Oxidative stress and cellular immunity in patients with recurrent aphthous ulcers

Recurrent aphthous ulcer (RAU) is an inflammatory condition of the oral mucosa characterized by painful, well-circumscribed, single or multiple round or ovoid ulcerations. The exact etiologic factor(s) of these ulcerations are not yet understood. The objective of this study was to evaluate inflammatory processes and free radical metabolism of 25 patients with RAUs compared to 25 healthy controls. The levels of malondialdehyde (MDA) and glutathione (GSH) were determined by high-performance liquid chromatography. Tumor necrosis factor-alpha (TNF-α), interleukin-2 (IL-2), IL-10, and IL-12 were determined by ELISA. Nitric oxide (NO), myeloperoxidase (MPO), total antioxidant status (TAS), and total oxidant status (TOS) levels were measured spectroscopically in serum. The levels of MDA, GSH, TNF-α, IL-2, IL-12, MPO, and TOS, and oxidative stress index (OSI) were higher, and the levels of NO, IL-10, and TAS were lower in patients with RAU than in controls. Statistical analysis showed that GSH, TNF-α, IL-2, IL-10, and OSI differed significantly in patients with RAU compared to controls. These parameters have important roles in oxidant/antioxidant defense.     

Protective and Therapeutic Effect of Molsidomine on Bleomycin-Induced Lung Fibrosis in Rats

We aimed to investigate the preventive and treatment effect of molsidomine (MOL) on bleomycin (BLC)-induced lung injury in rats. Rats were assigned into groups as follows: control group; MOL group, 10 mg/kg MOL was continued orally for 29 day; BLC group, a single intratracheal injection of BLC (2.5 mg/kg), MOL+BLC-preventive group, 10 mg/kg MOL was administered 1 day before the intratracheal BLC injection and continued for 14 days; BLC+MOL-treatment group 10 mg/kg MOL was given on 14th day after the intratracheal BLC injection and continued until sacrifice. All animals were sacrificed on 29th day after BLC administration. The semiquantitative histopathological assessment, tissue levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), total antioxidant status (TAS), total oxidant status (TOS), myeloperoxidase (MPO), and oxidative stress index (OSI) were measured. BLC-provoked histological changes were significantly detected compared to the control group. MOL restored these histological damages in different quantity in the treatment and preventive groups. BLC administration significantly decreased levels of GSH and TAS when compared to controls and these reductions was significantly ameliorated by MOL given prophylactic setting. However, therapeutic MOL administration significantly increased the TAS level decreased by BLC. The levels of MDA, MPO, and TOS were significantly increased with BLM, and these augmentations of MDA and TOS were significantly reduced by MOL given prophylactic setting. Furthermore, the OSI was higher in the BLC group, and this increase was reversed by the MOL administration before and after BLC treatment. In this study, both protective and therapeutic effects of MOL against BLC-induced lung fibrosis were demonstrated for the first time.     

Not Only Melatonin but also Caffeic Acid Phenethyl Ester Protects Kidneys against Aging-related Oxidative Damage in Sprague Dawley Rats

Microscopic features and antioxidant status of kidneys of young, old, and caffeic acid phenethyl ester (CAPE) and melatonin administered old Sprague Dawley rats were evaluated. Aging-related tubular and glomerular changes were evident. The most prominent tubular alterations were massive vacuole formation, mitochondrial degeneration, and lysosome accumulation. Mean tissue malondialdehyde (MDA) level was increased, mean tissue superoxide dismutase (SOD), catalase (CAT) (p < .001), and glutathione peroxidase (GPx) activities (p < .05), and total glutathione (GSH) level were decreased in old animals. Melatonin significantly reduced tissue MDA levels (p < .005), but increased tissue SOD (p < .001), CAT, and GPx activities (p < .05), and GSH levels (p < .005) in old animals. CAPE also significantly reduced tissue MDA levels (p < .005), but increased tissue SOD (p < .05), CAT (p < .005), GPx activities, and GSH levels (p < .001) in old rats. Mean tissue MDA levels of melatonin and CAPE-administered rats were even lower than those of young rats (p < .05). In conclusion, tubular and glomerular structures and tissue antioxidant enzyme activities were very well preserved in CAPE and melatonin-administered rats.     

