Investigation of protective effects of selenium and vitamin E against DNA oxidation, membrane damage and alteration of COMT metabolism in smoke-exposed male mice (Mus musculus, Balb/c)

In our study, the protective effects of vitamin E and Se (selenium) against cigarette smoke hazards on second-hand smoker (passive smoker) male mice (Balb/c) were investigated. Serum MDA levels in the smoke-exposed mice were found higher than serum MDA levels of control mice and Se- and vitamin E-treated mice. But, the MDA levels of smoke-exposed plus Se- and vitamin E-treated mice were found lower than MDA levels of smoke-exposed mice at the end of the three and five months. According to these results, application of vitamin E and Se, when given to smoke-exposed mice together, had an additive protective effect against cigarette smoke hazards (p < 0.05). Vitamin E also had protective effect on formation of 8-OHdG in smoke-exposed mice. The serum 8-OHdG amounts of smoke-exposed plus vitamin E-treated mice were found low, but the serum 8-OHdG amounts of smoke-exposed mice were found high. Also 8-OHdG levels in the serum of the smoke-exposed mice were increased which occurs as a result of DNA oxidation (p < 0.05). At the end of the three and five months, COMT (catechol-o-methyl transferase) activity of smoke-exposed mice livers were increased but, vitamin E and/or Se showed a significant protective effect on changing of COMT activity only at the end of the 5 months. Our results showed that MDA levels and 8-OHdG amounts were increased in the serum of smoke-exposed mice. On the other hand, vitamin E and Se had an additive protective effect against increasing MDA level. Also vitamin E had a protective effect against formation of 8-OHdG amounts and COMT activity alterations.     

镉对长江华溪蟹肝胰腺抗氧化酶活力的影响

重金属对环境的污染已成为全球面临的首要问题之一,其中镉(Cd2 )是一种广泛存在的毒性污染物,能通过消化道和呼吸道进入生物体,对机体造成损伤(Zyadah and Abdel-Baky,2000)。研究表明,Cd2 可以通过Ca2 通道穿过细胞膜进入机体(Roesijadi and Robinson,1994),诱导产生大量自由基和活性氧(ROS),从而形成氧胁迫(Toppi andGabbrielli,1994;Hegedus et al.,2001)。ROS可以与体内脂质、蛋白质和核酸反应,导致脂质过氧化、细胞膜损伤并且影响多种酶的活力,对生物体造成威胁。由于在水生生态系统中生物富集污染物的作用明显,故相对于陆地生…     

Effect of chronic cadmium exposure on antioxidant defense system in some tissues of rats: protective effect of selenium

The effects of selenium (Se) on antioxidant defense system in liver and kidneys of rats with cadmium (Cd)-induced toxicity were examined. Cd exposure (15 mg Cd/kg b.m./day as CdCl(2) for 4 weeks) resulted in increased lipid peroxidation (LP) in both organs (p<0.005 and p<0.01). Vitamin C (Vit C) was decreased in the liver (p<0.005), whereas vitamin E (Vit E) was increased in the liver and kidneys (p<0.005 and p<0.05) of Cd-exposed animals. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were decreased in both tissues (p<0.05 and p<0.005), whereas catalase (CAT) activity was decreased only in liver (p<0.005). Glutathione S-transferase (GST) increased in both tissues (p<0.005 and p<0.01). Treatment with Se (0.5 mg Se/kg b.m./day as Na(2)SeO(3) for 4 weeks) significantly increased liver and kidneys SOD and GSH-Px activities (p<0.05 to p<0.005), as well as CAT and GST activities only in the liver (p<0.01). In animals exposed to Se, both the concentrations of Vit C (p<0.01) and Vit E (p<0.005) were increased in both tissues. Co-treatment with Se resulted in reversal of oxidative stress with significant decline in analyzed tissues Cd burden. Our results show that Se may ameliorate Cd-induced oxidative stress by decreasing LP and altering antioxidant defense system in rat liver and kidneys and that Se demonstrates the protective effect from cadmium-induced oxidative damage.     

