Prophylactic effect of aqueous extract of Sesamum indicum seeds on ethanol-induced toxicity in male rats

The liver is vulnerable to alcohol-related injury because it is the primary site of alcohol metabolism. Additionally, a number of potentially dangerous by-products are generated as alcohol is broken down in the liver. However, dietary supplements may prevent or relieve some of alcohol''s deleterious effects. Therefore, this study was conducted to evaluate the prophylactic effect of aqueous extract of Sesamum indicum (SI) on ethanol induced toxicity in rats. Male Wistar albino rats were divided into control, ethanol, pre-treatment, simultaneous and post-treatment groups. In the prophylactic experiment, Sesamum indicum, (200 mg/kg body weight) was administered by oral gavage for 28 days; two hours before, simultaneously with or two hours after ethanol exposure. Toxicity was induced by administering 45% ethanol (4.8 g/kg bw) by oral gavage. Lipid peroxidation (TBARS) and reduced glutathione (GSH) levels and catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD) and gluthathione-S-transferase (GST) activities were then determined in the liver, serum triglyceride (TG) levels, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were monitored and histological examination was carried out. The results revealed that ethanol administration led to significant elevation of TBARS level while depleting in the level of GSH as well as CAT, GPx, SOD and GST activities. Similarly, TG level and ALT and AST activities were elevated. The SI pre-treated group significantly inhibited TBARS, restored GSH level, enhanced CAT, GPx, SOD and GST activities and significantly decreased the elevated level of serum TG, ALT and AST activities. SI treatment (simultaneously with ethanol) exhibited similar effects to those of the SI pre-treated groups, while the SI post-treated group did not show the same protection as the Pre-treated group. S. indicum possesses antioxidant and hepatoprotective properties, that eliminate the deleterious effects of toxic metabolites of ethanol.     

Response of Antioxidant System of Tilapia (Oreochromis niloticus) Following Exposure to Chromium and Copper in Differing Hardness

Tilapias (Oreochromis niloticus) were exposed to copper or chromium in soft water (SW) (~80 mg CaCO₃/L, conductivity 1.77 mS/cm) or hard water (HW) (~320 mg CaCO₃/L, conductivity 5.80 mS/cm) using 2 exposure protocols (20 μM for 48 h and 10 μM for 144 h). Following the exposures, antioxidant enzyme activities [superoxide dismutase (SOD); catalase (CAT); glutathione peroxidase; glutathione reductase; and glutathione S-transferase (GST)] and glutathione (GSH) levels were measured in the liver of fish. SOD and CAT activities of control fish kept in SW were significantly lower than control fish kept in HW. However, the other antioxidant indices (glutathione metabolism) of both control fish were unaffected from water hardness. Acute metal exposures did not alter the glutathione metabolism, whereas SOD activity in SW and CAT activity in both waters changed significantly. In subchronic duration, Cu exposure caused significant decreases in measured parameters, except for GST activity and GSH level. Similarly, GST activity and GSH level were unaffected from Cr exposure. This study showed that SOD and CAT were the most sensitive antioxidant indices, and that glutathione metabolism, in general, was not altered following metal exposures in different waters.     

Response of integrated biomarkers of fish (Lateolabrax japonicus) exposed to benzo[a]pyrene and sodium dodecylbenzene sulfonate

Fish Lateolabrax japonicus were exposed to 0.1 and 1mg/L of anion surfactant sodium dodecylbenzene sulfonate (SDBS) and to 2 and 20 microg/L of benzo[a]pyrene (B[a]P) for 6, 12, and 18 days, with control and solvent control groups. Liver antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), and glutathione S-transferase (GST), were determined; brain acetylcholinesterase (AChE) and liver inducible nitric oxide synthase (iNOS) activities were also measured. The results indicated that (1) L. japonicus avoided oxidative damage through antioxidant systems; (2) SOD, GPx, and GSH were induced, and GST was inhibited and then induced by B[a]P exposure; and (3) CAT, GPx, and AChE were induced while iNOS was inhibited, and GST was induced and then inhibited by SDBS stress in experimental period.     

