Temperature increase results in oxidative stress in goldfish tissues. 2. Antioxidant and associated enzymes

Activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GR), and glucose-6-phophate dehydrogenase (G6PDH) were measured in four tissues of goldfish, Carassius auratus L., over 1-12 h of high temperature (35 degrees C) exposure followed by 4 or 24 h of lower temperature (21 degrees C) recovery. SOD activity was strongly affected by heat shock, increasing 4-fold in brain, liver, and kidney, but was mainly reversed at recovery. In some tissues, activities of SOD, catalase, GPx, and G6PDH decreased significantly after 1 h heat shock exposure suggesting that thermal inactivation possibly occurred, but were renewed at further exposure. In many cases, 4 h of return to the initial temperature decreased enzyme activities. High correlation coefficients between SOD activities and levels of lipid peroxidation products suggest that these products might be involved in up-regulation of antioxidant defense. Several enzymes (SOD, GST, GR) responded to stress in coordinated manner.     

The interactive effect of elevated temperature on deltamethrin-induced biochemical stress responses in Channa punctata Bloch

There are reports showing interactive effect of environmental factors with the toxic outcome of chemicals. We studied the interactive effect of elevated temperature as an abiotic stressor on deltamethrin-induced biochemical stress responses in a freshwater fish, Channa punctata Bloch. Heat stress (∼12 °C above ambient temperature for 3 h) and pesticide exposure (deltamethrin 0.75 ppb for 48 h) showed significant induction of heat shock protein-70 (HSP70) in liver, kidney and gills of fishes. Elevated temperature when followed by deltamethrin exposure showed synergistic effect showing a high level of HSP70 in liver and gills whereas response in the kidney was opposite. On the contrary, when deltamethrin exposure followed the heat stress, no significant difference was observed. Protein carbonylation was found to be more pronounced in heat-stressed group compared with control fish group. A significant increase in lipid peroxidation (LPO) was observed in different tissues of fish exposed to either of the stressors. In the kidney of fish exposed to heat stress followed by deltamethrin, LPO was relatively lower as compared to other treatments. Thiols content such as reduced glutathione (GSH), total thiols (T-SH), non-protein thiols (NP-SH) and protein thiols (P-SH) showed no consistent pattern in different tissues. In deltamethrin-exposed group that was subsequently exposed to heat stress, the GSH content was higher in liver and lower in both kidney and gills when compared with other groups. Alteration in the activities of antioxidant enzymes such as catalase (CAT), glutathione S-transferase (GST), glutathione reductase (GR) and glutathione peroxidase (GPx) was also observed when fish were exposed to heat stress and/or deltamethrin. Our study demonstrated that heat stress modulated biochemical stress responses in fish showing a tissue specific pattern. This implies that fish has the capacity to elicit differential response to exposure to abiotic stressors in order to reduce the systemic magnitude of stress which may otherwise lead to severe dysfunction of vital tissues.     

The effects of selenium on oxidative stress biomarkers in the freshwater characid fish matrinxã, Brycon cephalus (Günther, 1869) exposed to organophosphate insecticide Folisuper 600 BR (methyl parathion)

Methyl parathion (MP), an organophosphate widely applied in agriculture and aquaculture, induces oxidative stress due to free radical generation and changes in the antioxidant defense system. The antioxidant roles of selenium (Se) were evaluated in Brycon cephalus exposed to 2 mg L(-1) of Folisuper 600 BR (MP commercial formulation - MPc, 600 g L(-1)) for 96 h. Catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione S-transferase (GST), reduced glutathione (GSH) and lipid peroxidation (LPO) levels in the gills, white muscle and liver were evaluated in fish fed on diets containing 0 or 1.5 mg Se kg(-1) for 8 weeks. In fish treated with a Se-free diet, the MPc exposure increased SOD and CAT activities in all tissues. However, the GPx activity decreased in white muscle and gills whereas no alterations were observed in the liver. MPc also increased GST activity in all tissues with a concurrent decrease in GSH levels. LPO values increased in white muscle and gills and did not change in liver after MPc exposure. A Se-supplemented diet reversed these findings, preventing increases in LPO levels and concurrent decreases in GPx activity in gills and white muscle. Similarly, GSH levels were maintained in all tissue after MPc exposure. These results suggest that dietary Se supplementation protects cells against MPc-induced oxidative stress.     