Superoxide dismutase, catalase and glutathione peroxidase activities in the brain of streptozotocin induced diabetic rats

Brain antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) levels were studied in the brains of early diabetic (72 hr) and long term diabetic (one month) rats. Diabetes was induced by injecting streptozotocin (50 mg/kg, i.p.) in citrate buffer. One group of diabetic rats was treated with insulin (1U/day/animal). The results indicate that early diabetic rats exhibit increased SOD and CAT activities with no alteration in the GPX activity. On the contrary, increased CAT decreased GPX activities with no alteration in the SOD activity, was noted in the long-term Diabetic rats. Insulin treatment reversed these alterations in both the groups. It can be concluded that, in diabetic condition antioxidant enzyme levels are elevated and insulin treatment attenuated these changes. Hence, diabetes mellitus, if left untreated, may initiate degenerative processes and other CNS complications due to accumulation of oxidative free radicals.     

Selenium deficiency activates mouse liver Nrf2-ARE but vitamin E deficiency does not

Selenium (Se) and vitamin E are antioxidant micronutrients. Se functions through selenoproteins and vitamin E reacts with oxidizing molecules in membranes. The relationship of these micronutrients with the Nrf2-antioxidant response element (ARE) pathway was investigated using ARE-reporter mice and Nrf2-/- mice. Weanling males were fed Se-deficient (0 Se), vitamin E-deficient (0 E), or control diet for 16 or 22 weeks. The ARE reporter was elevated 450-fold in 0 Se liver but was not elevated in 0 E liver. Antioxidant enzymes induced by Nrf2-ARE (glutathione S-transferase (GST), NAD(P)H quinone oxidoreductase (NQOR), and heme oxygenase-1 (HO-1)) were elevated in 0 Se livers but not in 0 E livers. Deletion of Nrf2 had varying effects on the inductions, with GST induction being abolished by it but induction of NQOR and HO-1 still occurring. Thus, Se deficiency, but not vitamin E deficiency, induces a number of enzymes that protect against oxidative stress and modify xenobiotic metabolism through Nrf2-ARE and other stress-response pathways. We conclude that Se deficiency causes cytosolic oxidative stress but that vitamin E deficiency does not. This suggests that the oxidant defense mechanisms in which these antioxidant nutrients function are independent of one another.     

Effect of physical restraint on oxidative stress in mice fed a selenium and vitamin E deficient diet

Physical restraint has been associated with increased oxidative damage to lipid, protein, and DNA. The purpose of this experiment was to determine whether physical restraint would further exacerbate oxidative stress in mice fed a selenium (Se) and vitamin E (VE) deficient diet. Three-week-old mice were fed a Torula yeast diet containing adequate or deficient Se and VE. Menhaden oil was added to the deficient diet to impose an additional oxidative stress. After 4 wk feeding, half the mice in each group were restrained for 5 d in well-ventilated conical tubes for 8 h daily. Mice fed the Se and VE deficient diets had increased liver thiobarbituric acid-reactive substance (TBARS) levels and decreased liver glutathione peroxidase (GPX1) activity and α-tocopherol levels. Plasma corticosterone levels were elevated in restrained mice fed the deficient diet compared to unrestrained mice fed the adequate diet. Restraint had no effect on liver TBARS or α-tocopherol levels. Liver GPX1 activity, however, was lower in restrained mice fed the adequate diet. In addition, liver superoxide dismutase (SOD) activity was lower in the restrained mice fed the adequate or deficient diet. Thus, under our conditions, Se and VE deficient diet, but not restraint, increased lipid peroxidation in mice. Restraint, however, decreased antioxidant protection in mice due to decreased activities of GPX1 and SOD enzymes.     

Combined effect of alcohol and cigarette smoke on lipid peroxidation and antioxidant status in rats

The effect of long-term administration of alcohol and cigarette smoke independently and both in combination on lipid peroxidation and antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione-S-transferase (GST) was studied in liver, kidney, heart and lungs of albino rats. The levels of peroxidation products viz., malondialdehyde, hydroperoxides and conjugated dienes were increased in all the tissues of alcohol administered and smoke-exposed rats. Activities of SOD and CAT were decreased in alcohol-treated and alcohol and smoke combination groups, but increased in smoke-exposed group. Activities of GPx and GST have shown an increase, while concentration of reduced glutathione was found decreased in all the three groups.     