Protective effect of Indigofera oblongifolia in CCl4-induced hepatotoxicity

The present study aimed at assessing the protective effect of Indigofera oblongifolia on carbon tetrachloride (CCl4-induced hepatotoxicity. Hepatotoxicity was induced in male Wistar rats using CCl4 (1 mL/day at an interval of 72 hours). CCl4-induced animals were treated with I. oblongifolia at different doses. Hepatoprotection was assessed from activities of marker enzymes in serum and antioxidant status in the liver after an experimental period of 10 days. The activities of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and lactate dehydrogenase were significantly (P < .001) increased in serum of CCl4-induced animals when compared with control animals. Antioxidant status was significantly lowered in CCl4-treated animals with a significant (P < .001) increase in the levels of lipid peroxides [thiobarbituric acid-reactive substances (TBARS)], significantly lower levels of glutathione (GSH), and lowered activities of superoxide dismutase (SOD), catalase (CAT), and GSH peroxidase (GPx). The protective effect of I. oblongifolia was evident from lowering of levels of marker enzymes in serum and maintenance of antioxidant status in the liver as seen from lowered levels of TBARS, increased levels of GSH, and increased activities of SOD, CAT, and GPx. These results show the protective effect of I. oblongifolia and suggest the antioxidant property of the extract.     

Oxidative Stress Biomarkers in the Digestive Gland of Theba pisana Exposed to Heavy Metals

The in vivo toxic effects of sublethal treatment of 40 and 80% of 48-h LD₅₀ of topically applied trace metals [copper (Cu), lead (Pb), and zinc (Zn)] on oxidative stress biomarkers in the digestive gland of Theba pisana were examined. Oxidative individual perturbations were assessed by measuring nonenzymatic (glutathione; GSH) and enzymatic (catalase, CAT; glutathione peroxidase, GPx; and glutathione-S-transferase, GST) antioxidants in digestive gland of the snails. Lipid peroxidation (LPO) was also evaluated as a marker of cell damage. The results indicated that the copper ion was the most potent metal against this snail, followed by zinc and lead, for which the corresponding LD₅₀ values were 37.88, 261.72, and 652.55 μg/snail, respectively. The no-observed effect concentration (NOEC) values for Cu, Zn, and Pb were 10, 50, and 500 μg/snail, respectively, and the corresponding lowest-observed effect concentration (LOEC) values were 50, 100, and 1000 μg/snail. All trace metals resulted in a significant increase in the level of LPO, whereas a significant decline in the content of GSH was observed when compared with untreated controls. Treatment with both sublethal doses of the metals caused significant increase in CAT activity, except in the case of 40% LD₅₀ Zn and 80% LD₅₀ Cu, which exhibited no alteration in CAT when compared to control animals. GPx was significantly increased in snails exposed to 40% LD₅₀ Cu and Pb as well as 80% LD₅₀ Cu. However, an opposite effect was observed in snails exposed to 80% LD₅₀ Pb and in either 40 or 80% LD₅₀ of Zn-intoxicated animals. Treatment with Pb at two sublethal doses significantly increased GST activity, whereas treatment the animal with Cu caused significant inhibition in this enzyme. Snails exposed to 40% LD₅₀ Zn showed significant enhancement of GST, whereas snails exposed to 80% LD₅₀ showed ignificantly reduced GST activity. Biphasic responses were observed for CAT, GPx, and GST activities in snails exposed to Cu, Pb, and Zn, respectively. This study suggests that upregulation of the antioxidant enzyme activities, elevation of LPO, and the reduction in GSH content is related to oxidative stress in this species that could be useful as biomarkers for the evaluation of contaminated terrestrial ecosystems.     

急性光气吸入对大鼠抗氧化酶及一氧化氮和一氧化氮合酶的影响

目的　研究光气急性吸入对机体抗氧化酶活力以及一氧化氮 (NO)、一氧化氮合酶(NOS)的影响。方法　利用三光气在N ,N 二甲基甲酰胺作用下分解生成光气的方法 ,设对照组采用SD大鼠进行动态恒量染毒 ,2h后处死实验动物 ,取肺组织测定湿干比 ,取全血、血清和肝组织分别测定谷胱甘肽硫转移酶 (GST)、过氧化氢酶 (CAT)、超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH Px)、NO、NOS活力和总蛋白含量。结果　染毒组实验动物的肺湿干比明显大于对照组 ,差异有显著性(P <0 .0 1) ,血清和肝组织匀浆的GST活力明显升高 ,差异有显著性 (P <0 .0 5 ) ,血清和肝组织中SOD、全血CAT以及全血、血清、肝组织GSH Px活力明显提高 ,差异有显著性 (P <0 .0 5 ) ,血清和肝组织匀浆NO含量明显降低 ,差异有显著性 (P <0 .0 1) ,NOS活力明显升高 ,差异有显著性 (P <0 .0 1)。结论　大鼠光气急性吸入可以明显改变机体抗氧化酶系的活力 ,并且存在着一定程度的急性肝损伤 ,而这种损伤与活性氧密切相关 ,但多种抗氧化酶活力的升高却提示抗氧化治疗非光气急性中毒救治的首选。     