铜对梨形环棱螺抗氧化酶活性和金属硫蛋白含量的影响

本实验采用暴露重金属的方法,研究了不同浓度硫酸铜（Cu2+ 分别为0、0.005、0.01、0.02、0.05 mg/L）在不同暴露时间（0—14d）下对梨形环棱螺（Bellamya purificata）过氧化氢酶(CAT)、超氧化物歧化酶（SOD）、谷胱甘肽硫转移酶（GST）的活性、还原性谷胱甘肽（GSH）和金属硫蛋白（MT）含量的影响,以探讨Cu2+ 对梨形环棱螺的氧化损伤及其防御作用的机理,并为水环境Cu2+ 污染的早期诊断及生态风险评价提供科学的依据。结果表明：Cu2+对梨形环棱螺肝脏和鳃中CAT、SOD、GST、GSH 和MT 均有明显影响,表现出时间剂量效应。SOD在前4天、CAT在前3天酶活性总体上表现出诱导趋势, GST在前4天酶活性处于诱导状态,随着暴露时间的延长,酶活性下降,到第5天时表现出抑制趋势;随着时间的进一步增长,至14d时, 0.005 mg/L剂量组酶活性维持在正常值附近波动, 0.01 mg/L剂量组酶活性被诱导, 0.02 mg/L剂量组酶活性在肝脏中表现为诱导而在鳃中则被抑制,0.05 mg/L剂量组酶活性被抑制。肝脏和鳃GSH含量的变化与GST相似,在短时间内表现出诱导效应,肝脏GSH在暴露的前5天、鳃GSH在暴露的前4天均处于诱导状态,随着暴露时间的延长,0.005 mg/L剂量组表现出诱导,0.05 mg/L剂量组则受到抑制。MT在整个实验期间均处于诱导状态,各剂量组在0.5d被极显著诱导,随后MT含量出现起伏波动,有上升和下降,至第14天时达到一稳定水平。其中,0.01 mg/L剂量组肝脏的MT在整个实验期间均被极显著地诱导（P <0.01）,0.01 mg/L 剂量组的鳃组织MT除第10天外也被极显著诱导（P <0.01）。在暴露14d时,除0.05 mg/L剂量组的肝脏MT外,其余处于极显著诱导状态（P <0.01）。     

Oxidative stress biomarkers in the freshwater characid fish, Brycon cephalus, exposed to organophosphorus insecticide Folisuper 600 (methyl parathion)

Methyl parathion (MP) is an organophosphorus insecticide used worldwide in agriculture and aquaculture due to its high activity against a broad spectrum of insect pests. The effect of a single exposure to 2 mg L(- 1) of a commercial formulation of MP (MPc: Folisuper 600(R), MP 600 g L(- 1)) on catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione S-transferase (GST), reduced glutathione (GSH) and lipid peroxidation (LPO) of the liver, white muscle and gills of Brycon cephalus was evaluated after 96 h of treatment. MPc exposure resulted in a significant induction of SOD, CAT and GST activity in all tissues. However, the GPx activity decreased significantly in white muscle and gills, whereas no alterations were observed in hepatic GPx activity. MPc also induced a significant increase in LPO values in the white muscle and gills, while hepatic LPO levels did not show any significant alteration. The current data suggest that MPc has oxidative-stress-inducing potential in fish, and that gills and white muscle are the most sensitive organs of B. cephalus, with poor antioxidant potentials. The various parameters studied in this investigation can also be used as biomarkers of exposure to MPc.     