Antioxidant response of the bivalve Pinna nobilis colonised by invasive red macroalgae Lophocladia lallemandii

Invasive species represent a risk to natural ecosystems and a biodiversity hazard. The present work aims to determine the antioxidant enzyme response – superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX), the phase II detoxifying enzyme – glutathione S-transferase (GST) – and markers of oxidative damage – thioredoxin reductase (TR) and malondialdehyde (MDA) – in gills and digestive gland of Pinna nobilis and to study the antioxidant response effects in the bivalve colonised by the invasive macroalgae Lophocladia lallemandii. Colonised specimens were collected in a control area without L. lallemandii and another area completely colonised by L. lallemandii. All enzyme activities were found to be present in gills and digestive gland, with some tissue differences. CAT and SOD activities were higher in gills than digestive gland, whereas GST activity and MDA levels were higher in digestive gland. The presence of L. lallemandii induced a significant increase in the activities of antioxidant enzymes in both gills and digestive gland, except for CAT activity in gills. GST and TR activities were also increased in both tissues, as well as the MDA concentration. We can conclude that the presence of L. lallemandii colonising P. nobilis induces a biological stress and oxidative damage to the fan mussel.     

Skeletal muscle oxidative capacity, antioxidant enzymes, and exercise training

The purposes of this study were to determine whether exercise training induces increases in skeletal muscle antioxidant enzymes and to further characterize the relationship between oxidative capacity and antioxidant enzyme levels in skeletal muscle. Male Sprague-Dawley rats were exercise trained (ET) on a treadmill 2 h/day at 32 m/min (8% incline) 5 days/wk or were cage confined (sedentary control, S) for 12 wk. In both S and ET rats, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX) activities were directly correlated with the percentages of oxidative fibers in the six skeletal muscle samples studied. Muscles of ET rats had increased oxidative capacity and increased GPX activity compared with the same muscles of S rats. However, SOD activities were not different between ET and S rats, but CAT activities were lower in skeletal muscles of ET rats than in S rats. Exposure to 60 min of ischemia and 60 min of reperfusion (I/R) resulted in decreased GPX and increased CAT activities but had little or no effect on SOD activities in muscles from both S and ET rats. The I/R-induced increase in CAT activity was greater in muscles of ET than in muscles of S rats. Xanthine oxidase (XO), xanthine dehydrogenase (XD), and XO + XD activities after I/R were not related to muscle oxidative capacity and were similar in muscles of ET and S rats. It is concluded that although antioxidant enzyme activities are related to skeletal muscle oxidative capacity, the effects of exercise training on antioxidant enzymes in skeletal muscle cannot be predicted by measured changes in oxidative capacity.     

Glutathione peroxidase-1 gene knockout on body antioxidant defense in mice

To determine the in vivo role of cellular glutathione peroxidase (E.C.1.11.1.9, GPX1), we challenged the GPX1 knockout [GPX1(-/-)], the GPX1 overexpressing [GPX1(+)], and their respective wild-type (WT) mice of different Se and vitamin E status with acute oxidative stress. After these mice were injected with pro-oxidants paraquat or diquat at 12 to 125 mg/kg of body weight, their survival rate and time were a function of their GPX1 activity levels. The GPX1 protection was associated with attenuation of NADPH and NADH oxidation, protein carbonyl and F(2)-isoprostanes formation, and alanine transaminase release in various tissues, and was irreplaceable by high levels of dietary vitamin E or other selenoproteins. The GPX1 expression was also protective against moderate oxidative stress induced by low levels of paraquat or diquat, particularly in the Se-deficient mice. Alteration of GPX1 expression showed no impact on the expression of other selenoproteins and antioxidant enzymes in unstressed mice. Total Se content in liver of the Se-adequate GPX1(-/-) mice was reduced by 60% the WT controls. In conclusion, normal expression of GPX1 is essential and overexpression of GPX1 is beneficial to protect mice against acute oxidative stress.     

Age-related changes in antioxidant and glutathione S-transferase enzyme activities in the Asian clam