Time-Course Variations of DNA Damage and Biomarkers of Oxidative Stress in Tilapia (Oreochromis niloticus) Exposed to Effluents From a Swine Industry

DNA damage (Comet assay), lipoperoxidation levels (TBARS), and several biomarkers of oxidative stress such as catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione S-transferase (GST), and contents of reduced (GSH) and total (TG) glutathione were measured in liver and blood (Comet assay) of tilapia (Oreochromis niloticus) exposed for 7, 15, 30 (subchronic exposure), 60, and 90 days (chronic exposure) to two treatment lagoons of a swine-processing plant, the first an anaerobic lagoon and the second a final treatment lagoon. After the 15th day, TBARS increased in fish exposed to both lagoons, decreased on the 30th day, and on the 90th day remained similar to controls. Fish exposed subchronically and chronically to both effluents showed consistently greater DNA damage. The CAT and GPx activities showed similar profiles and were induced only during the first week and during the first and second months. GST activity was induced throughout the experimental period. On the other hand, GR activities showed inverted profiles, with progressively decreased activities in the liver of fish exposed to the anaerobic lagoon, and progressively increased activities in fish exposed to the final lagoon. GSH showed higher contents in liver after 60 and 90 days of exposure to the final lagoon. GSSG contents were higher in fish exposed to the final lagoon throughout the experimental period. After 15 days, tilapia exposed to both lagoons showed enhanced total glutathione contents. The hepatic antioxidant system and biomarkers of oxidative stress such as DNA fragmentation and TBARS contents of tilapia exposed to both lagoons presented biphasic profiles. These changes in the antioxidant status also indicate that the industrial treatment is not adequate to avoid damaging environmental effects.     

Evaluation of oxidative stress in some cases of argimone oil poisoning during a recent outbreak of epidemic dropsy in India

The study was designed to evaluate the oxidative stress and modulation of anti-oxidant enzymes in 10 accidental argimone oil poisoning cases admitted in a hospital in Delhi, India during a recent outbreak of epidemic dropsy in 1998. Serum malondialdehyde (MDA) level, oxygen free-radical scavenging enzymes such as superoxide dismutase (SOD) and catalase (CAT), and glutathione (GSH) and related enzymes, e.g. glutathione reductase (GR), glutathione peroxidase (GPx), gamma glutamyl transpeptidase (GGT) and glutathione-S-transferase (GST) in erythrocytes were assayed. The sanguinarine level in serum was measured by high-performance liquid chromatography. The serum MDA level was higher and the GSH level in erythrocytes was lower in argimone oil poisoning cases than those in controls. There was a significant decrease in SOD and GPx activities in erythrocytes of epidemic dropsy cases but no changes were observed in CAT, GR and GST assay. The depletion of GSH in erythrocytes, serum MDA level and clinical severity were dependent on serum sanguinarine level. The results indicate that sanguinarine (argimone oil) poisoning creates an oxidative stress in humans. The oxidative stress and differential modulation of anti-oxidant enzymes by sanguinarine might play a pathogenic role in epidemic dropsy, which suggests the incorporation of anti-oxidant drugs in the treatment protocol of the disease.     