Dehydroepiandrosterone improves hepatic antioxidant reserve and stimulates Akt signaling in young and old rats

This study examined, in the liver of young and old (3- and 24-month-old, respectively) healthy Wistar rats, the in vivo effect of dehydroepiandrosterone (DHEA) (10mg/kg body weight) administered subcutaneously for 5 weeks. Reduced (GSH) and oxidized (GSSG) glutathione levels, glucose-6-phosphate dehydrogenase (G6PDH), glutathione-S-transferase (GST), glutathione peroxidase (GPx) and catalase (CAT) activities, hydrogen peroxide concentration, GST and p-Akt/Akt immunocontent ratio were assessed in hepatic tissue. DHEA treatment significantly increased total glutathione content (17%) and GSH (22%) in 3- and 24-month-old treated groups when compared to control groups. The aging factor increased G6PDH (51%) and GPx (22%) activities as well as the hydrogen peroxide concentration (33%), independently of treatment. DHEA treatment increased p-Akt (54%) and p-Akt/Akt ratio (36%) immunocontents in both treated groups. Increased serum levels of alanine aminotransferase (ALT) in aged rats were reduced by DHEA treatment (34%).     

磷酸戊糖途径的调节对红豆杉细胞生长及紫杉醇合成的影响

在正常的红豆杉细胞悬浮培养过程,葡萄糖-6-磷酸脱氢酶(G6PDH)活性的变化趋势与生物量的基本相似。而在chitosan处理的细胞中G6PDH活性升高而生物量下降。100 mg·L^-1 chitosan和500mg·L^-1 chitosan均对细胞G6PDH具有诱导作用,且后者的诱导强度较前者的高。乙二醇双2-氨基乙基醚四乙酸(EGTA)的加入降低chitosan对细胞G6PDH的诱导程度,显示chitosan对G6PDH的诱导需要Ca²⁺的参与。谷胱甘肽(GHS)的处理可反馈抑制chitosan对细胞G6PDH的诱导。通过分析调节后G6PDH的各种活性与细胞中紫杉醇产量的关系,认为采用合适的处理方法调节磷酸戊糖途径,有利于红豆杉细胞合成紫杉醇。     

Tissue lipid peroxidation and glutathione‐dependent enzyme status in patients with oral squamous cell carcinoma

We examined the extent of lipid peroxidation and the status of reduced glutathione (GSH) and the GSH‐dependent enzymes—glutathione peroxidase (GPx) and glutathione‐S‐transferase (GST)—in oral tumour tissues from 33 adult oral cancer patients and an equal number of age‐ and sex‐matched normal subjects. Diminished lipid peroxidation in the oral tumour tissue was accompanied by a significant decrease in phospholipids and an increase in the cholesterol/phospholipid (C/P) ratio. The concentration of glutathione and the activities of GPx and GST were elevated in oral tumour tissues. These findings suggest that GSH‐ and GSH‐dependent enzymes play a crucial role in tobacco‐related tumourigenesis and may be considered as markers of carcinogen exposure. Copyright © 1999 John Wiley & Sons, Ltd.     

IGF and GH mRNA levels are suppressed upon exposure to micromolar concentrations of cobalt and zinc in rainbow trout white muscle

The objective of this study was to assess the effects of cobalt and zinc exposure of rainbow trout (Oncorhynchus mykiss) on insulin like growth factors (IGF) and growth hormone (GH). Mature rainbow trouts were exposed to 0.42, 2.1, 4.2, 21 and 42μmol/L Co(2+) (added as CoCl(2)·6H(2)O) and 0.34, 1.7, 3.4, 17 and 34μmol/L Zn(2+) (added as ZnSO(4)i·7H(2)O). After 6, 12, 24 and 48h of treatment, expressions of white muscle IGF-I, IGF-II and GH mRNAs were measured by means of quantitative Real Time PCR. During the exposure experiments, no mortalities occurred. The most effective metal concentrations, which caused significant alterations, were determined to be 42μmol/L Co(2+) (10mg CoCl(2)·6H(2)O/L) and 3.4μmol/L Zn(+2) (1mg ZnSO(4)·7H(2)O/L). The following results were obtained for these concentrations. Expression of IGF-I did not change at 6h in zinc treatment while the decrease (p<0.05) was observed at 12h and 24h, and this decrease became stronger at 48h. Cobalt exposure caused a decrease in IGF-I mRNA level at 6h, 12h, 24h and 48h (p<0.05). Both zinc and cobalt exposure resulted in significant decreases in GH expression at 6h. Exposure of trout to Zn resulted in a decrease in expression of IGF-II starting from 6h whereas the significant decrease started at 6h in cobalt exposure and this decrease elevated at 24h. The results indicate that micromolar cobalt and zinc exposure causes significant attenuation in the expressions of these three genes' time dependently. Our findings show that IGF-I is the most resistant and GH is the most sensitive component against cobalt and zinc exposure. We conclude that IGF/GH axis might be strongly affected by the short term exposure to low micromolar concentrations of zinc and cobalt due to alterations of these genes.     