Ethanol induced adaptive changes in blood for the pathological and toxicological effects of chronic ethanol consumption in humans

Alcohol consumption is associated with a number of toxicological changes in blood and the oxidant–antioxidant system. The present study was performed to investigate the alcohol induced toxicological, pathological changes in blood and an adaptive role of erythrocyte antioxidant system in chronic alcoholics. Human male volunteers aged 44 ± 6 years with similar dietary habits were divided into two groups, namely non-alcoholic controls and chronic alcoholics. We measured hematological parameters, erythrocyte lipid peroxidation, NO production, erythrocyte antioxidant and liver function test enzyme activities. Alcoholics had increased erythrocyte nitric oxide levels and also elevated erythrocyte lipid malondialdehyde (MDA) concentrations. Strikingly, increments in reduced glutathione and markedly increased activities of certain antioxidant enzymes such as glutathione reductase (GR), superoxide dismutase (SOD), and another related enzyme G-6 phosphate dehydrogenase (G6-PDH) with no alterations in the activities of glutathione S-transferase (GST), glutathione peroxidase (GPx), and catalase (CAT) in chronic alcoholics were observed compared to controls. Furthermore, erythrocyte NO levels were positively correlated with lipid peroxidation, SOD, GSH, GR and G6PDH in chronic alcoholics. In addition, increased AST/ALT ratio and a significant increase in WBC and platelets were also noticed. Together, these results indicate that, antioxidants and defense enzymes appear to be rendering protection as a consequence of chronic adaptation in alcoholics.     

糖尿病大鼠心肌病理变化及脂质过氧化和一氧化氮的改变

目的：研究糖尿病心肌的病理变化及其发生机制。方法：用光镜及透射电镜观察四氧嘧啶诱导的糖尿病1个月大鼠心肌形学改变,并测定心肌细胞超氧化物歧化酶（SOD）、谷膛甘肽过氧化物酶（GSH－Px)、一氧化氮合酶（NOS）的活性及一氧化氮（NO）、丙二醛（MDA）含量。结果：光镜下见心肌细胞萎缩、嗜酸性变及空泡变性,间质纤维增生,透射电镜下见线粒体扩张、嵴变短,内质网扩张,骨原纤维破坏,间质胶原纤维增生。SOD、GSH－Px活性下降,NOS活性及NO、MDA含量增加。结论：糖尿病大鼠心肌病变主要为心肌萎缩、线粒体扩张及肌原纤维破坏,间质纤维增生,脂质过氧化作用及NO所致的损伤可参与其中。     

Overloaded training increases exercise-induced oxidative stress and damage.

We hypothesized that overloaded training (OT) in triathlon would induce oxidative stress and damage on muscle and DNA. Nine male triathletes and 6 male sedentary subjects participated in this study. Before and after a 4-week OT, triathletes exercised for a duathlon. Blood ratio of reduced vs. oxidized glutathione (GSH/GSSG), plasma thiobarbituric acid reactive substances (TBARS), leukocyte DNA damage, creatine kinase (CK), and CK-MB mass in plasma, erythrocyte superoxide dismutase (SOD) activity, erythrocyte and plasma glutathione peroxidase (GSH-Px) activities, and plasma total antioxidant status (TAS) were measured before and after OT in pre- and postexercise situations. Triathletes were overloaded in response to OT. In rest conditions, OT induced plasma GSH-Px activity increase and plasma TAS decrease (both p < 0.05). In exercise conditions, OT resulted in higher exercise-induced variations of blood GSH/GSSG ratio, TBARS level (both p < 0.05), and CK-MB mass (p < 0.01) in plasma; and decreased TAS response (p < 0.05). OT could compromise the antioxidant defense mechanism with respect to exercise-induced response. The resulting increased exercise-induced oxidative stress and further cellular susceptibility to damage needs more study.     

