Oxidative stress in toadfish (Halobactrachus didactylus) cardiac muscle. Acute exposure to vanadate oligomers

Vanadate solutions as ‘metavanadate’ (containing ortho and metavanadate species) and ‘decavanadate’ (containing manly decameric species) (5 mM; 1 mg/kg) were injected intraperitoneously in Halobatrachus didactylus (toadfish), in order to evaluate the contribution of decameric vanadate species to vanadium (V) intoxication on the cardiac tissue. Following short-term exposure (1 and 7 days), different changes on antioxidant enzyme activities—superoxide dismutase (SOD), catalase (CAT), selenium-glutathione peroxidase (Se-GPx), total glutathione peroxidase (GPx), lipid peroxidation and subcellular vanadium distribution were observed in mitochondrial and cytosolic fractions of heart ventricle toadfish. After 1 day of vanadium intoxication, SOD, CAT and Se-GPx activities were decreased up to 25%, by both vanadate solutions, except mitochondrial CAT activity that increased (+23%) upon decavanadate administration. After 7 days of exposure, decavanadate versus metavanadate solutions promoted different effects mainly on cytosolic CAT activity (−56% versus −5%), mitochondrial CAT activity (−10% versus +10%) and total GPx activity (+1% versus −35%), whereas lipid peroxidation products were significantly increased (+82%) upon 500 μM decavanadate intoxication. Accumulation of vanadium in total (0.137±0.011 μg/g) and mitochondrial (0.022±0.001 μg/g) fractions was observed upon 7 days of metavanadate exposure, whereas for decavanadate, the concentration of vanadium increased in cytosolic (0.020±0.005 μg/g) and mitochondrial (0.021±0.009 μg/g) fractions. It is concluded that decameric vanadate species are responsible for a strong increase on lipid peroxidation and a decrease in cytosolic catalase activity thus contributing to oxidative stress responses upon vanadate intoxication, in the toadfish heart.     

Double blind, cluster randomised trial of low dose supplementation with vitamin A or beta carotene on mortality related to pregnancy in Nepal. The NNIPS-2 Study Group

ObjectiveTo assess the impact on mortality related to pregnancy of supplementing women of reproductive age each week with a recommended dietary allowance of vitamin A, either preformed or as β carotene.DesignDouble blind, cluster randomised, placebo controlled field trial.SettingRural southeast central plains of Nepal (Sarlahi district).Subjects44 646 married women, of whom 20 119 became pregnant 22 189 times.Intervention270 wards randomised to 3 groups of 90 each for women to receive weekly a single oral supplement of placebo, vitamin A (7000 μg retinol equivalents) or β carotene (42 mg, or 7000 μg retinol equivalents) for over 3½ years.ResultsMortality related to pregnancy in the placebo, vitamin A, and β carotene groups was 704, 426, and 361 deaths per 100 000 pregnancies, yielding relative risks (95% confidence intervals) of 0.60 (0.37 to 0.97) and 0.51 (0.30 to 0.86). This represented reductions of 40% (P<0.04) and 49% (P<0.01) among those who received vitamin A and β carotene. Combined, vitamin A or β carotene lowered mortality by 44% (0.56 (0.37 to 0.84), P<0.005) and reduced the maternal mortality ratio from 645 to 385 deaths per 100 000 live births, or by 40% (P<0.02). Differences in cause of death could not be reliably distinguished between supplemented and placebo groups.ConclusionSupplementation of women with either vitamin A or β carotene at recommended dietary amounts during childbearing years can lower mortality related to pregnancy in rural, undernourished populations of south Asia.