Aging is accompanied by increased production of free oxygen radicals and impairment of normal cellular functions. The aim of this work was to provide preliminary data on age-related differences in the activities of antioxidant enzymes and phase II biotransformation enzyme glutathione S-transferase (GST) in a wild population of the Asian clam Corbicula fluminea. The antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), and GST were assessed in visceral mass of four age classes (0+-, 1+-, 2+-, and 3+-year-old) of C. fluminea clams. Age-related changes were seen in antioxidant enzyme status: levels of total SOD (totSOD) (P < 0.05), MnSOD, and CuZnSOD (P < 0.05) activities increased progressively during aging from younger to older clams. Changes in CAT and GR activities with advancing age were found, the levels being the highest in age class II, then being lower in age classes III and IV (P < 0.05). Activities of GPX and GST were lower in the senescent individuals (2+- and 3+-year-old clams) compared with young individuals (0+- and 1+-year-old clams). Overall, the decline of glutathione-dependent enzyme activities, coupled with higher and lower activities of totSOD and CAT, respectively, as the individual grows older, may render the older animals more susceptible to oxidative stress. Data reported here are not intended to be exhaustive since they concern only age/size structure of the population at one locality, so more detailed studies on both the developmental stages and levels of antioxidant enzymes of this new alien species in Serbian rivers are required.     

Developmental changes in antioxidant enzymes and oxidative damage in kidneys, liver and brain of bcl-2 knockout mice.

While programmed cell death is induced by a variety of internal and external stimuli, including reactive oxygen species, the anti-apoptotic protein Bcl-2 is involved in opposing cell death and affects the antioxidant status of cells. Since the exact mechanism of its action is uncertain, in this study we examined the role of Bcl-2 using a loss of function model, Bcl-2 knockout mice. The consequence of Bcl-2 knockout was assessed in kidneys, liver and brain, using protein carbonyls and cellular levels of antioxidant enzymes as markers of oxidative stress. Kidney extracts from 8 days-old Bcl-2-knockout mice had 59% higher content of protein carbonyls relative to the wild type, but similar levels of oxidized proteins at the age of 30 days. By marked contrast, in liver and brain, levels of protein carbonyls were similar at 8 days but by 30 days the liver of knockout animals (and brains, as we have shown previously) show 36% higher protein carbonyls. Measures of glutathione reductase (GRX), glutathione transferase (GST) and catalase revealed significantly higher levels in kidneys of 8 days old Bcl-2-knockout mice compared to wild type. By 30 days activities of glutathione-related enzymes and catalase increased and abolished the differences between the knockout and wild type. At 8 days, in liver there were no significant differences in activities of all enzymes between the mice, however by 30 days, the specific activity of GRX was significantly higher in Bcl-2-knockout mice, relative to controls. From day 8 to day 30 there was an increase in liver catalase activity that resulted in significantly higher levels in Bcl-2-knockout animals. Catalase activity in brains of Bcl-2-knockout, 8 days old mice was significantly higher compared to the wild type, and significantly lowers at 30 days. Taken together our findings indicate that Bcl-2 knockout results in significant perturbations of oxidative metabolism and antioxidant status of in kidney, liver and brain. Such changes are tissue specific with respect to age, magnitude and type of enzyme affected.     

Interaction of vitamin E and exercise training on oxidative stress and antioxidant enzyme activities in rat skeletal muscles

It has been shown that free radicals are increased during intensive exercise. We hypothesized that vitamin E (vit E) deficiency, which will increase oxidative stress, would augment the training-induced adaptation of antioxidant enzymes. This study investigated the interaction effect of vit E and exercise training on oxidative stress markers and activities of antioxidant enzymes in red quadriceps and white gastrocnemius of rats in a 2x2 design. Thirty-two male rats were divided into trained vit E-adequate, trained vit E-deficient, untrained vit E-adequate, and untrained vit E-deficient groups. The two trained groups swam 6 h/day, 6 days/week for 8 weeks. The two vit E-deficient groups consumed vit E-free diet for 8 weeks. Vitamin E-training interaction effect was significant on thiobarbituric acid reactive substances (TBARSs), glutathione peroxidase (GPX), and superoxide dismutase (SOD) in both muscles. The trained vit E-deficient group showed the highest TBARS and GPX activity and the lowest SOD activity in both muscles. A significant vit E effect on glutathione reductase and catalase was present in both muscles. Glutathione reductase and catalase activities were significantly lower in the two vit E-adequate groups combined than in the two vit E-deficient groups combined in both muscles. This study shows that vit E status and exercise training have interactive effect on oxidative stress and GPX and SOD activities in rat skeletal muscles. Vitamin E deprivation augmented the exercise-induced elevation in GPX activity while inhibiting exercise-induced SOD activity, possibly through elevated oxidative stress.     

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.     