Heat stress‐induced alterations of antioxidants in the freshwater fish Channa punctata Bloch

The effect of elevated temperature on the antioxidants in the freshwater fish Channa punctata was investigated. Fish stressed with an elevated temperature of 12° C, range ± 1° C over the ambient temperature for 3 h showed a significant ( P  < 0·05–0·01) reduction in the levels of antioxidants: reduced glutathione (GSH) and non‐protein thiols. Activity of glutathione reductase was also reduced in all the tissues (liver, kidney and gills) after 3 h of heat stress and 24 h recovery. Catalase (CAT) showed enhanced activity in liver in both the conditions while gills and kidney showed a decreased CAT activity. Glutathione S‐transferase (GST) activity in kidney and liver decreased significantly ( P  < 0·05–0·01) after 3 h of heat stress. At 24 h GST activity showed a tendency to normalize in all the tissues along with a concomitant increase in the GSH level in the kidney. Total and protein thiols in heat stressed fish when matched with controls, showed significant ( P  < 0·05) reduction in the kidney only with a transient increase in liver and gills. Heat shock also induced lipid peroxidation in 3 h heat‐treated and recovery groups when compared with controls. Elevated temperature therefore resulted in tissue specific and time‐dependent alterations of antioxidants in the fish. It also induced lipid peroxidation in various tissues.     

Proteasome and antioxidant responses in Cottus gobio during a combined exposure to heat stress and cadmium

Temperature and trace metals are common environmental stressors, and their importance is increasing due to global climate change and anthropogenic pollution. Oxidative damage and antioxidant properties have been studied in liver and gills of the European bullhead (Cottus gobio) subjected to cadmium (CdCl(2) at nominal concentrations of 0.01 and 1mg/L) for 4 days at either 15°C or 21°C. First, exposure to 1mg Cd/L induced a high mortality rate (67%) in fish held at 21°C. Regarding the antioxidant enzymes, exposure to 0.01 mg Cd/L significantly increased the activity of superoxide dismutase (SOD) and decreased the activity of glutathione reductase (GR) in liver, independently of heat stress. In gills, exposure to 21°C resulted in a significantly increased activity of glutathione peroxidase (GPx), whereas the activity of glutathione S-transferase (GST) was significantly reduced as compared to fish exposed to 15°C. Furthermore, regardless of Cd stress, exposure to elevated temperature resulted in a significant decrease of lipid peroxidation (LPO) level in liver and in a significant increase in the activity of chymotrypsin-like 20S proteasome in both studied tissues of C. gobio. Overall, the present results indicated that elevated temperature and cadmium exposure independently influenced the antioxidant defense system in bullhead with clear tissue-specific and stress-specific antioxidant responses. Further, elevated temperature affected the hepatic lipid peroxidation and the activity of 20S proteasome in both tissues.     

Aortic-banding induces myocardial oxidative stress and changes in concentration and activity of antioxidants in male Wistar rats

Myocardial activity and gene expression of antioxidant defenses and oxidative damage were examined in an experimental model of pressure overload hypertrophy. Male Wistar rats were divided into abdominal aortic-banded or sham-operated groups. After 30 days, arterial pressure and heart rate were measured. Heart, lung, and liver were extracted and weighted to evaluate cardiac hypertrophy and pulmonary and hepatic congestion. Heart homogenates were prepared to quantify lipid peroxidation (LPO); the activities of superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx) and glutathione reductase (GR); and Cu-Zn SOD and GST concentrations. Total glutathione (GSH) myocardial content was also measured. Arterial pressure (142 +/- 17 mmHg) and cardiac hypertrophy index (3.4 +/- 0.45 mg/g) were significantly increased (by 38% and 22%, respectively, p<0.0001) in the aortic-banded group. LPO was enhanced by 55% in the aortic-banded group (11891 +/- 766 cps/mg protein, p<0.001) compared with that in the controls. SOD activity and concentration were higher (40% and 38%, 15.15 +/- 1.03 U/mg protein, 49.187 pixels, respectively, p<0.05) in the aortic-banded group than in the controls. Aortic-banding induced a decrease by 28% in GST (48 +/- 10 pmol/min/mg protein, p<0.005), by 36% in GPx (38.2 +/- 9.5 nmol/min/mg protein, p<0.005), by 31% in GR activities (1.55 +/- 0.23 nmol/mg protein, p<0.0005), and by 43% in GSH content (0.13 +/- 0.02 nmol/mg protein, p<0.005). In conclusion, in this model it was observed that myocardial oxidative stress induces alterations in antioxidant enzyme activities and protein expression. The follow up of these parameters could afford an early therapeutical window to avoid heart failure progression.     