Effects of Subchronic Manganese Chloride Exposure on Tambaqui (Colossoma macropomum) Tissues: Oxidative Stress and Antioxidant Defenses

This study aimed to evaluate oxidative stress parameters in juvenile tambaqui (Colossoma macropomum) exposed to 3.88 mg l^?1 Mn²⁺ for 96 hours. Biomarkers of oxidative stress, such as thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), and glutathione-S-transferase (GST) activities, as well as content of reduced glutathione (GSH), were analyzed in gill, liver, brain, and kidney. The presence of Mn²⁺ in the water corresponded to increased levels of Mn²⁺ accumulation according to the following sequence: gill > kidney > brain > liver. There was a significant increase in TBARS levels (40 %) and SOD activity (80 %) in addition to a significant decrease in GSH content (41 %) in gills of fish exposed to waterborne Mn²⁺. In hepatic tissue of the exposed animals, TBARS levels decreased significantly (35 %), whereas SOD (82 %) and GST activities (51 %) as well as GSH content (43 %) increased significantly. In brain of exposed juvenile fish, only significant decreases in SOD (32 %) and CAT activities (65 %) were observed. Moreover, the kidney of exposed fish showed a significant increase in TBARS levels (53 %) and a significant decrease in SOD activity (41 %) compared with the control. Thus, the changes in biomarkers of oxidative stress were different in the tissues, showing a specific toxicity of this metal to each organ.     

The Impact of Element–Element Interactions on Antioxidant Enzymatic Activity in the Blood of White Stork (Ciconia ciconia) Chicks

The aim of this work was to determine interrelationships among macroelements Na, K, Ca, Mg, and Fe, microelements Zn, Cu, Mn, and Co, and toxic heavy metals Pb and Cd in the blood of white stork Ciconia ciconia, during postnatal development, in different Polish environments, and their impact on the activity of antioxidant enzymes. We considered the content of thiobarbituric acid-reactive substances (TBARSs), i.e., malondialdehyde (MDA), and activity of superoxide dismutase (SOD), catalase (CAT), ceruloplasmine (CP), glutathione peroxidase (GPx), and glutathione reductase (GR). Blood samples were collected from storks developing at Odra meadows (Kłopot; southwestern Poland). They were compared with blood of chicks from several suburban sites located 20 km away from Zielona Góra (0.1 million inhabitants; southwestern Poland) and near Głogów, where a copper smelter is situated. We also conducted research in the Pomeranian region (Cecenowo; northern Poland). We collected blood samples via venipuncture of the brachial vein of chicks in 2005–2007. They were retrieved from the nest and placed in individual ventilated cotton sacks. The blood was collected using a 5-ml syringe washed with ethylenediaminetetraacetic acid (EDTA). We found significant interactions between macro- and microelements and enzymatic activity and TBARS products. We noticed the predominance of Cd and Pb participation in element–enzyme interactions. Simultaneously, we found interrelationships between cadmium and Na, K, Ca, Mg, and Fe and the activity of antioxidant enzymes SOD, CAT, CP, GR, and TBARS products in the blood of white stork chicks. In the case of lead these relationships were not numerous and they were significant for Ca, Mg, Cu, Mn, and Co. Correlations with enzymes were significant for Pb-CAT and Pb-TBARS. We noted that activities of most enzymes (SOD, CAT, CP, GR) and TBARS products are determined by their interactions with physiological elements Na, Ca, Mg, Fe, and Zn and toxic heavy metals. White stork chicks ranged in age from 17 to 59 days. Concentrations of elements in the blood were age related. Among enzymes, only SOD, CAT, and GPx were age related. Young storks differed in the case of element concentration (except for Ca, Zn, and Cd) and enzymatic activity. We found that significant element–element interaction/enzyme activity predominated in the case of physiological elements and toxic metals, which we explain by the intensive and prevailing access of toxic metals in redox reactions. This causes changes in the priority of these metals, reflected by their influence on the enzymatic activity of antioxidant enzymes. The content of Cd and Pb in blood of young storks from different regions tends to affect the lipid peroxidation process negatively. However, in many cases we observed an increase in enzymatic activity with an increase in heavy metals. This indicates the changes in oxidative stress intensity in chicks in response to environmental differentiation. The increase in lipoperoxidation modifies antioxidant enzyme activity and causes changes in SOD, CAT, CP, GPx, and GR activity in chicks from various regions, principally increases in enzyme activity in chicks from polluted environments and suburbs. We suggest that the source of heavy metals in chicks’ blood might be used as a biological test system of adaptation to oxidative stress. We also report that a high level of heavy metals is accompanied by increased lipid peroxidation. Thus young storks are probably significantly susceptible to environmental conditions. They demonstrated initiation of lipoperoxidation and oxidative modification of proteins that coincide with chemical elements, as a possible antioxidant defense system.     