Protective effect of vitamin E in dimethoate and malathion induced oxidative stress in rat erythrocytes

Organophosphate (OP) pesticides such as dimethoate and malathion intoxication has been shown to produce oxidative stress due to the generation of free radicals and alter the antioxidant defense system in erythrocytes. It is possible that vitamin E being present at the cell membrane site may prevent OP-induced oxidative damage. In the present study, rats were pretreated orally with vitamin E (250 mg/kg body wt, twice a week for 6 weeks) prior to oral administration of a single low dose of dimethoate and/or malathion (0.01% LD(50)). The result showed that treatment with OP increased lipid peroxidation (LPO) in erythrocytes, however, vitamin E pretreated rats administered OP's showed decreased LPO in erythrocytes. The increase in the activities of superoxide dismutase (SOD) and catalase (CAT) and total-SH content in erythrocytes from dimethoate and/or malathion treated rats as compared to control appears to be a response towards increased oxidative stress. Vitamin E pretreated animals administered OP's showed a lowering in these parameters as compared to OP treated rats which indicates that vitamin E provide protection against OP-induced oxidative stress. The glutathione-S-transferase (GST) activity in erythrocytes was inhibited in OP intoxicated rats which partially recovered in vitamin E pretreated animals administered OP's. Inhibition in erythrocyte and serum acetylcholinesterase (AChE) activity was not relieved in vitamin E pretreated rats administered OP's probably due to the competitive nature of enzyme inhibition by OP's. The results show that vitamin E may amelierate OP-induced oxidative stress by decreasing LPO and altering antioxidant defense system in erthrocytes.     

镉对泥蚶抗氧化酶系统的影响

研究了不同浓度的重金属Cd²⁺对泥蚶抗氧化酶活性的影响。设置了四组镉的梯度(0、0.025、0.05和0.1 mg·L^-1,分别在第12、24、48、96和144 h对各组织取样,用泥蚶内脏团与鳃制成酶样,对非特异性免疫抗氧化酶SOD、CAT、GST、GPX进行指标测定。结果表明,在开始的12～24 h,中低浓度组SOD酶的活力与对照组相比有显著性地提高,高浓度组SOD酶的活力变化不显著,随着暴露时间的延长和Cd²⁺浓度的增加,随后至144 h,高中浓度组SOD酶的活力降至低于对照组水平(P<0.05);GPX和GST活力的变化与SOD变化相似,它们的活性在12～48 h的范围内达到顶峰,然后与对照组相比出现显著下降;中低浓度组的CAT酶活力在第144 h时与对照组相比无显著差异(P<0.05)。在一定程度的Cd²⁺胁迫会对泥蚶体内的抗氧化酶系统造成损伤。     

Induction of oxidative stress and DNA damage in cervix in acute treatment with benzo[a]pyrene

Benzo[a]pyrene [B(a)P] is one of the most prevalent environmental carcinogens and genotoxic agents. However, the mechanisms of B(a)P-induced oxidative damage in cervical tissue are still not clear. The present study was to investigate the oxidative stress and DNA damage in cervix of ICR female mice induced by acute treatment with B(a)P. Oxidative stress was assayed by analysis of malondialdehyde (MDA), superoxide anion and H(2)O(2), and antioxidant enzymes. The alkaline single-cell electrophoresis (SCGE) was used to measure DNA damage. The contents of MDA and glutathione (GSH), and the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST) were significantly increased in cervix 24, 48 and 72h after B(a)P treatment of a single dose of 12.5 and 25mg/kg, while GSH, CAT, SOD and GST had no significant difference with the dose of 50mg/kg B(a)P at post-treatment time 48 and 72h except for SOD activity at 48h which was significant. The maximum values of SOD, CAT, GST and GSH were peaked at 24h and then decreased gradually while GPx activities and MDA levels persisted for up to 72h. Superoxide anion, H(2)O(2) and DNA damage changed similarly as the activity of SOD, CAT or GST. Additionally, increases of formamidopyrimidine DNA glycosylase (FPG) specific DNA damage were observed and can be greatly rescued by vitamin C pretreatment. Overall, B(a)P demonstrated a time- and dose- related oxidative stress and DNA damage in cervix.     