Protective role of aminoguanidine on gentamicin-induced acute renal failure in rats

The toxicity of aminoglycosides including gentamicin (GEN), the most widely used drug in this category, is believed to be related to the generation of reactive oxygen species (ROS) in the kidney. Aminoguanidine (AG) is known as an effective antioxidant and its free radical scavenger effects may protect GEN-induced acute renal failure (ARF). Therefore, this study was focused on investigating the possible protective effect of AG against GEN-induced nephrotoxicity in an in vivo rat model. We investigated the effects of AG on GEN-induced changes in renal tissue malondialdehyde (MDA) levels; nitric oxide (NO) generation; glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities; glutathione (GSH) content; serum creatinine (Cr) and blood urea nitrogen (BUN) levels. Morphological changes in the kidney were also examined using light microscopy. GEN administration to control group rats increased renal MDA and NO levels but decreased GSH-Px, SOD, CAT activities and GSH content. AG administration with GEN injection resulted in significantly decreased MDA, NO generation and increased GSH-Px, SOD, CAT activities and GSH content when compared with GEN alone. Serum levels of Cr and BUN significantly increased as a result of nephrotoxicity. Also, AG significantly decreased Cr and BUN levels. Morphological changes in the kidney, including tubular necrosis, intracellular edema, glomerular and basement membrane alterations were evaluated qualitatively. Both biochemical findings and histopathological evidence showed that administration of AG reduced the GEN-induced kidney damage. We propose that AG acts in the kidney as a potent scavenger of free radicals to prevent the toxic effects of GEN both at the biochemical and histological level.     

Evaluation of Oxidative Stress and Antioxidant Status in Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a common respiratory condition involving the airways and characterized by airflow limitation. Gaseous and noxious particles play an important role in this process. Antioxidants are the substances that may protect cells from the damage caused by unstable molecules known as free radicals. The increased oxidative stress in patients with COPD is the result of an increased burden of inhaled oxidants, as well as increased amounts of reactive oxygen species (ROS) generated by various inflammatory, immune and epithelial cells of the airways. A total of 150 subjects with COPD and 100 healthy controls subjects were enrolled in this study from the period October 2015 to January 2016. The investigation included measurements of plasma superoxide dismutase activity (SOD), catalase activity (CAT), glutathione content (GSH) reduced form, (GPx) glutathione peroxidase, glutathione reductase (GR) and lipid peroxidation (LPO). Absorbance was measured by UV spectrophotometer. The estimated values of SOD, catalase, GPx, GSH and GR were found to be significantly (P = 0.0001) lower among the cases compared with controls. But, the levels of MDA were higher (P = 0.0001) in cases as compared to control group and there was significant difference in the oxidative stress parameters among the various stages of COPD. The post hoc analysis revealed that SOD was significantly (P < 0.01) lower among the mild, moderate and severe patients compared with very severe patients. The catalase was also observed to be significantly (P = 0.01) lower among mild, moderate and severe patients than very severe patients. The GPx was found to be significantly (P = 0.002) lower among the mild, moderate and severe patients compared with very severe patients. MDA was observed to be significantly higher in mild, moderate and severe patients compared with very severe (P = 0.001). GR was significantly (P = 0.003) lower among mild, moderate and severe patients than very severe patients. However, there was no significant difference in GSH among severity of COPD patients. This study suggests that oxidant and antioxidant imbalance plays an important role in various stages of severity of COPD. These results revealed the presence of an oxidative stress in subjects with COPD, and it is proportionate to the severity of disease.     