Key messages

• Maternal vitamin A deficiency, evident as night blindness or low serum retinol concentration during pregnancy, is widely prevalent in rural south Asia
• In Nepal, women of reproductive age who were given 7000 μg retinol equivalents of vitamin A on a weekly basis showed a reduction in mortality related to pregnancy of 40%
• Weekly dosing with 42 mg β carotene (also providing 7000 μg retinol equivalents) lowered their mortality by 49%
• Preventing maternal vitamin A deficiency in rural South Asia can lower the risk of mortality of women during and after pregnancy

     

Absorption and retention of selenium from shrimps in man

This study was undertaken to evaluate the bioavailability of selenium in shrimps, a possible good source of selenium, by measurements of the absorption and retention of selenium and the effects on plasma selenium concentration and glutathione peroxidase activity. Twelve healthy young subjects (9F and 3M) received 100 g of shrimps each day for six weeks in addition to their habitual diet. In the third week of the study a balance period was inserted in which the subjects received all food from the department and collected faeces and urine over 5 days. Blood samples were collected at commencement of the study, after 2, 4, and 6 weeks. The selenium intake increased from 39.4 ± 15.3 μg/d to 127 ± 5.5 μg/d with the addition of shrimps. The apparent absorption of selenium from shrimps was 83 ± 4%. Faecal and urinary selenium excretion was 32.5 ± 17.0 μg/d and 21.2 ± 9.0 μg/d, respectively and the total retention of selenium was 3.1 ± 1.1 mg. Plasma selenium concentrations were 95.2 ± 9.7 μg/L and 101.5 ± 9.7 μg/L before and after six weeks of shrimp intake, respectively (p<0.05). Plasma and erythrocyte glutathione peroxidase activities were not influenced by shrimp intake. Thus, despite the high absorption and retention, plasma selenium concentrations were only moderately affected by an increase in selenium intake of about 100 μg/d in the chemical forms found in shrimp. Whether the accumulation of selenium from shrimps in tissues may represent a potential hazard is to be further investigated.     

Effect of posttraining and pretest β-endorphin and ACTH administration in normal and protein malnourished rats

Rats were submitted to a normal (25% casein) or a low protein diet (8% casein) from the day of birth until the age of 110 to 120 days. Hypothalamic β-endorphin-like immunoreactivity was lower in the animals raised and maintained with the low protein diet, and, in addition, it did not respond to training in a step-down inhibitory avoidance task with or without footshock with a depletion, as was the case with the normal diet animals. In the animals submitted to the normal protein diet posttraining ACTH (0.2 μg/kg) and β-endorphin (1.0 μg/kg) caused retrograde amnesia of a step-down inhibitory avoidance task, and pretest administration of these substances had no effect of its own, but was able to reverse the amnesia induced by their previous posttraining administration. In the animals submitted to the low protein diet, results were similar except that pretest β-endorphin caused amnesia on its own. On the basis of previous findings which suggest that pretest actions of ACTH and β-endorphin depend on their endogenous release at the time of training, the present results are compatible with a malfunction of the brain β-endorphin system in the undernourished animals.     

牛樟芝多糖对HepG2细胞酒精性氧化损伤的保护作用

研究了不同剂量(100、200和400μg/mL)的牛樟芝粗多糖(CP)和醇提物后的水提物(WEE)对酒精诱导的HepG2细胞氧化损伤的保护作用.研究结果表明:与模型组比较,各剂量组的CP和200、400μg/mL的WEE均能极显著提高HepG2细胞的细胞活力.100μg/mL的CP和WEE均能极显著降低细胞培养液的A...     

The effects of surimi and pelleted diets on the laboratory survival, growth, and feeding rate of the cuttlefish Sepia officinalis L.