镉对尖紫蛤抗氧化酶活性及脂质过氧化的影响

为阐明镉(Cd2+)对尖紫蛤消化盲囊和鳃抗氧化酶的毒性影响程度,研究了不同浓度的Cd2+(0.005、0.05、0.5 mg/L)在不同暴露时间(24h、72h、120h)对尖紫蛤鳃和消化盲囊中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-PX)的活性以及丙二醛(MDA)含量的影响。结果表明,在Cd2+浓度为0.005 mg/L时,在整个实验期间Cd2+对消化盲囊和鳃内的SOD、CAT、GSH-PX活性并无显著影响。在Cd2+浓度为0.05 mg/L和0.5 mg/L时,SOD、CAT、GSH-PX在鳃和消化盲囊中的活性都呈现出明显的时间剂量依赖关系。在0.05 mg/L暴露时,鳃和消化盲囊中的SOD、CAT和GSH-PX的活性随时间逐渐增强,在72h时达到最大值,但在120h时略有降低。在0.5 mg/L暴露时,消化盲囊中SOD、CAT及鳃中CAT活性在24h时上升达到最大值,但鳃中SOD直到72h才达到最大值,并均在120h下降到最低,其中消化盲囊中SOD和CAT活性在120h低于对照组,这可能与消化盲囊对Cd2+的敏感性高于鳃有关。在0.5 mg/L暴露的鳃中,GSH-PX在24h、72h活性并不上升,在120h甚至低于正常水平,0.5 mg/L暴露的消化盲囊中,24h时迅速增高,然后逐渐下降到正常值。这可能与Cd2+结合了GSH-PX的活性中心,降低了GSH-PX的活性有关。与3种酶活性随着时间延长和剂量的增加,酶活性会降低的变化趋势不同,鳃和消化盲囊中的MDA的含量随时间延长和剂量的增加而增加,并不出现下降,这表明尖紫蛤鳃和消化盲囊中的MDA含量可以灵敏的反映机体内的氧化损伤程度,但不能敏感的反映水体中Cd2+的污染情况。     

Effects of cadmium exposure on lipid peroxidation and the antioxidant system in fourth-instar larvae of Propsilocerus akamusi (Diptera: Chironomidae) under laboratory conditions

Enzymatic antioxidants such as selenium-dependent glutathione peroxidase (GPx), glutathione transferase (GST), glutathione reductase (GR), and superoxide dismutases (SOD), as well as the concentration of hydrogen peroxide (H2O2) and malondialdehyde (MDA, an indicator of lipid peroxidation) were determined to identify which antioxidant enzymes participate in the efficient scavenging of ROS generated upon exposure to high doses of Cd2+ in fourth-instar Propsilocerus akamusi (Tokuna) (Diptera: Chironomidae) larvae after 72-h exposure. A significant increase in MDA levels and a change in GR and GPx activities in the Cd(2+)-treated P. akamusi were observed. The MDA in 25.0 and 50.0 mmol/liter treatments was significantly higher than that of the control dose after 72 h exposure. GPx activity was significantly induced by Cd2+ exposure only in the 50.0-mmol/liter treatment with a 0.59-fold increase in the control. All doses of Cd2+ significantly suppressed GR activity compared with the findings for the control dose, with an inhibited rate up to 0.55-fold in the 25.0 mmol/liter Cd2+ treatment. SOD and GST activities were not altered. The results indicate that Cd2+ can induce oxidative stress as indicated by the changes in lipid peroxidation and antioxidant status. For P. akamusi, an increase in the dose that the threshold needed for defense (namely, MDA level and GPx activity) activation was achieved. From this, organisms can be hypothesized to enable cells to avoid oxidant stress up to a certain extent where damage is again measurable (higher Cd2+ concentration).     