Ascorbic acid does not increase the oxidative stress induced by dietary iron in C3H mice

Iron is a potent prooxidant that can induce lipid peroxidation. Ascorbic acid, a potent antioxidant, has prooxidant effects in the presence of iron in vitro. We investigated whether ascorbic acid and iron co-supplementation in ascorbic acid-sufficient mice increases hepatic oxidative stress. C3H/He mice were fed diets supplemented with iron to 100 mg/kg diet or 300 mg/kg diet with or without ascorbic acid (15 g/kg diet) for 3 wk. Liver iron concentration, malondialdehyde (MDA), glutathione (GSH), glutathione S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) were measured. High dietary iron increased liver iron concentrations slightly (P < 0.05), whereas it dramatically increased hepatic MDA (P < 0.0001). Ascorbic acid increased MDA but only in mice fed the low-iron diet (P < 0.05). The high-iron diet reduced GPx (P < 0.0001), CAT (P < 0.0005), SOD (P < 0.05), and GST (P < 0.005) activities regardless of ascorbic acid supplementation. In contrast, ascorbic acid reduced GPx (P < 0.0001) and CAT (P < 0.05) activities only in mice fed the low-iron diet. In conclusion, ascorbic acid supplementation can have prooxidant effects in the liver. However, ascorbic acid does not further increase the oxidative stress induced by increased dietary iron.     

Ameliorating effects of quercetin and chrysin on 2,3,7,8-tetrachlorodibenzo- p-dioxin-induced nephrotoxicity in rats

The aim of this study is to investigate the beneficial effects of the quercetin (Q) and chrysin (CH) against nephrotoxicity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a persistent environmental contaminant, in rats. Rats were divided randomly into six equal groups. TCDD, Q and CH were administered by gavages dissolved in corn oil at the doses of 2?μg/kg/week, 20?mg/kg/day and 50?mg/kg/day, respectively. The kidney samples were taken from all rats on day 60 for the determination of thiobarbituric acid reactive substances (TBARS), glutathione (GSH), catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) levels by spectrophotometric method. The results indicated that TCDD significantly induced lipid peroxidation and reduced antioxidant activities in rats. In contrast, Q and CH significantly prevented toxic effects of TCDD via increased GSH, CAT, GPx and SOD levels but decreased formation of TBARS. Also, it was determined that exposure to TCDD leads to significant histological damage in kidney tissue, and these effects can be eliminated with Q and CH treatment. In conclusion, the current study showed that exposure to TCDD can exert nephrotoxicity in rats. When Q and CH were given together with TCDD, they prevented nephrotoxic effects of TCDD. Their preventive effect lends more support to the role of oxidative and histological damage in the overall toxicity of TCDD.     

Antioxidant and antiapoptotic effects of capsaicin against carbon tetrachloride-induced hepatotoxicity in rats

The aim of the study was to evaluate the potential hepatoprotective utility of capsaicin against carbon tetrachloride (CCl?)-induced liver injury and to explore the possible mechanisms whereby this agent mediated its beneficial effects. We randomized 40 rats into four groups for treatment with corn oil, CCl?, capsaicin and both CCl? and capsaicin, respectively, for 8 weeks. At the end of the experiment, blood samples were collected and used for determination of aspartylaminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin, while the liver tissues were subjected to hematoxylin and eosin examination; evaluation of malondialdehyde (MDA), reduced glutathione (GSH) and active caspase-3 contents; and evaluation of superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST) activities. Animals treated with CCl? exhibited significant elevation in AST, ALT, total bilirubin and caspase-3 and exhibited significant decrease in activities of SOD, CAT, GST and GSH contents. The combination (both capsaicin and CCl?) group has preserved the liver histology, liver enzymes and bilirubin close to normal, exhibited significant induction in the activities of CAT, SOD and GST, increased the liver content of GSH and active caspase-3 and conversely showed significant decrease in liver MDA content compared to CCl? challenged rats. Capsaicin confers an appealing hepatoprotective effect which might be explained partially via diminishing the generation of MDA, induction of antioxidant systems and inhibition of active caspase-3.     