Not Only Melatonin but also Caffeic Acid Phenethyl Ester Protects Kidneys against Aging-related Oxidative Damage in Sprague Dawley Rats

Microscopic features and antioxidant status of kidneys of young, old, and caffeic acid phenethyl ester (CAPE) and melatonin administered old Sprague Dawley rats were evaluated. Aging-related tubular and glomerular changes were evident. The most prominent tubular alterations were massive vacuole formation, mitochondrial degeneration, and lysosome accumulation. Mean tissue malondialdehyde (MDA) level was increased, mean tissue superoxide dismutase (SOD), catalase (CAT) (p < .001), and glutathione peroxidase (GPx) activities (p < .05), and total glutathione (GSH) level were decreased in old animals. Melatonin significantly reduced tissue MDA levels (p < .005), but increased tissue SOD (p < .001), CAT, and GPx activities (p < .05), and GSH levels (p < .005) in old animals. CAPE also significantly reduced tissue MDA levels (p < .005), but increased tissue SOD (p < .05), CAT (p < .005), GPx activities, and GSH levels (p < .001) in old rats. Mean tissue MDA levels of melatonin and CAPE-administered rats were even lower than those of young rats (p < .05). In conclusion, tubular and glomerular structures and tissue antioxidant enzyme activities were very well preserved in CAPE and melatonin-administered rats.     

肠缺血再灌注时肠粘膜抗氧化系统及肝、肾功能改变的实验研究

目的：研究肠缺血再灌注损伤时肠粘膜抗氧化系统的改变及对肝、肾功能的影响。 方法： 复制大鼠肠缺血再灌注模型，采用分光光度计生化测定方法检测肠粘膜的还原型谷胱甘肽GSH、谷胱甘肽-S-转移酶GST、过氧化氢酶CAT、丙二醛MDA、超氧化物岐化酶SOD、谷胱甘肽过氧化物酶GSH-Px及血清谷丙转氨酶ALT、谷草转氨酶AST、尿素氮BUN、肌酐Cr的改变。 结果： 肠粘膜MDA含量于再灌注2 h显著高于假手术组(P<0.05)，再灌注4 h较假手术组高116%(P<0.05)，24 h较前有所降低但仍高于假手术组(P<0.05)；GSH含量于再灌注2 h显著低于假手术组(P<0.05)，再灌注4 h低至假手术组的40%（P<0.01），12 h恢复；肠粘膜CAT、SOD和GSH-Px活性未见明显改变；GST活性于再灌注2 h较假手术组低39%，再灌注4 h达最低，较假手术组低43%(P<0.05)，12 h恢复至假手术组水平；血清ALT、AST、 BUN及Cr于再灌注2 h显著高于假手术组(P<0.05)，再灌注4 h分别较假手术组高208%、100%、103%、41%（P<0.01），24 h基本恢复。 结论： 肠缺血45 min再灌注使肠粘膜GSH含量和GST活性降低，MDA含量增加，并造成肝肾功能的可逆性损伤。     

Oxidative stress and enzymatic antioxidant status in patients with nonalcoholic steatohepatitis

Oxidative stress is an important pathophysiological mechanism in nonalcoholic steatohepatitis (NASH). To assess whether there are relationships between oxidative stress and antioxidant enzymes in the development of NASH, we investigated oxidative stress by measuring serum malondialdehyde (MDA) and nitric oxide (NO) and antioxidant status by measuring serum glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione reductase (GR), and superoxide dismutase (SOD). The study included 18 patients (13 men, 5 women; mean age 42 yr) with biopsy proven NASH and 16 healthy volunteers (10 men, 6 women; mean age 38 yr). Serum levels of MDA, NO, GSH, GSH-Px, GR and SOD were determined by spectrophotometric methods. Serum levels (mean +/- SD) of MDA (6.7 +/- 1.6 vs 2.8 +/- 1.7 nmol/ml, p 0.0001), NO (135 +/- 28 vs 113 +/- 35 mmol/L, p 0.04), GSH (919 +/- 137 vs 770 +/- 128 mmol/L, p 0.003) were increased in patients with NASH vs controls. Serum levels of GSH-Px (1063 +/- 152 vs 1000 +/- 94 U/L) and GR (47 +/- 22 vs 40 +/- 21 U/L) were not singnificantly different in the patients vs controls. However, the serum level of SOD (1.24 +/- 0.32 vs 1.51 +/- 0.37 U/ml, p: 0.04) was significantly decreased. Impaired antioxidant defense mechanisms may be an important factor in the pathogenesis of NASH. Treatment approaches that affect the antioxidant enzymes may be beneficial in patients with NASH.     

