pro- and anti-oxidative processes; however, these disturbances do not improve in patients in remission after three months of fluoxetine therapy.     

Aluminium Phosphide Poisoning and Oxidative Stress

According to previous animal studies, aluminium phosphides (AlPs) may induce oxidative stress leading to generation of free radicals and alteration in antioxidant defense system. This study was conducted to evaluate the existence and degree of oxidative stress in patients with acute AlP ingestion. A total of 44 acute AlP ingested patients as well as 44 age- and sex-matched controls were included. All patients had acute poisoning symptoms with AlP at the time of presentation and had blood samples analyzed for lipid peroxidation, total antioxidant capacity and total thiol. Our findings showed that there is a significant increase in lipid peroxidation in AlP ingested group along with a reduction in total antioxidant capacity and total thiols groups. These clinical data confirm previous experimental models that showed AlP exposure might significantly augment lipoperoxidative damage with simultaneous alterations in the antioxidant defense system. Hence, our findings might justify use of antioxidants in treatment of acute AlP poisoning which needs to be clarified by additional clinical trials.     

Antioxidant effects of piperine in in-vivo chick embryo cataract model induced by steroids

Purpose: The etiopathogenesis of steroid-induced cataracts is unknown. One hypothesis is that the higher reactive oxygen species (ROS) levels play an important role in the pathogenesis of several disorders, including the evolution of cataracts. This study investigated the antioxidant effects of piperine in our steroid-induced chick embryo lens model.

Methods: The study included 36 specific pathogen-free (SPF) fertilized eggs divided into six groups: phosphate buffer saline (PBS, pH 7.4 Saline Solution (0.9%) isotonic) group (G1), hydrocortisone succinate sodium (HC)-treated group (G2), 100?mg/kg piperine and HC treated group (G3), 50?mg/kg piperine and HC treated group (G4), 25?mg/kg piperine and HC treated group (G5), and 10?mg/kg piperine and HC treated group (G6). On the 15th day of incubation, the SPF eggs in the six groups were removed from the incubator; all were injected using insulin injectors into the chorioallantoic membrane. On day 17, all of the chick embryos were removed from the eggs and all lenses were dissected from the embryos. Cataract formation was evaluated in all lenses, and total antioxidant status (TAS), total oxidant status (TOS), reduced glutathione (GSH), and lipid peroxidation (MDA, malondialdehyde) levels were measured in all lens.

Results: The lenses in the G1 group had higher levels of GSH and TAS (p?p?p?p?p?p?p?Conclusion: Steroid therapy causes a decrease in GSH and TAS levels and an increase in TOS and MDA levels in lens tissues, indicating increased oxidative stress. Piperine exerts its effects as an antioxidant substance, in increasing doses.     

Protective effects of antioxidant supplementation on plasma lipid peroxidation in smokers

This study was designed to investigate the possible protective effects of antioxidants (vitamin E, beta-carotene, vitamin C, and red ginseng) on lipid peroxidation in smokers (> or = 20 cigarettes/day). Male student smokers were given antioxidant supplements for 4 wk. Smokers had significantly higher plasma levels of total cholesterol, triacylglycerols, and malondialdehyde (MDA) than nonsmokers. No corresponding significant differences in lipid profiles were found between smokers and nonsmokers. Smokers had significantly lower baseline concentrations of plasma vitamin C, beta-carotene, and alpha-tocopherol. After antioxidant (200 IU vitamin E, 9 mg beta-carotene, 500 mg vitamin C, or 1.8 g red ginseng) supplementation for 4 wk, smokers had significantly higher concentrations of plasma antioxidants. After 4 wk of antioxidant supplementation with betacarotene, high-density lipoprotein (HDL) cholesterol concentrations in smokers were significantly increased. Overall, plasma MDA concentrations gradually decreased after antioxidant supplementation over the 4-wk period. Moreover, a significant reduction in plasma MDA concentrations was observed after vitamin E supplementation. The results of our study support the hypothesis that lipid peroxidation concentrations are inversely correlated with plasma antioxidant concentrations. Our data suggest that smokers have insufficient concentrations of antioxidant vitamins in plasma and that supplementation with antioxidants might protect smokers from oxidative damage.     