Dietary selenium and antioxidant status: toxic effects of 1,2-dimethylhydrazine in rats

Weanling male Sprague-Dawley rats were used to determine whether the mechanism of the previously reported toxicity of 1,2-dimethylhydrazine (DMH) in selenium-deficient rats was related to a diminished capacity for detoxification of reactive oxygen species via glutathione peroxidase (GSH-Px) as well as by other known pathways of detoxification, including catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST) and levels of glutathione (GSH). A 3 x 3 factorial experimental design was used to examine the acute effects of DMH treatment (0, 10 and 20 mg/kg body weight) interacting with dietary Se levels (less than 0.02, 0.1 and 0.5 mg/kg diet as sodium selenite). Animals were maintained on the test diets for 4 wk prior to challenge with DMH. Preliminary kinetics studies indicated the most appropriate time to examine antioxidant status was 3 h after DMH injection. At that time, livers and colons were analyzed for tissue levels of GSH-Px, CAT, SOD, GST and GSH. Data analysis demonstrated that Se deficiency impaired the ability of both liver and colon to mount an induced detoxification response to the acute oxidative stress generated by DMH challenge and may explain the toxicity of DMH in Se-deficient rats.     

Protective effect of Raphanus sativus on D-galactosamine induced nephrotoxicity in rats

The aim of the present study was to evaluate nephroprotective effect of Raphanus sativus ethanolic extract (RSEt) on tissue defense system in galactosamine (GalN) induced renal damage in rats. GalN was administered intraperitoneally at a dose of 400 mg/kg/b.w for three alternate days and the renal toxicity was manifested by a significant (P < 0.05) increase in the levels of renal markers such as urea, creatinine and uric acid. This was found to be associated with decreased activities of renal antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx) and glutathione reductase (GR) and depletion of renal reduced glutathione (GSH), vitamin C and vitamin E. Administration of the RSEt (850 mg/kg/body weight, oral) for 15 days to rats reduced the levels of renal markers and significantly increased the level of antioxidants. The activities of gamma glutamyl transpeptidase (GGT) and thiobarbituric acid reactive substances (TBARS) were also decreased in the kidney of RSEt treated group. Renal histology examination confirmed the damage to the kidney as it reveals severe necrosis of the proximal renal tubules with haemorrhage which was ameliorated by the treatment with RSEt. These results suggest that the R. sativus has protective effects on GalN-mediated nephrotoxicity and this may be related to the action of the antioxidant content of the extract.     

Antioxidant effect of diphenyl diselenide on oxidative damage induced by smoke in rats: involvement of glutathione

In the present study, the involvement of glutathione system in the restorative effect of diphenyl diselenide (PhSe)(2) on damage induced by cigarette smoke was investigated. Rat pups were progressively exposed to four, five, and six cigarettes for exposure periods of 15 min during their first, second, and third weeks of life. Thiobarbituric acid reactive species (TBARS) levels, components of the enzymatic antioxidant defenses (superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) activities), and non-enzymatic antioxidant defenses (vitamin C and non-protein thiol (NPSH) levels) were examined in lungs of pups. The results demonstrated an increase in lipid peroxidation and the alteration in non-enzymatic and enzymatic antioxidant defenses induced by cigarette smoke exposure in lung of pups. Administration of (PhSe)(2) (0.5mg/kg) restored TBARS levels and antioxidant defenses in lungs of rat pups exposed to cigarette smoke. (PhSe)(2) treatment increased NPSH levels and GST activity per se in lungs of rat pups. Together these results indicate that (PhSe)(2) restored oxidative damage induced by cigarette smoke exposure in lungs of rat pups. The glutathione system is involved in antioxidant effect of this compound.     

不同剂量乙醇对大鼠血清抗氧化系统的动态影响及银杏黄酮的保护效应

目的研究不同剂量乙醇对大鼠血清抗氧化系统的影响及银杏黄酮的保护作用。方法雄性SD大鼠按体重随机分为正常对照组、低、中、高乙醇组(分别为0.8、1.6、2.4g/kg)和低、高干预组(48或96mg/kg银杏黄酮+2.4g/kg乙醇)和黄酮对照组(银杏黄酮96mg/kg)。试验D30、D60、D90取尾血测定血清还原型谷胱甘肽(GSH)、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)、丙二醛(MDA)活性或水平。结果大鼠摄入低剂量乙醇后,血清SOD、CAT和GSH-Px活性逐渐升高;摄入中剂量乙醇后,SOD与CAT在30d时升高,随后降至正常水平,而GSH水平在60、90d时明显下降,MDA水平持续升高;摄入高剂量乙醇后,实验期间抗氧化酶及GSH水平持续下降,MDA不断升高。银杏黄酮干预,尤其是在高剂量干预后,抭氧化酶失活与GSH消耗程度明显下降,MDA升高幅度也相应降低。结论低剂量乙醇摄入激活了机体的抗氧化系统,高剂量则导致严重的氧化应激;银杏黄酮对高剂量乙醇所致的氧化-抗氧化失衡有明显的调节和保护作用     