The effects of feeding a prepared surimi diet (fish-based) and a prepared pelleted diet (shrimpbased) on the survival, growth and feeding rate of the cuttlefish Sepia officinalis L. were evaluated during a 45-day experiment. One hundred and twenty juveniles of laboratory cultured cuttlefish (74.5 ± 12.36 g) were divided into three treatments and were fed thawed shrimp (control), pellets or surimi. Survival rates on these diets were 95.0%, 67.5% and 22.5%, respectively. Preliminary data indicated that the low survival of cuttlefish fed surimi may have been caused by low levels of copper in their blood (131 vs 244 μg/ml) since copper is required for their respiratory blood pigment, hemocyanin. Instantaneous growth rates were 2.71 % body weight BW/day for cuttlefish fed raw shrimp, 0.33% BW/day for cuttlefish fed pellets, and 0.54% BW/day for cuttlefish fed surimi. The feeding rate of cuttlefish fed shrimp was high (6–8% BW/day). The feeding rate on pellets increased with time (from < 1 to 3% BW/day) but never reached the level for raw shrimp. The feeding rate on surimi increased to equal the rate for raw shrimp during days 1–30 (8 to 9% BW/day) and thereafter decreased (<4% BW/day). In conclusion, there was a major distinction between the palatability of a prepared diet and the ability of that diet to support growth. Surimi was highly palatable but resulted in poor survival, suggesting low nutritional quality. In contrast, pellets were less palatable but produced maintenance growth. Development of practical surimi diets will require supplementation of the surimi with soluble micro- and macronutrients.     

Radiation-induced clastogenic factors: Anticlastogenic effect of ginkgo biloba extract

Clastogenic factors (CFs) were first described in the blood of persons irradiated accidentally or for therapeutic reasons. Work of our laboratory has shown that they occur also under other circumstances, which are characterized by oxidative stress, and that CF-induced chromosome damage is regularly prevented by superoxide dismutase (SOD). Recently we found CFs in a high percentage of salvage personnel of the Chernobyl reactor accident. These liquidators represent a high-risk population and might benefit from cancer chemoprevention by antioxidants. SOD would have to be injected and is not appropriate for longterm prophylactic treatment. In the present study, we therefore evaluated the anticlastogenic effect of the Ginkgo biloba extract EGb 761, which is known for its superoxide scavenging properties. EGb 761 was tested on CF-treated blood cultures of healthy donors. After establishing the optimal protective EGb concentration, using CFs produced by irradiation of whole blood from healthy volunteers, the extract was tested on cultures exposed to CFs from plasma of persons irradiated as liquidators. The anticlastogenic effect could be confirmed for a final concentration of 100μg/ml. In 12 consecutive experiments, CFs induced an average of 18.00 ± 4.41 aberrations/100 cells. This was reduced to 7.33 ± 3.08 in the parallel cultures receiving 100μg/ ml EGb 761 (p < .001). SOD was anticlastogenic in the same system at concentrations of 30 cytochrome C units/ml (approximately 10μg/ml). Preliminary results obtained in a small series of liquidators showed regression or complete disappearance of CFs in the plasma after 2 months of treatment with EGb 761 (3 × 40 gmg/d).     

Short-term very low calorie diet reduces oxidative stress in obese type 2 diabetic patients

Oxidative stress is higher in obese diabetic than in non-diabetic subjects. This pilot study evaluates oxidative stress during short-term administration of a very low calorie diet in obese persons. Nine obese Type 2 diabetic patients (age 55+/-5 years, BMI 35.9+/-1.9 kg/m2) and nine obese non-diabetic control subjects (age 52+/-6 years, BMI 37.3+/-2.1 kg/m2) were treated by a very low calorie diet (600 kcal daily) during 8 days stay in the hospital. Serum cholesterol, triglycerides, non-esterified fatty acids (NEFA), beta-hydroxybutyrate (B-HB), ascorbic acid (AA), alpha-tocopherol (AT), plasma malondialdehyde (MDA) and superoxide dismutase (SOD) activity in erythrocytes were measured before and on day 3 and 8 of very low calorie diet administration. A decrease of serum cholesterol and triglyceride concentrations on day 8 was associated with a significant increase of NEFA (0.30+/-0.13 vs. 0.47+/-0.11 micromol/l, p<0.001) and B-HB (0.36+/-.13 vs. 2.23+/-1.00 mmol/l, p<0.001) in controls but only of B-HB (1.11+/-0.72 vs. 3.02+/-1.95 mmol/l, p<0.001) in diabetic patients. A significant decrease of plasma MDA and serum AT together with an increase of SOD activity and AA concentration (p<0.01) was observed in control persons, whereas an increase of SOD activity (p<0.01) was only found in diabetic patients after one week of the very low calorie diet. There was a significant correlation between NEFA or B-HB and SOD activity (p<0.01). We conclude that one week of a very low calorie diet administration decreases oxidative stress in obese non-diabetic but only partly in diabetic persons. Diabetes mellitus causes a greater resistance to the effects of a low calorie diet on oxidative stress.     