Protective effect of resveratrol and vitamin E against ethanol-induced oxidative damage in mice: biochemical and immunological basis

The metabolism of ethanol gives rise to the generation of excess amounts of reactive oxygen species and is also associated with immune dysfunction. We examined the efficacy of resveratrol and vitamin E on the immunomodulatory activity and vascular function in mice with liver abnormalities induced by chronic ethanol consumption by measuring the protein, liver-specific transaminase enzymes, antioxidant enzymes and non-enzymes such as reduced glutathione (GSH) content, thiobarbituric acid reactive substance (TBARS) level, nitrite level, and activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione peroxidase (GPx) and glutathione-S-transferase (GST), and cytokines such as interleukin (IL)-2, IL-4, IL-10, tumor necrosis factor (TNF)-alpha, gamma interferon (IFN-gamma), vascular endothelial growth factor (VEGF)-A and transforming growth factor (TGF)-beta1 in mice blood. Ethanol (1.6 g/kg body wt/day) exposure for 12 wks significantly increased TBARS and nitrite levels and GST activity, and significantly decreased GSH content and the activities of SOD, CAT, GR and GPx in whole blood hemolyzate of 8-10 wks-old male BALB/c mice (weighing 20-30 g). Ethanol exposure also elevated the activities of transaminase enzymes (AST and ALT), IL-10, TNF-alpha, IFN-gamma, VEGF-A and TGF-beta1, while decreasing the albumin concentration and IL-4 activity in the serum. Both resveratrol (5 mg kg(-1) day(-1)) and vitamin E (80 mg kg(-1) day(-1)) treatment significantly reduced AST, ALT, GST, IL-10, TNF-alpha, IFN-gamma, VEGF-A and TGF-beta1 activities and levels of TBARS and nitrite, and elevated albumin content, GSH level and activities of SOD, CAT, GR and GPx, compared to ethanol-treated group. Thus, results from the study demonstrated that both resveratrol (5 mg kg(-1) day(-1)) and vitamin E (80 mg kg(-1) day(-1)) can effectively ameliorate ethanol (1.6 g kg(-1) day(-1))-induced oxidative challenges, immunomodulatory activity and angiogenesis processes.     

Oxidative stress in digestive gland and gill of the brown mussel (Perna perna) exposed to air and re-submersed

Mussels Perna perna were exposed to air for 24 h showing a clear increase in the levels of lipid peroxidation and oxidative DNA damage, measured as 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodGuo). The levels of lipid peroxidation increased both in the digestive gland and gills, while oxidative DNA damage increased only in the gills. After the 24 h of air exposure, mussels were re-submersed for a period of 3 h, leading values to return to a pre-aerial exposure levels. Control animals were kept immersed during the whole period. Several antioxidant and complementary enzymes (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PDH), glutathione S-transferase (GST) and the levels of total glutathione (Total GSH) were assayed in a second set of experiments where one group of mussels were exposed to air for 18 h and other to 1 h re-submersion after 18 h aerial exposure. Only a 52% increase in the glutathione S-transferase activity was observed in the digestive gland, which remained elevated to about 40% after 1 h re-submersion, showing that defense systems can be modulated even during oxygen deprivation in P. perna. The DNA and lipid oxidative damage observed after aerial exposure indicates that mussels face an oxidative challenge, and are able to counteract such an “insult” as values of lipid peroxidation and DNA damage returned to control values after 3 h re-submersion.     