Repeated acetaminophen dosing in rats: adaptation of hepatic antioxidant system

Repeated dosing of acetaminophen (paracetamol) to rats is reported to decrease their sensitivity to its hepatotoxic effects, which are associated with oxidative stress and glutathione depletion. We determined if repeated acetaminophen dosing produced adaptive response of key antioxidant system enzymes. Male rats (Sprague-Dawley, 10 weeks) were given 800, 1200, or 1600 mg/kg/day acetaminophen by oral gavage for 4 days. Liver was assayed for oxidative stress and antioxidant markers: malondialdehyde (MDA), thiobarbituric acid reactive substance (TBARS), total antioxidant status (TAS), glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), glucose-6-phosphate dehydrogenase (G6PD), catalase (CAT), and superoxide dismutase (SOD), and alanine transaminase (ALT) as a marker of hepatocellular injury. Acetaminophen at 1200/1600 mg/kg decreased GSH 26/47%, GPx 21/26%, CAT 35/28%, SOD 21/12%; and TAS 28/18% (correlated with CAT, r=0.91; SOD, r=0.66; GPx, r=0.45). Despite antioxidant deficiencies, and no TBARS change, MDA decreased 26%/33%/37% at 800/1200/1600 mg/kg, which correlated with increased GR (61%/62%/76%, r=0.77) and G6PD (130%/110%/190%, r=0.78). Both MDA (r=0.68) and G6PD (r=0.71) correlated with hepatic ALT, which decreased 27%/43%/48%, respectively. Resistance to acetaminophen hepatotoxicity produced by repeated exposure is partially attributable to upregulation of hepatic G6PD and GR activity as an adaptive and protective response to oxidative stress and glutathione depletion.     

Selenium-mediated cardioprotection against adriamycin-induced mitochondrial damage

Adriamycin (ADR) causes morphological and functional alterations in mitochondrial structure in the heart. The study′s aim was to determine whether there is a protective effect of selenium (Se) on ADR-induced cardiac damage. Rats were divided into four groups: The first group was injected saline intraperitoneally (i.p.) for 21 days; the second group received 4?mg/kg i.p. ADR every alternate day for 8 days; the third group received 50 µg/kg i.p. Se for 21 days; and the fourth received the Se (for 21 days) and ADR (for 8 days) coadministration i.p. Left ventricular functions, electrocardiography parameters, and blood pressures were assessed. Mitochondrial membrane potential (MMP), adenosine triphosphate (ATP) level, and thioredoxin reductase (TrxR) activity were determined. Total antioxidant (TAS) and oxidant status (TOS) in cytosol, mitochondria of myocytes, and plasma were measured. Left ventricular data demonstrated left ventricular systolic pressure (LVSP) decreased, left ventricular developed pressure (LVDP) decreased, and left ventricular end-diastolic pressure (LVEDP) increased in ADR-treated animals, compared to the control and Se groups. ADR decreased the membrane potential and ATP level in myocyte mitochondria. TrxR activity decreased in the ADR group, compared to the Se group. Cytosolic and mitochondrial TAS decreased and mitochondrial and plasma TOS increased in the ADR group, compared to the control. The coadministration of Se with ADR attenuated left ventricular dysfunction, improved MMP and ATP levels, and prevented oxidative stress by increasing antioxidants (especially TrxR) and decreasing oxidants. We concluded that Se is effective against ADR-induced cardiac damage via the restoration of TAS and TOS, which prevented mitochondrial damage.     