低剂量辐射对荷瘤鼠放疗后血清中抗氧化酶活性的影响

目的 观察低剂量辐射对荷瘤鼠放疗后血清中抗氧化酶活性的影响。方法 采用化学比色法测定不同照射时相点血清中超氧化物歧化酶(SOD)、谷胱甘肽-S转移酶(GST)和过氧化氢酶(CAT)活性。结果 低剂量全身照射组血清中SOD、GST、CAT活力高于相应对照组;低剂量+局部放疗组(d₃ d₅)血清中SOD、GST、CAT活力显著高于局部大剂量组(c₃,c₅);尤以连续三天照射组明显。结论 低剂量辐射激活荷瘤机体抗氧化物酶可能是低剂量辐射抑瘤作用的部分机制     

Behavioral and histologic neuroprotection of aqueous garlic extract after reversible focal cerebral ischemia

The objective of the present study was to investigate the effects of aqueous garlic extract (AGE) on neurobehavioral activities, malondialdehyde (MDA) and reduced glutathione (GSH) levels, glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), superoxide dismutase (SOD), catalase (CAT), and sodium-potassium ATPase (Na(+),K(+)-ATPase) activities, and glutamate and aspartate content in a middle cerebral artery (MCA) occlusion (MCAO) model of acute cerebral ischemia in rats. The right MCA of male Wistar rats was occluded for 2 hours using intraluminal 4-0 monofilament, and reperfusion was allowed for 22 hours. MCAO caused significant depletion in GSH and its dependent enzymes (GPx, GR, and GST) and significant elevation of MDA, glutamate, and aspartate. The activities of Na(+),K(+)- ATPase, SOD, and CAT were decreased significantly by MCAO. The neurobehavioral activities (grip strength, spontaneous motor activity, and motor coordination) were also decreased significantly in the MCAO group. All of the alterations induced by ischemia were significantly attenuated by pretreatment with AGE (500 mg/mL/kg of body weight, i.p.) 30 minutes before the induction of MCAO and correlated well with histopathology by decreasing the neuronal cell death following MCAO and reperfusion. These findings suggest that AGE effectively modulates neurobehavioral and neurochemical changes in focal ischemia, most probably by virtue of its antioxidant properties.     

Lead-induced dysregulation of superoxide dismutases, catalase, glutathione peroxidase, and guanylate cyclase

Previous studies from this laboratory have demonstrated the presence of oxidative stress and its role in the pathogenesis of lead-induced hypertension. This study was designed to determine whether oxidative stress in animals with lead-induced hypertension is associated with dysregulation of the activities of the main antioxidant enzymes, namely superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX). In addition, we aimed to determine the effect of lead on the regulation of guanylate cyclase (GC) expression. Male Sprague-Dawley rats were randomly assigned to control and lead-exposed groups, and immunodetectable Cu/Zn SOD, Mn SOD, CAT, and GPX were determined by immunoblotting in the thoracic aorta. Additionally, the activities of these enzymes were measured in the renal cortex, medulla, and thoracic aorta. Furthermore, immunodetectable GC was determined in the thoracic aorta. In the thoracic aorta, lead exposure resulted in significant upregulation of aortic Cu/Zn SOD activity, while CAT and GPX activity and CuZn SOD, Mn SOD, and CAT protein abundance were unchanged. Conversely, GC protein abundance was decreased in thoracic aorta. In renal cortex and medulla, CAT and Cu/Zn SOD activities were increased, while GPX activity was unchanged. Lead-exposed animals exhibited upregulation of some antioxidant enzyme activities, most likely as a compensatory response to lead exposure. However, other enzymes did not compensate in the face of oxidative stress, suggestive of an antioxidant/oxidant imbalance. These findings, combined with decrease in aortic GC protein abundance, provide further evidence for dysregulation of antioxidant/oxidant balance and hypertension in this model.