Seasonal changes in antioxidant defence system of liver and gills of Salmo trutta caspius, Salmo trutta labrax and Salmo trutta macrostigma

Seasonal changes in antioxidant enzyme activities (superoxide dismutase, SOD, EC 1.15.1.1; catalase, CAT, EC 1.11.1.16; glutathione peroxidase, GPx, EC 1.11.1.9; glutathione reductase, GR, EC 1.6.4.2; glucose-6-phosphate dehydrogenase, G6PD, EC 1.1.1.49 and glutathione S -transferase, GST, EC 1.5.1.18) and lipid peroxidation (LPO) levels of livers and gills of female Caspian trout Salmo trutta caspius , Black Sea trout Salmo trutta labrax and mountain trout Salmo trutta macrostigma were investigated. SOD, CAT, GPx, G6PD and GST activities were higher in liver compared to gills of all sub-species; concomitantly, the GR activity was also higher in the livers of S. t. caspius and S. t. labrax , but the reverse was seen in S. t. macrostigma . LPO levels were higher in the gills compared to the liver of all sub-species. There was no general trend in the seasonal changes in the gill antioxidant enzyme (AE) activities or LPO levels. Higher AE activities, however, were found in the liver of each sub-species during autumn, and this coincided with an increase in the gonado-somatic index.     

Selenium-induced changes in activities of antioxidant enzymes and content of photosynthetic pigments in Spirulina platensis

Spirulina platensis exposed to various selenium （Se） concentrations （0, 10, 20, 40, 80, 150, 175, 200, 250 mg/L） accumulated high amounts of Se in a dose- and time-dependent manner. Under low Se concentrations （〈150 mg/L）, Se induced increases in biomass concentration, content of photosynthetic pigments, and activities of glutathione peroxidase （GPX）, superoxide dismutase （SOD）, catalase （CAT） and Gua-dep peroxidases （POD）, which indicates that antioxidant enzymes play an important role in protecting cells from Se stress. Higher Se concentrations （≥175 mg/L） led to higher Se accumulation and increases in activities of GPX, SOD, CAT and POD, but also induced lipid peroxidation （LPO） coupled with potassium leakage and decreases in biomass concentration and contents of photosynthetic pigment. The results indicate that increases in activities of the antioxidant enzymes were not sufficient to protect cell membranes against Se stress. Time-dependent variations in the activities of antioxidant enzymes, contents of chlorophyll a and carotenoid and the LPO level were also investigated under representative Se concentrations of 40 and 200mg/L. Opposite variation trends between SOD-CAT activities, and GPX-POD-APX activities were observed during the growth cycles. The results showed that the prevention of damage to cell membranes of S. platensis cells could be achieved by cooperative effects of SOD-CAT and GPX-POD-APX enzymes. This study concludes that S. platensis possessed tolerance to Se and could protect itself from phytotoxicity induced by Se by altering various metabolic processes.     

Oxidative stress and antioxidant status in mouse kidney: effects of dietary lipid and vitamin E plus iron

The purpose of this study was to determine the effects of dietary fat, vitamin E, and iron on oxidative damage and antioxidant status in kidneys of mice. Sixty 1-month-old male Swiss-Webster mice were fed a basal vitamin E-deficient diet that contained either 8% fish oil + 2% corn oil or 10% lard with or without 1 g all-rac-alpha-tocopherol acetate or 0.74 g ferric citrate per kilogram of diet for 4 weeks. Significantly (P < 0.05) higher levels of lipid peroxidation products, thiobarbituric acid reactants (TBAR), and conjugated dienes were found in the kidneys of mice fed with fish oil compared with mice fed lard irrespective of vitamin E status. Mice maintained on a vitamin E-deficient diet had significantly higher renal levels of TBAR, but not conjugated dienes, than the supplemented group. Fish oil fed mice receiving vitamin E supplementation had lower levels of alpha-tocopherol than did mice in the lard fed group. Significantly higher levels of ascorbic acid were also found in the kidneys of mice fed with fish oil than were found in mice fed lard. The levels of protein carbonyls and glutathione (GSH), and activities of catalase, superoxide dismutase, selenium (Se)-GSH peroxidase, and non-Se-GSH peroxidase were not significantly altered by dietary fat or vitamin E. Dietary iron had no significant effect on any of the oxidative stress and antioxidant indices measured. The results obtained provide experimental evidence for the pro-oxidant effect of high fish oil intake in mouse kidney and suggest that dietary lipids play a key role in determining cellular susceptibility to oxidative stress.