氯乙醇急性肝脏毒性研究：Ⅰ.氯乙醇中毒与脂质过氧化效应

用大鼠急性经口染毒模型研究了氯乙醇脂质过氧化效应与其肝损害作用之间的关系。结果表明,中、高剂量组肝匀浆丙二醛含量随作用时间延长而逐步上升,至12小时达到高峰。肝脏萄葡糖-6-磷酸酶活性与微粒体丙二醛含量升高呈高度负相关,线粒体琥珀酸脱氢酶活力则与线粒体丙二醛含量呈高度正相关。血清甘胆酸含量出现先升高后降低的双相反应。肝脏还原型谷胱甘肽含量在染毒1小时后大幅度下降,12小时已恢复正常水平。肝脏主要的病理改变为小叶中央区肝细胞脂肪变性。     

右美托咪定对腹腔镜全子宫切除术患者氧化应激反应的影响

目的：观察并评价右美托咪定（dexmedetomidine,Dex）对腹腔镜全子宫切除术患者氧化应激反应的影响。方法择期全麻行腹腔镜全子宫切除术患者40例,随机分为两组：D组（Dex组,n＝20）,Dex静脉泵注负荷剂量为1μg·kg－1（15 min内输注完）,然后以0．5μg·kg－1·h－1持续泵注至手术结束前30 min。C组（对照组,n＝20）,同样方式输注生理盐水。于麻醉前（T0）、气腹结束即刻（T1）、气腹结束后30 min（T2）和术后24 h（T3）4个时间点记录平均动脉压（MAP）、心率（HR）并抽取静脉血,测定血清过氧化氢（H2 O2）、丙二醛（MDA）和总抗氧化态（TAS）浓度。结果与T0相比,C组MAP在T1、T2时间点差异有显著性（P＜0．05）。与T0相比,T1、T2时间点C组、D组H2O2、MDA增高,TAS降低（P＜0．05）。T3时D组H2O2、MDA与T0比较差异无显著性（P＞0．05）,而C组仍较高（P＜0．05）;与C组相比,D组T2、T3时间点H2O2、MDA浓度低,TAS浓度高（P＜0．05）。两组在T1时间点H2O2、MDA差异无显著性（P＞0．05）,但D组较C组TAS浓度高（P＜0．05）。结论右美托咪定可减轻腹腔镜全子宫切除术患者氧化应激反应。     

Ursolic acid ameliorates cognition deficits and attenuates oxidative damage in the brain of senescent mice induced by D-galactose

Ursolic acid (UA), a pentracyclic triterpene, is reported to have an antioxidant activity. Here we assessed the protective effect of UA against the d-galactose (D-gal)-induced neurotoxicity. We found that UA markedly reversed the D-gal induced learning and memory impairment by behavioral tests. The following antioxidant defense enzymes were measured: superoxide dismutases (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR). The content of the lipid peroxidation product malondialdehyde (MDA) was also analyzed. Our results indicated that the neuroprotective effect of UA against D-gal induced neurotoxicity might be caused, at least in part, by the increase in the activity of antioxidant enzymes with a reduction in lipid peroxidation. And UA also inhibited the activation of caspase-3 induced by D-gal. Furthermore, we found that UA significantly increased the level of growth-associated protein GAP43 in the brain of D-gal-treated mice. These results suggest that the pharmacological action of UA may offer a novel therapeutic strategy for the treatment of age-related conditions.     

Possible new organoselenium supplement – evaluation of its influence on the kidneys in comparison with inorganic sodium selenite

The aim of this work was to evaluate the possibility of using of the new selenoorganic ring compound, 3-(o-chlorobenzoylamino)-2-(o-tolylimino)-4-methyl-4-selenazoline, as a selenium supplement by investigating the influence of its short-term administration on Se accumulation and antioxidant status in kidney. For 10 days, adolescent male Wistar rats were treated with saline (control group), Na₂SeO₃ (Se-IN group) or the studied compound (Se-ORG group) (5 × 10^?4 mg Se/g of once a day) via a stomach tube. The selenium concentration, total antioxidant status (TAS), activities ofthe antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx), concentrations of ascorbic acid (AA) and reduced glutathione (GSH) and concentration of malonyldialdehyde (MDA) were determined in the kidney homogenates. TAS was significantly reduced in the Se-ORG group compared to the control. Reduced glutathione was markedly decreased in Se-treated animals compared to the control and in the Se-ORG group compared to the Se-IN group. Malonyldialdehyde was significantly increased in the Se-supplemented groups compared to the control group but considerably less so in the Se-ORG group. All other studied parameters displayed no significant differences. No increase in the accumulation of selenium and the partial impairment of the antioxidant status and enhancement of lipid peroxidation in the kidneys resulting from Se treatment could suggest that in the first period of administration, excess selenium was excreted with urine, leading to a disturbance of kidney functions. Comparison of the effect of our compound with that exerted by inorganic Na₂SeO₃ suggests that the studied compound could be considered as a possible supplement after further investigations, including determination of selenium excretion with urine, as well as repetition of this study using a wide range of doses and periods of supplementation.     

alpha-Tocopherol supplementation restores the reduction of erythrocyte glucose-6-phosphate dehydrogenase activity induced by forced training.