高压氧与环孢素A对皮肤移植小鼠脾活性氧及一氧化氮含量的影响

目的:探讨高压氧与环孢素A对皮肤移植小鼠脾中活性氧、一氧化氮含量的影响。方法:供鼠BALB/C,受鼠C⁵⁷BL/6,皮肤移植,环孢素A组每日腹腔注射CsA5mg/kg,高压氧(HBO)组每日用99.2%氧气0.25MPa作用1.5h,14d后,取脾称重,测脾中丙二醛(MDA)的含量,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、过氧化氢酶(CAT)的活性和一氧化氮(NO)的含量,一氧化氮合酶(NOS)的活性。结果:(1)移植组、高压氧组和环孢素A组的MDA含量,GSH-PX、CAT的活性均高于对照组;环孢素A组GSH-PX、CAT活性低于、SOD的活性高于移植组;高压氧组GSH-PX活性低于、CAT和SOD活性高于移植组(P<0.01)。(2)移植组的NOS活性及NO含量高于对照组;高压氧组的NO含量低于、NOS活性高于移植组(P<0.01);环孢素A组的NO含量、NOS活性变化无显著意义。结论:皮肤移植小鼠脾细胞过氧化增强,NO含量及NOS活性增高;高压氧与环孢素A对上述二个系统具有一定作用,这可能与其抑制排斥反应有关。     

Separate and combined effects of heat stress and exercise on circulatory markers of oxidative stress in euhydrated humans

Combined heat stress, dehydration, and exercise is associated with enhanced oxidative stress in humans, but the separate and combined effects of heat stress and exercise on circulatory markers of oxidative stress without the influence of dehydration remain uncertain. The purpose of this study was to determine the effects of whole body heat stress alone and in combination with exercise on blood markers of oxidative stress in euhydrated humans. Eight males wore a water-perfused suit at rest and during 6 min of one-legged knee extensor exercise under control and heat stress conditions while maintaining euhydration. Following the control trial and a 15 min resting period, hot water was perfused through the suit in order to increase core, skin, and mean body temperatures by ~1, ~6, and ~2°C, respectively. Blood samples were taken to measure reduced glutathione (GSH), oxidized glutathione (GSSG), superoxide dismutase (SOD) and plasma isoprostanes. Heat stress alone did not alter GSH, SOD activity, or plasma isoprostanes, but increased GSSG leading to a reduction in the GSH/GSSG ratio. No changes in these variables were observed with exercise alone. Conversely, combined heat stress and exercise increased both GSH and GSSG, decreased SOD activity, but did not alter GSH/GSSG ratio or isoprostanes. In conclusion, these findings suggest that heat stress, independently of dehydration, induces non-radical oxidative stress at rest but not during moderate exercise because an increase in antioxidant defense compensates the heat stress-induced non-radical oxidative stress.     

Antioxidant and antiapoptotic effects of green tea polyphenols against azathioprine-induced liver injury in rats