Effects of Different Copper Sources and Levels on Plasma Superoxide Dismutase, Lipid Peroxidation, and Copper Status of Lambs

This study was performed to determine the effects of different copper (Cu) sources and levels on plasma superoxide dismutase (SOD), lipid peroxidation, and Cu status of lambs. Fifty Dorper × Mongolia wether lambs (approximately 3?month of age; average BW?=?23.8?±?0.6?kg) were divided into five equal groups each with ten animals according to their weight. Treatments consisted of (1) control (no supplemental Cu), (2) 10?mg Cu/kg DM from Cu-lysine, (3) 20?mg Cu/kg DM from Cu-lysine, (4) 10?mg Cu/kg DM from tribasic copper chloride (Cu(2)(OH)(3)Cl; TBCC), and (5) 20?mg Cu/kg DM from TBCC. The Cu concentration was 6.74?mg/kg DM in the basal diet. Plasma copper concentrations and ceruloplasmin activities were not affected on day?30 by Cu supplementation. Copper supplementation increased plasma and liver copper concentrations and ceruloplasmin activities on day?60. Muscle Cu concentrations were not affected by Cu supplementation. There were no differences in plasma, liver, and muscle Cu concentrations and ceruloplasmin activities between Cu-lysine and TBCC. Liver copper concentrations and plasma ceruloplasmin activities were increased in lambs supplemented with 20?mg Cu/kg DM than in those supplemented with 10?mg Cu/kg DM on day?60. However, copper levels had no effects on Cu concentrations in plasma and muscle. Malondialdehyde (MDA) concentrations were decreased in plasma and liver tissues, but not affected in muscle by Cu supplementation. Plasma SOD activities were increased by Cu supplementation. There were no differences in plasma, liver, and muscle MDA concentrations and plasma SOD activities between Cu sources and levels. These results indicated that Cu supplementation increased plasma SOD activity, lipid oxidative stability, and copper status of lambs, but did not influence lipid oxidative stability in sheep muscle. Cu-lysine and TBCC were of similar availability when offered to finishing sheep.     

Upregulation of Respiratory Burst of Polymorphonuclear Leukocytes By A Bleomycin Derivative, Peplomycin

The influence of peplomycin (PLM) on the respiratory burst of peripheral blood polymorphonuclear leukocytes (PMN) was investigated. Short-term (5 min) treatment of human PMN with 0.1μg/ml to 100μg/ml of PLM increased phorbol myristate acetate (PMA)-and formyl-methionyl-leucyl-phenylalanine (FMLP)-induced luminol-dependent chemiluminescence. PMN, as well as alveolar macrophages from rabbits treated with 0.5 to 1.0 mg/kg of peplomycin per day for 5 days, generated more superoxide (O₂^-) than the cells from untreated rabbits. In both PLM-treated and untreated PMN, chemiluminescence induced by FMLP and PMA was decreased to less than 50% of the control by staurosporine, superoxide dismutase (SOD) and catalase. However, the peak intensity in PLM-untrcated PMN was decreased to about 30% of the control by genislein, while this agent induced a slight decrease in peak intensity in the PLM-treated PMN. Inositol triphosphate and diacyl glycerol levels were not clearly increased by PLM, but an increase of intracellular Ca and a shift of protein kinase C (PKC) to the membrane occurred in PMN within 1 min after PLM treatment. Western blotting revealed that the tyrosine phosphorylation of a 115 kDa protein was upregulated by 5 to 50μg/ml of PLM. While, PLM suppressed SOD activity in alveolar macrophages and PMN. These results seem to indicate that PLM increases the respiratory burst of PMN and macrophages both by way of direct PKC activation and by the upregulation of protein tyrosine phosphorylation. This increased reactive oxygen generation, together with the suppression of SOD activity seems to be tissue-impairing.     