BACKGROUND: Erythrocyte glucose-6-phosphate dehydrogenase (G6PD) activity is closely related to free radical production. alpha-Tocopherol (alpha-T) is implicated with the reduction of lipid peroxidation. AIM: To investigate the effect of training and alpha-T supplementation on the erythrocyte G6PD activity. METHODS: Blood was obtained from 10 basketball players pre-game (group A), post-game (group B) and after 30 days on alpha-T (dl-alpha-tocopheryl-acetate, 200mg 24h(-1) orally) supplementation pre- (group C) and post-training (group D). alpha-T and catecholamines were evaluated with HPLC methods and creatine kinase, lactate dehydrogenase, total antioxidant status (TAS) and G6PD activity with commercial kits. RESULTS: TAS was increased in the groups with alpha-T addition (groups C and D). Post-exercise, TAS and G6PD activity were remarkably higher (2.10+/-0.13mmoll(-1), 7.92+/-1.5Ug(-1)Hb, respectively) in group D than those in group B (0.92+/-0.10mmoll(-1), 4.8+/-1.4Ug(-1)Hb, p<0.01, respectively). G6PD activity positively correlated with TAS (r=0.64, p<0.001) in all the studied groups. CONCLUSIONS: Supplementation with alpha-T may protect G6PD activity from reduction induced by forced training.     

Effects of Pycnogenol on cisplatin-induced optic nerve injury: an experimental study

Aim: To determine the effects of Pycnogenol on cisplatin-induced optic nerve damage.

Material and method: Totally 18 albino Wistar male rats were assigned into three groups, with six rats in each group as follows: healthy controls (HC group), only cisplatin (2.5?mg/kg) administered group (CIS group) and Pycnogenol (40?mg/kg)?+?cisplatin (2.5?mg/kg) administered group (PYC group). We analyzed the levels of malondialdehyde (MDA) as a marker of lipid peroxidation and oxidative stress, total glutathione (tGSH) as a marker of antioxidant status, nuclear factor-kappa B (NF-κB) and tumor necrosis factor alpha (TNF-α) as inflammatory markers, total oxidative status (TOS) and total antioxidant status (TAS) on eye tissue together with histopathological evaluation of optic nerve in an experimental model.

Results: In CIS group MDA, TOS, TNF-α and NF-κB levels were statistically significantly higher (p?p?p?p?Conclusion: Pycnogenol pretreatment was highly effective in preventing augmentation of cisplatin-induced oxidative stress and inflammation in eye tissue.     

Hypotensive effect of atorvastatin is not related to changes in inflammation and oxidative stress

We sought to determine if atorvastatin lowers blood pressure in patients with previously diagnosed and well-controlled essential arterial hypertension and if this effect could be related to anti-inflammatory and anti-oxidative effects. Among 92 patients with essential arterial hypertension, we studied 56 non-smoking and normolipemic: 39 were randomized to receive 80 mg atorvastatin daily for 3 months (statin-treated patients, ST), and the rest continued a previous hypotensive therapy (statin-free patients, SF). Blood pressure was measured using a 24-h ambulatory blood pressure measurement device. Serum levels of high-sensitivity C-reactive protein (hs-CRP), total antioxidant status (TAS) and plasma peroxides (assessed by Oxystat) were measured in both groups. The mean change in systolic BP (SBP) for atorvastatin was -5.7 mmHg (95% confidence interval CI, -4.1 to -7.2 mmHg), and the mean change in diastolic BP (DBP) was -3.9 mmHg (95% CI, -2.7 to -5.0 mmHg). No change in BP in SF patients was observed. In the ST group, hs-CRP and peroxides did not significantly decrease. In the SF group, concentrations of hs-CRP proceeded to decrease while peroxides increased. In the ST group, changes in hs-CRP correlated with changes in total cholesterol and low-density lipoprotein cholesterol (r = 0.41, p = 0.013 and r = 0.35, p = 0.04, respectively) but did not correlate with changes in BP. The hypotensive statin effect was independent of the hypolipemic effect. During three months of observation, TAS concentrations in both groups remained stable. In this randomized study, additionally administered atorvastatin to non-smoking and normolipemic patients with well-controlled essential arterial hypertension resulted in reduction of BP. This effect was not followed by significant changes in hs-CRP, TAS or Oxystat concentrations. The hypotensive effect of atorvastatin did not depend on anti-inflammatory, anti-oxidative or hypolipemic actions.     