Amelioration of cadmium-induced cardiac impairment by taurine

The present study has been designed to investigate the protective role of taurine (2-aminoethanesulfonic acid), a sulfur containing conditionally essential amino acid, against cadmium-induced cardiac dysfunction in mice. Cadmium chloride (CdCl(2)) was used as the source of cadmium and it was administered orally at a dose of 4mg/kg body weight for 6 days. Cadmium exposure caused significant accumulation of the cadmium and iron in mice hearts tissue. Levels of serum specific markers related to cardiac impairments, e.g. total cholesterol, HDL cholesterol and triglyceride were altered due to cadmium toxicity. Reduction in the activities of antioxidant enzymes, namely, superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPx) and glucose-6-phosphate dehydrogenase (G6PD) have been observed in cadmium exposed mice. Cadmium intoxication also decreased the cardiac glutathione (GSH) and total thiols contents and increased the levels of oxidized glutathione (GSSG), lipid peroxidation end products, protein carbonyl content and the extent of DNA fragmentation. Oral administration of taurine at a dose of 100mg/kg body weight for 5 days, however, prevented all the toxin-induced oxidative impairments mentioned above. "Ferric Reducing/Antioxidant Power (FRAP) assay" showed that taurine could protect the cardiac tissue by preventing cadmium-induced reduction of the intracellular antioxidant power. Histological examination of cardiac segments also supported the beneficial role of taurine against cadmium-induced damages in the murine hearts. Effect of a well established antioxidant, vitamin C has been included in the study as a positive control. Combining all, results suggest that taurine attenuates cadmium-induced impairment in mice hearts.     

Modulation of antioxidant defence system in brain of rainbow trout (Oncorhynchus mykiss) after chronic carbamazepine treatment

We investigated the effect of long-term exposure to CBZ on the antioxidant system in brain tissue of rainbow trout. Fish were exposed to sublethal concentrations of CBZ (1.0 μg/L, 0.2 mg/L or 2.0 mg/L) for 7, 21, and 42 days. Oxidative stress indices (LPO and CP) and activities of antioxidant enzymes (SOD, CAT, GPx and GR) in fish brain were measured. In addition, non-enzymatic antioxidant (GSH) was determined after 42 days exposure. Carbamazepine exposure at 0.2 mg/L led to significant increases (p < 0.05) of LPO and CP after 42 days and, at 2.0 mg/L, after 21 days. Activities of the antioxidant enzymes SOD, CAT, and GPx in CBZ-treated groups slightly increased during the first period (7 days). However, activities of all measured antioxidant enzymes were significantly inhibited (p < 0.05) at 0.2 mg/L exposure after 42 days and after 21 days at 2.0 mg/L. After 42 days, the content of GSH in fish brain was significantly lower (p < 0.05) in groups exposed to CBZ at 0.2 mg/L and 2.0 mg/L than in other groups. Prolonged exposure to CBZ resulted in excess reactive oxygen species formation, finally resulting in oxidative damage to lipids and proteins and inhibited antioxidant capacities in fish brain. In short, a low level of oxidative stress could induce the adaptive responses of antioxidant enzymes, but long-term exposure to CBZ could lead to serious oxidative damage in fish brain.     

Effects of cadmium on carbohydrate and protein metabolisms in the freshwater crab Sinopotamon yangtsekiense

The physiological impact of Cd(2+) on Sinopotamon yangtsekiense was evaluated through changes of selected parameters considered as key elements of carbohydrate and protein metabolisms. Crab were exposed to 0.725, 1.45, 2.9mg·L(-1) Cd(2+) for 7, 14 and 21 days. A time- and/or concentration- dependent decrease in muscle glycogen and increase in LDH activity suggested that glycolysis was accelerated during the treatments. Increased protease activity, lowering of FAA and the initially increased and subsequently decreased aminotransferase activities suggest an enhanced protein mobilization during early Cd(2+) exposure followed by a metabolic impairment during late exposure. Decreased hemolymph glucose level was observed in the crabs treated with 2.9mg·L(-1) Cd(2+) for 21d, suggesting an impaired gluconeogenesis. Ammonia level barely changed during the 14d Cd(2+) exposure most likely due to the increased urea and glutamine production; After 1.45 and 2.9mg·L(-1) Cd(2+) treatment for 21d, ammonia was observed increased followed by an exclusive increase in glutamine. Taken together, our results indicate that carbohydrate and protein are mobilized to a varying degree as a compensatory metabolism to response to the energy stress during acute Cd(2+) exposure. As the time lapsed, some symptoms on metabolism obstacle reflect the toxic effect of sublethal Cd(2+).