Green tea polyphenols (GTP) is considered to have protective effects against several diseases. The hepatotoxicity of azathioprine (AZA) has been reported and was found to be associated with oxidative damage. This study was conducted to evaluate the role of GTP to protect against AZA-induced liver injury in rats. AZA was administered i.p. in a single dose (50 mg kg⁻¹) to adult male rats. AZA-intoxicated rats were orally administered GTP (either 100 mg kg⁻¹ day⁻¹ or 300 mg kg⁻¹ day⁻¹, for 21 consecutive days, started 7 days prior AZA injection).AZA administration to rats resulted in significant elevation of serum transaminases (sALT and sAST), alkaline phosphatase (sALP), depletion of hepatic reduced glutathione (GSH), catalase (CAT) and glutathione peroxidase (GPx), accumulation of oxidized glutathione (GSSG), elevation of lipid peroxides (LPO) expressed as malondialdehyde (MDA), reduction of the hepatic total antioxidant activity (TAA), decrease serum total proteins and elevation of liver protein carbonyl content. Significant rises in liver tumor necrosis factor-alpha (TNF-α) and caspase-3 levels were noticed in AZA-intoxicated rats. Treatment of the AZA-intoxicated rats with GTP significantly prevented the elevations of sALT, sAST and sALP, inhibited depletion of hepatic GSH, GPx, CAT and GSSG and inhibited MDA accumulation. Furthermore, GTP had normalized serum total proteins and hepatic TAA, CAT, TNF-α and caspase-3 levels of AZA-intoxicated rats. In addition, GTP prevented the AZA-induced apoptosis and liver injury as indicated by the liver histopathological analysis. The linear regression analysis showed significant correlation in either AZA-GTP100 or AZA-GTP300 groups between TNF-α and each of serum ALT, AST, ALP and total proteins and liver TAA, GPX, CAT, GSH, GSSG, MDA and caspase-3 levels. However, liver TNF-α produced non-significant correlation with the serum total proteins in both AZA-GTP100 and AZA-GTP300 groups.In conclusion, our data indicate that GTP protects against AZA-induced liver injury in rats through antioxidant, anti-inflammatory and antiapoptotic mechanisms. However, further merit investigations are needed to verify these results and to assess the efficacy of GTP therapy to counteract the liver injury and oxidative stress status.     

Effects of graded exercise-induced dehydration and rehydration on circulatory markers of oxidative stress across the resting and exercising human leg

Exercise in the heat enhances oxidative stress markers in the human circulation, but the contribution of active skeletal muscle and the influence of hydration status remain unknown. To address this question, we measured leg exchange of glutathione (GSH), glutathione disulfide (GSSG), superoxide dismutase activity (SOD) and isoprostanes in seven males at rest and during submaximal one-legged knee extensor exercise in the following four conditions: (1) control euhydration (0% reduction in body mass), (2) mild-dehydration (2%), (3) moderate-dehydration (3.5%), (4) rehydration (0%). In all resting and control exercise conditions, a net GSH uptake was observed across the leg. In contrast, a significant leg release of GSH into the circulation (−354 ± 221 μmol/min, P < 0.05) was observed during exercise with moderate-dehydration, which was still present following full rehydration (−206 ± 122 μmol/min, P < 0.05). During exercise, mild and moderate-dehydration decreased both femoral venous erythrocyte SOD activity (195 ± 6 vs. 180 ± 5 U/L, P < 0.05) and plasma isoprostanes (30 ± 1.1 vs. 25.9 ± 1.3 pg/L, P < 0.05), but during rehydration these were not different from control. In conclusion, these findings suggest that active skeletal muscles release GSH into the circulation under moderate dehydration and subsequent rehydration, possibly to enhance the antioxidant defense.     

Effects of vitamin E supplementation on oxidative stress in streptozotocin induced diabetic rats: investigation of liver and plasma