抗氧化剂减轻造血干细胞移植术对肝肾毒性的研究

目的 研究抗氧化剂对减轻造血干细胞移植术预处理相关肝肾毒性的作用。方法 随机,单盲设计,选择100名移植患者随机分为2组,试验组于预处理前给予Vit C（300 mg/d）以及Vit E（600 mg/d）,对照组不予补充。其余处理两组相同。测定预处理前后两组患者的血浆谷氨酸丙酮酸转移酶（ALT）、尿素氮（BUN）、肌酐（Cr）水平以及血浆总抗氧化力TAC、脂质过氧化物MDA。结果 预处理后两组ALT、BUN、Cr 及TAC、MDA水平均有显著差异。结论 移植预处理前外源性补充抗氧化剂提高了患者机体的抗氧化力,减少了预处理中脂质过氧化物的产生,有效减轻了移植术相关肝肾毒性。     

血浆载脂蛋白水平及apoB/apoA1与急性冠脉综合征的相关性研究

目的探讨血浆载脂蛋白A1,B(apoA1,B)水平及apoB/apoA1比值与急性冠综合征(ACS)的相关性。方法入选我院经冠脉造影检查的119例可疑冠心病患者,其中不稳定型心绞痛组(UA组)54例,急性心肌梗死组(AMI组)33例,冠脉造影阴性者设为对照组32例。分别测定血浆总胆固醇(TC)、低密度脂蛋白(LDL-C)、高密度脂蛋白(HDL-C)及apoA1、apoB,计算apoB/apoA1比值,比较各组各项测定指标及apoB/apoA1的水平变化,并进行多因素logistic回归分析。结果 UA组与AMI组apoA1分别为(1.10±0.12)mmol/L,(1.07±0.14)mmol/L,与对照组(1.19±0.17)mmol/L相比显著偏低(P均<0.01);UA组与AMI组apoB分别为(1.00±0.14)mmol/L,(1.10±0.13)mmol/L,与对照组(0.92±0.14)mmol/L相比显著偏高(P<0.05,P<0.01);UA组与AMI组的apoB/apoA1分别为0.91±0.19,0.97±0.18,与对照组(0.79±0.18)相比显著偏高(P<0.05,P<0.01)。多因素logistic回归分析示apoB/apoA1(OR=4.462,95%CI2.153～9.255,P<0.001)及apoB(OR=2.764,95%CI1.174～6.511,P<0.001)与ACS显著相关。结论 apoB与apoB/apoA1均是ACS的独立危险因素,而apoB/apoA1是ACS最显著的独立危险因素。     

Lipid peroxidation and glutathione peroxidase activity in chronic obstructive pulmonary disease exacerbation: prognostic value of malondialdehyde.