Manganese complexes of curcumin and its derivatives: evaluation for the radical scavenging ability and neuroprotective activity

In this study, three manganese complexes of curcumin (Cp) and related compounds, diacetylcurcumin (AcylCp) and ethylenediamine derivative (CpED), were synthesized and evaluated in vitro for antilipid peroxidation and superoxide dismutase activity. The manganese complexes exhibited a great capacity to protect brain lipids against peroxidation with IC₅₀ of 6.3–26.3 μM. All manganese complexes showed much greater SOD activity than their corresponding antioxidant ligands as well as trolox with IC₅₀ values of 8.9–29.9 μM. AcylCp and curcumin manganese complexes (AcylCpCpx and CpCpx) also gave the highest inhibitory activity to H₂O₂-induced cell damage (oxidative stress) at 0.1 μg/ml (< 0.2 μM) in NG108-15 cells, which were more potent than curcumin and related compounds. The neuropharmacological tests in mice supported the idea that the SOD mimicking complexes were able to penetrate to the brain as well as their role in the modulation of brain neurotransmitters under the aberrant conditions. The complexes significantly improved the learning and memory impairment induced by transient ischemic/reperfusion. AcylCpCpx, CpCpx, and CpEDCpx showed significant protection at 6.25, 25, and 50 mg/kg (i.p.), respectively, whereas manganese acetate and curcumin had no effect at doses of 50 mg/kg. In addition, treatment of AcylCpCpx and curcumin significantly attenuated MPTP-induced striatal dopamine depletion in mice, which was in accordance with the increase in the density of dopaminergic neurons when compared with MPTP-treated mice. These results support the important role of manganese in importing SOD activity and consequently, the enhancement of radical scavenging activity. AcylCpCpx and CpCpx seem to be the most promising neuroprotective agents for vascular dementia.     

Carotene production from waste cooking oil by Blakeslea trispora in a bubble column reactor: The role of oxidative stress

The oxidative stress induced by hydroperoxides and reactive oxygen species (ROS) during carotene production from waste cooking oil (WCO) and corn steep liquor (CSL) by the fungus Blakeslea trispora in a bubble column reactor was investigated. The specific activities of the intracellular enzymes superoxide dismutase (SOD) and catalase (CAT) as well as the micromorphology of the fungus were measured in order to study the response of the fungus to oxidative stress. The changes of the morphology of microorganism leaded to pellets formation and documented using a computerized image analysis system. As a consequence of the mild oxidative stress induced by hydroperoxides of WCO and ROS a significant increase in carotene production was obtained. The highest carotene concentration (980.0 mg/l or 51.5 mg/g dry biomass) was achieved in a medium consisted of CSL (80.0 g/L) and WCO (50.0 g/L) at an aeration rate of 5 vvm after 6 days of fermentation. In this case the carotenes produced consisted of β‐carotene (71%), γ‐carotene (26%), and lycopene (3%). The strong oxidative stress in the fungus caused a significant increase of γ‐carotene concentration. Bubble column reactor is a useful fermentation system for carotene production in industrial scale.     

Hyperglycinemia due to folate deficiency in rats: evidence for the lack of involvement of the hepatic glycine cleavage system