This experimental study was designed to investigate the effects of vitamin E supplementation, especially on lipid peroxidation and antioxidant status elements 3/4 namely, glutathione (GSH), CuZn superoxide dismutase (CuZn SOD), and glutathione peroxidase (GSH Px), both in blood and liver tissues of streptozotocin (STZ) diabetic rats. The extent to which blood can be used to reflect the oxidative stress of the liver is also investigated. In diabetic rats, plasma lipid peroxide values were not significantly different,from control,whereas erythrocyte CuZn SOD (p < 0.01), GSH Px (p < 0.001) activities and plasma vitamin E levels (p < 0.001), were significantly more elevated than controls. Vitamin E supplementation caused significant decreases of erythrocyte GSH level (p < 0.01) in control rats and of erythrocyte GSH Px activity (p < 0.05) in diabetic rats. Liver findings revealed significantly higher lipid peroxide (p < 0.001) and vitamin E (p < 0.01) levels and lower GSH (p < 0.001), CuZn SOD (p < 0.001) and GSH Px (p < 0.01) levels in diabetic rats. A decreased hepatic lipid peroxide level (p < 0.01) and increased vitamin E/lipid peroxide ratio (p < 0.001) were observed in vitamin E supplemented, diabetic rats. A vitamin E supplementation level which did not cause any increase in the concentration of the vitamin in the liver or blood, was sufficient to lower lipid peroxidation in the liver. Vitamin E/lipid peroxide ratio is suggested as an appropriate index to evaluate the efficiency of vitamin E activity,independent of tissue lipid values. Further, the antioxidant components GSH, GSH Px and CuZn SOD and the relationships among them, were affected differently in the liver and blood by diabetes or vitamin E supplementation.     

配比油对家兔体内抗氧化酶类活性的影响

观察不同配比n-3,n-6系脂肪酸的配比油对家兔体内几种抗氧化酶活性的影响，实验用家兔，共50只随机分为5组。对照组喂饲基础饲料，高脂组喂饲富含猪油和胆固醇（Ch)的饲料，配比油组（配比1组。配比2组，配比3组）喂饲的饲料中除了猪油和胆固醇外，还有不同配比n-3,n-6系脂肪酸的配比油，实验三个月中每间隔一个月耳缘静脉取血一次，检测各组家兔红细胞中超氧化物歧化酶（SOD）。过氧化氢酶（CAT），谷胱甘肽过氧化物酶9GSH-Px)。活性的变化，结果表明配比油使SOD，CAT活性均明显增强，但不同油脂对GSH-Px活性的影响较复杂，说明不同配比n-3,n-6系脂肪酸的混合油均可增强抗氧化系统酶活性，其增强作用与不同配比剂量密切相关。     

Blood antioxidant parameters in patients with diabetic retinopathy

It has been postulated that enhanced generation of reactive oxygen species (ROS) may take part in a pathogenesis of diabetic microvascular complication - retinopathy. There are two types of diabetic retinopathy, non-proliferative (simplex) and proliferative. ROS are anihilated by an intracelluar enzymatic system composed mainly of glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT). Beta-carotene, tocopherols and ascorbic acid are major components of serum antioxidants. All serum antioxidants are usually measured together as total antioxidant status (TAS). Erythrocyte activities of GPx, SOD, CAT and TAS were measured in diabetic patients without retinopathy, with non-proliferative and proliferative retinopathy. Obtained results were correlated with a period of diabetic history and a period of insulin treatment. SOD was significantly elevated in diabetics with non-proliferative retinopathy compared to patients without retinopathy. TAS was significantly lower in patients with proliferative retinopathy than in diabetics not developing retinopathy. Only CAT was significantly negatively correlated with the period of insulin treatment. This significant negative correlation was also observed in a subgroup of patients with proliferative retinopathy.     

Alterations in the erythrocyte antioxidant system of blood stored in blood bags

In the present study, we measured the concentrations of reduced glutathione (GSH) and malonyldialdehyde (MDA) and the activities of glutathione peroxidase (GSH-Px), glutathione S-transferase (GSH-S-T), superoxide dismutase (SOD), catalase (CAT) and glucose-6-phosphate dehydrogenase (G-6-PD) in erythrocytes obtained freshly from adult male donors which was preserved with CPDA-1 anticoagulant (citrate,phosphate, dextrose, adenine) on different days of storage. At the end of the study, storage-associated alterations in antioxidant activities were noted and discussed. GSH, GSH-Px, GSH-S-T, SOD, CAT and G-6-PD activities decreased, but erythrocyte MDA levels, as anindex of lipid peroxidation, increased during the storage period. According to our results, glutathione-dependent antioxidant systems in erythrocytes might be depleted during long storage in blood bags.