Results of recent studies have indicated that during exacerbation of chronic obstructive pulmonary disease (COPD), antioxidant capacity is lower and the levels of lipid peroxidation products are higher than those in age-matched healthy subjects. The aim of this study was to assess the time course of changes in oxidant stress during the treatment of exacerbation of COPD. For this purpose, we measured erythrocyte glutathione peroxidase (GPx) activity and serum levels of the lipid peroxidation product malondialdehyde (MDA) in 18 male patients with acute exacerbation of COPD. Fifteen healthy non-smokers having no history of lung disease served as control subjects. Mean erythrocyte GPx values of patients were 45.54 +/- 9.04 u/gHb on admission and had increased to 72.77 +/- 9.68 by the tenth day of treatment, but still remained lower than those of healthy subjects (83.13 +/- 10.91) (p=0.007). Serum MDA values in patients were Vol. 12, No. 1, 2001 significantly higher (2.68 +/- 1.28 nmol/ml) than those in control subjects (1.04 +/- 0.36 nmol/ml) (p=0.000) and returned to normal values by the tenth day of treatment (1.08 +/- 0.36 nmol/ml) (p=0.766). Erythrocyte GPx values in patients who were current smokers (39.87 +/- 3.82 u/gHb) were lower than those in ex-smokers (49.15 +/- 9.67 u/gHb) (p=0.021). Moreover, serum MDA values in patients who were current smokers (3.32 +/- 1.18 nmol/ml) were higher than those in ex-smokers (1.66 +/- 0.60 nmol/ml) (p=0.007). The results show that oxidative stress in patients with acute exacerbation of COPD is related to higher MDA levels that return to normal conditions during the course of treatment. In conclusion, the results suggest that MDA levels can serve as a marker of prognosis and of the success of treatment of the exacerbation of COPD.     

The beneficial effect of L-cysteine supplementation on DNA oxidation induced by forced training.

BACKGROUND: Forced training is closely implicated with free radicals production and indication of tissue damage as well as DNA oxidation. AIM: To investigate the effect of L-cysteine (L-cys) supplementation on DNA oxidative damage found in basketball players after forced training. SUBJECTS AND METHODS: Blood was obtained from 10 players pre-game (group A), post-game (group B) and after 1 month L-cys (0.5 g 24 h(-1), orally) supplementation, pre- (group C) and post-training (group D). Total antioxidant status (TAS) and the biomarker of DNA oxidative damage 8-hydroxy-2-deoxyguanosine (8-OHdG) as well as creatine kinase (CK) and lactate dehydrogenase (LDH) were measured with commercial kits. RESULTS: TAS was increased in the groups with L-cys (group C and group D). Post-exercise 8-OHdG levels, CK and LDH were remarkably lower (0.16+/-0.03 ng ml(-1), 115+/-15 U l(-1), 417+/-90 U l(-1), respectively) in group D than those in group B (0.36+/-0.05 ng ml(-1), 286+/-12 U l(-1), 688+/-88U l(-1), p<0.001, respectively). 8-OH dG levels were negatively correlated with TAS(r=-0.718, p<0.01) and positively with CK levels(r=0.590, p<0.01). CONCLUSIONS: L-cys supplementation in basketball players may reduce DNA damage induced by training. The sulfur-containing amino acid may protect muscle cells "death" by increasing TAS and the cellular defense against oxidative stress.     

Oxidative stress increases in carbon monoxide poisoning patients

Objective: Carbon monoxide poisoning (COP) is one of the important causes of morbidity and mortality in toxicological cases. In this study, we aimed to find out more about the pathophysiology of COP by investigating the effects of COP on oxidative stress parameters such as total oxidant status (TOS) and total antioxidant status (TAS). Methods: Eighty-eight patients admitted to the emergency department of our hospital with acute COP and 35 healthy adults as control group were included in this study. Blood samples were collected from all COP patients at the time of initial emergency department evaluation to determine the oxidative stress parameters. Then, serum levels of total antioxidant status and total oxidant status levels were measured. Results: A total of 88 patients poisoned by carbon monoxide (CO; mean age 37.1 ± 18.2 years; 54'% women) were enrolled. TOS and carboxyhemoglobin (COHb) levels in COP patients were increased when compared to control group (p = 0.001). TOS, oxidative stress index (OSI) and COHb levels in COP patients were significantly lower after the treatment. (respectively, p = 0.016; p = 0.023; p = 0.001). On the other hand, no statistical differences were observed in TAS levels of study and control group as well as there were no changes with treatment. Conclusion: Measurements of TOS, TAS and OSI levels may be useful markers to find out the pathophsiology of COP.