In addition to a well-recognized hyperhomocysteinemic state, folate deficiency also leads to profound hyperglycinemia. To further characterize the latter observation, two trials were conducted using a folate-deficient rat model to (1) determine the sensitivity of plasma glycine to folate repletion and (2) test the hypothesis that hyperglycinemia results from a reduced flux through the folate-dependent glycine cleavage system (GCS). Weanling male Sprague–Dawley rats were used, and they consumed an amino acid-defined diet with either 0 (FD) or 1 (FA) mg/kg of crystalline folic acid. In Trial 1, 30 rats consumed the FD diet for 28 days. Rats then consumed diets containing 0.1, 0.2, 0.3 or 0.4 mg/kg of folic acid for 14 days before termination. In Trial 2, 16 rats were allocated to receive either the FA (n=8) or FD (n=8) diet for 30 days before termination. Liver mitochondria were isolated and flux through the GCS (measured as ¹⁴CO₂ production from 1-¹⁴C-glycine) was determined. Plasma from blood collected at termination was analyzed for folate, homocysteine and glycine. In Trial 1, both homocysteine and glycine responded linearly to increased dietary folic acid (milligrams per kilogram) levels (P<.05). In Trial 2, plasma folate (FA=25.85 vs. FD=0.66; S.E.M.=1.4 μM), homocysteine (FA=11.1 vs. FD=55.3; S.E.M.=1.7 μM) and glycine (FA=564 vs. FD=1983; S.E.M.=114 μM) were significantly affected by folate deficiency (P<.0001). However, glycine flux through hepatic GCS was not affected by folate deficiency (P>.05). These results provide evidence that in a folate-deficient rat model, both homocysteine and glycine are sensitive to dietary folic acid levels; however, the observed hyperglycinemia does not appear to be related to a reduced flux through the hepatic GCS.     

Beta-lactotensin and neurotensin rapidly reduce serum cholesterol via NT2 receptor

β-Lactotensin, a neurotensin NT₂ agonist derived from β-lactoglobulin, has hypocholesterolemic activity after administration for 2 days at a dose of 30 mg/kg (i.p.) or 100 mg/kg (p.o.) for 2 days in mice fed a high-cholesterol/cholic acid diet. The onset of hypocholesterolemic activity of β-lactotensin was observed 90 min after a single i.p. or p.o. administration at the same dose as described above. Neurotensin also induced hypocholesterolemic activity 90 min after single i.p. administration at a dose of 2 μg per mouse but was ineffective after oral administration. The rapid onset of hypocholesterolemic activities of β-lactotensin and neurotensin was blocked by levocabastine (50 μg/kg), an NT₂ antagonist, and raclopride (0.5 mg/kg), a dopamine D₂ antagonist.     

Estrogen effects on NADH oxidase and superoxide dismutase in prepubertal female rats

Thirty-four day old, ovariectomised rats were treated with increasing doses of estradiol, 2-hydroxyestradiol 2,3-dimethyl ether (23E₂), 4-hydroxyestradiol 3,4-dimethyl ether (34E₂) and 4-methoxy-estradiol (4ME₂) for five days by subcutaneous injection. Superoxide dismutase, phenol activated NADH oxidase and uterine dry weights were determined. Only estradiol was found to be uterotrophic and increased NADH oxidase activity in these experiments. Both 23E₂ and 34E₂ treatment reduced the enzyme activity significantly. Though 4ME₂ showed a decrease in NADH oxidase at 0.05μg/100gm body weight there was no further decrease at higher dose (5μg/100gm). The Superoxide dismutase (SOD) in uterus and liver was unaffected by estradiol, while 23E₂, 34E₂, and 4ME₂ significantly reduced SOD in both liver and uterus. These results indicate that 23E₂, 34E₂ and 4ME₂, in spite of their non-uterotrophic property, affect uterine metabolism. Furthermore, in view of the reports indicating the importance of SOD levels in various tumors and since catecholestrogens are observed to reduce SOD levels in liver and uterus, it is suggestive that catecholestrogens may play an important role in the pathophysiology of certain tumors.     

Weak antioxidant defenses make the heart a target for damage in copper-deficient rats

Copper deficiency causes more salient pathologic changes in the heart than in the liver of rats. Although oxidative stress has been implicated in copper deficiency-induced pathogenesis, little is known about the selective toxicity to the heart. Therefore, we examined the relationship between the severity of copper deficiency-induced oxidative damage and the capacity of antioxidant defense in heart and liver to investigate a possible mechanism for the selective cardiotoxicity. Weanling rats were fed a purified diet deficient in copper (0.4 μg/g diet) or one containing adequate copper (6.0 μg/g diet) for 4 weeks. Copper deficiency induced a 2-fold increase in lipid peroxidation in the heart (thiobarbituric assay) but did not alter peroxidation in the liver. The antioxidant enzymatic activities of superoxide dismutase, catalase, and glutathione peroxidase were, respectively, 3-, 50- and 1.5-fold lower in the heart than in the liver, although these enzymatic activities were depressed in both organs by copper deficiency. In addition, the activity of glutathione reductase was 4 times lower in the heart than in the liver. The data suggest that a weak antioxidant defense system in the heart is responsible for the relatively high degree of oxidative damage in copper-deficient hearts.     

Effects of Feed Contaminant Deoxynivalenol on Plasma Cytokines and mRNA Expression of Immune Genes in the Intestine of Broiler Chickens

An experiment was conducted to investigate the individual and combined effects of dietary deoxynivalenol (DON) and a microbial feed additive on plasma cytokine level and on the expression of immune relevant genes in jejunal tissues of broilers. A total of 40 broiler chicks were obtained from a commercial hatchery and divided randomly into four groups (10 birds per group). Birds were reared in battery cages from one day old for 5 weeks. The dietary groups were 1) control birds fed basal diet; 2) DON group fed basal diet contaminated with 10 mg DON/ kg feed; 3) DON + Mycofix group fed basal diet contaminated with 10 mg DON/ kg feed and supplemented with a commercial feed additive, Mycofix® Select (MS) (2.5 kg/ton of feed); 4) Mycofix group fed basal diet supplemented with MS (2.5 kg/ton of feed). At 35 days, the plasma levels of tumor necrosis factor alpha (TNF-α) and interleukin 8 (IL-8) were quantified by ELISA test kits. Furthermore, the mRNA expression of TNF-α, IL-8, IL-1β, interferon gamma (IFNγ), transforming growth factor beta receptor I (TGFBR1) and nuclear factor kappa-light-chain-enhancer of activated B cells 1 (NF-κβ1) in jejunum were quantified by qRT-PCR. The results showed that the plasma TNF-α decreased in response to DON, while in combination with MS, the effect of DON was reduced. DON down-regulated the relative gene expression of IL-1β, TGFBR1 and IFN-γ, and addition of MS to the DON contaminated diet compensates these effects on IL-1β, TGFBR1 but not for IFN-γ. Furthermore, supplementation of MS to either DON contaminated or control diet up-regulated the mRNA expression of NF-κβ1. In conclusion, DON has the potential to provoke and modulate immunological reactions of broilers and subsequently could increase their susceptibility to disease. The additive seemed to have almost as much of an effect as DON, albeit on different genes.     

Lymphocyte propionyl-CoA carboxylase and accumulation of odd-chain fatty acid in plasma and erythrocytes are useful indicators of marginal biotin deficiency small star,filled

BACKGROUND: Recent studies indicate marginal biotin deficiency is more common than previously thought. That conclusion's validity rests on two indicators of biotin status that depend on renal function.OBJECTIVE: Assessing the validity of two indicators of biotin status that do not depend upon renal function: 1) activity of the biotin-dependent enzyme propionyl-CoA carboxylase (PCC) in lymphocytes and 2) accumulation of odd-chain fatty acids in the lipids of plasma and erythrocytes.DESIGN: Marginal biotin deficiency was induced in 11 healthy adults by egg-white feeding for 28 days. Blood and 24-h urine samples were collected before commencing the diet and twice weekly thereafter. After depletion, biotin status was restored with a general diet with or without 80 &mgr;g/day or 328 nmol/day biotin supplement. Activity of PCC was determined by an optimized NaH 14CO(3) incorporation assay. Fatty acid composition was determined by gas chromatography.RESULTS: With time on the egg-white diet, lymphocyte PCC activity decreased significantly (P <0.0001); C15:0 and C17:0 content increased significantly in the lipids of plasma and erythrocytes (P <0.015). In eight of 11 subjects, lymphocyte PCC activity returned to normal within three weeks of resuming general diets with or without biotin supplement. With repletion, C15:0 and C17:0 in plasma lipids decreased (P <0.02), but odd-chain content of erythrocytes did not decrease significantly.CONCLUSIONS: Lymphocyte PCC activity is an early and sensitive indicator of marginal biotin deficiency. Odd-chain fatty acids accumulate in blood lipids more gradually during marginal deficiency and return to normal more gradually after biotin repletion.     

Vitamin E and Hippophea rhamnoides L. extract reduce nicotine‐induced oxidative stress in rat heart

The effects of vitamin E and Hippophea rhamnoides L. extract (HRe‐1) on nicotine‐induced oxidative stress in rat heart were investigated. There were eight rats per group and supplementation period was 3 weeks. The groups were: nicotine [0.5 mg kg^?1day^?1, intraperitoneal (i.p.)]; nicotine plus vitamin E [75 mg kg^?1day^?1, intragastric (i.g.)]; nicotine plus HRe‐1 (250 mg kg^?1day^?1, i.g.); and the control group (receiving only vehicles). Nicotine increased the malondialdehyde level, which was prevented by both vitamin E and HRe‐1. Glutathione peroxidase (GPx) activity in nicotine plus vitamin E supplemented group was higher than the others. Glutathione S‐transferase (GST) activity in nicotine plus HRe‐1 supplemented group was increased compared with the control group. Catalase activity was higher in nicotine group compared with others. GPx activity in nicotine plus vitamin E supplemented group was elevated compared with the others. Total and non‐enzymatic superoxide scavenger activities in nicotine plus vitamin E supplemented group were lower than nicotine plus HRe‐1 supplemented group. Superoxide dismutase (SOD) activity was higher in nicotine plus HRe‐1 supplemented group compared with others. Glutathione reductase activity and nitric oxide level were not affected. Increased SOD and GST activities might have taken part in the prevention of nicotine‐induced oxidative stress in HRe‐1 supplemented group in rat heart. Flavonols such as quercetin, and isorahmnetin, tocopherols such as α‐tocopherol and β‐tocopherol and carotenoids such as α‐carotene and β‐carotene, reported to be present in H. rhamnoides L. extracts may be responsible for the antioxidant effects of this plant extract. Copyright © 2010 John Wiley & Sons, Ltd.     

Oxidative stress in toadfish (Halobactrachus didactylus) cardiac muscle: Acute exposure to vanadate oligomers

Vanadate solutions as ‘metavanadate’ (containing ortho and metavanadate species) and ‘decavanadate’ (containing manly decameric species) (5 mM; 1 mg/kg) were injected intraperitoneously in Halobatrachus didactylus (toadfish), in order to evaluate the contribution of decameric vanadate species to vanadium (V) intoxication on the cardiac tissue. Following short-term exposure (1 and 7 days), different changes on antioxidant enzyme activities—superoxide dismutase (SOD), catalase (CAT), selenium-glutathione peroxidase (Se-GPx), total glutathione peroxidase (GPx), lipid peroxidation and subcellular vanadium distribution were observed in mitochondrial and cytosolic fractions of heart ventricle toadfish. After 1 day of vanadium intoxication, SOD, CAT and Se-GPx activities were decreased up to 25%, by both vanadate solutions, except mitochondrial CAT activity that increased (+23%) upon decavanadate administration. After 7 days of exposure, decavanadate versus metavanadate solutions promoted different effects mainly on cytosolic CAT activity (−56% versus −5%), mitochondrial CAT activity (−10% versus +10%) and total GPx activity (+1% versus −35%), whereas lipid peroxidation products were significantly increased (+82%) upon 500 μM decavanadate intoxication. Accumulation of vanadium in total (0.137±0.011 μg/g) and mitochondrial (0.022±0.001 μg/g) fractions was observed upon 7 days of metavanadate exposure, whereas for decavanadate, the concentration of vanadium increased in cytosolic (0.020±0.005 μg/g) and mitochondrial (0.021±0.009 μg/g) fractions. It is concluded that decameric vanadate species are responsible for a strong increase on lipid peroxidation and a decrease in cytosolic catalase activity thus contributing to oxidative stress responses upon vanadate intoxication, in the toadfish heart.