Effects of nicotine and vitamin E on 6-phosphogluconate dehydrogenase activity in some rat tissues in vivo and in vitro

The aim of this study was to investigate whether nicotine affects 6-phosphogluconate dehydrogenase (6PGD) enzyme activity in some rat tissues, and to see the modulatory effects of vitamin E on this effect in vivo. In addition, the effects of nicotine and vitamin E on 6PGD activity were also tested in vitro. The groups were: nicotine [0.5 mg/kg/day, intraperitoneal (i.p.)]; nicotine + vitamin E [75 mg/kg/day, intragastric (i.g.)]; and control group (receiving only vehicles). There were eight rats per group and supplementation period was 3 weeks. The results of in vivo study showed that nicotine activated the muscle, lungs, and testicular 6PGD enzyme activity but had no effect on heart and liver 6PGD activity. Also, nicotine + vitamin E activated the muscle, testicle, and liver 6PGD enzyme activity, while this combination had no effect on heart, and lungs in vivo. When nicotine is administered with vitamin E the increase in 6PGD enzyme activity in muscle and testicles were lower. On the other hand the increase in 6PGD enzyme activity was eliminated by vitamin E in lungs, while 6PGD enzyme activity was increased by vitamin E, which was not affected by nicotine only. In vitro results correlated well with in vivo experimental results. Our results suggest that vitamin E may favourably increase 6PGD enzyme activity in liver in nicotine treated rats, while it has negligible effects on this enzyme activity in other tissues.     

Dietary vitamin A requirement of juvenile Amur sturgeon (Acipenser schrenckii)

The present experiment was conducted to determine the dietary vitamin A requirement of juvenile Amur sturgeon (Acipenser schrenckii) by formulating seven semipurified diets containing 10, 258, 510, 1050, 2020, 4100 and 8300 IU vitamin A (as retinol acetate) kg^?1 diet, respectively. Each experimental diet was fed to triplicate groups of 20 juveniles each with initial average weights of 12.09 ± 0.22 g in 405‐L aquaria and maintained at 25.0 ± 2.0°C for 8 weeks. Fish fed the basal diet (10 IU vitamin A kg^?1 diet) exhibited poor appetite and activity, whereas these signs were not observed in any group fed vitamin A‐supplemented diets. Weight gain, feed efficiency and hepatosomatic index increased significantly with increases in the dietary vitamin A level, reaching a peak with the vitamin A 1050 IU kg^?1 diet, and then decreasing. Muscle chemical compositions were not affected by the dietary vitamin A levels. Vitamin A concentrations in liver and muscle increased significantly as the vitamin A levels increased within a range of 10～4100 IU kg^?1 diet; above this level there were no significant changes. Broken‐line regression analysis of weight gain and liver vitamin A concentration against the dietary vitamin A level showed that juvenile Amur sturgeon required a minimum of 923 IU vitamin A kg^?1 in the diet for maximal growth, and 1981 IU kg^?1 for highest liver vitamin A accumulation.     

The effects of vitamins and selenium mixture against brain tissue induced by d‐galactosamine

Brain damage is a major complication of fulminant hepatic failure. d ‐Galactosamine (d ‐GalN)‐induced liver toxicity causes damage to brain. The effects of vitamins and selenium mixture against d ‐GalN stimulated brain injury were investigated in this study. Sprague‐Dawley female rats aged 2.0‐2.5 months were used for the study. The rats were divided into four categories. A 0.9% NaCl solution was intraperitoneally given to the experimental rats in the first group. Using gavage technique, the second group of animals were subjected to a formulation consisting of 100 mg·kg^?1·day^?1 vitamin C, 15 mg·kg^?1·day^?1 of β‐carotene, 100 mg·kg^?1·day^?1 of α‐tocopherol in addition to 0.2 mg·kg^?1·day^?1 of sodium selenate for 3 days. The third group was given a single dose of d ‐GalN hydrochloride at the concentration of 500 mg·kg^?1 through a saline injection. The final group was given similar concentrations of both the antioxidant combination and d ‐GalN. Tissue samples were collected under ether anesthesia. The rats treated with d ‐GalN showed brain damage; increased myeloperoxidase, catalase, glutathione peroxidase, glutathione‐S‐transferase, lactate dehydrogenase, and superoxide dismutase activities; and decreased glutathione levels. Treatment with vitamins and selenium combination resulted in alleviation of these alterations in the rats. These findings suggest that administration of the vitamins and selenium combination suppresses oxidative stress and protects brain cells from injury induced by d ‐GalN.     

Protective effects of antioxidant combination against D‐galactosamine‐induced kidney injury in rats

The protective effects of an antioxidant combination in kidney injury induced by the injection of D‐galactosamine (D‐GaIN) were examined in the present study. Sprague Dawley female rats were used and divided into four groups as follows: (1) animals injected physiological saline solution, intraperitoneally, (2) animals treated with the combination of ascorbic acid (100 mg kg^?1 day^?1), β‐carotene (15 mg kg^?1 day^?1), α‐tocopherol (100 mg kg^?1 day^?1), and sodium selenate (0.2 mg kg^?1 day^?1) for three days orally, (3) rats injected D‐GaIN (500 mg kg^?1) intraperitoneally as a single dose, and (4) animals treated with the antioxidant combination for three days, then injected D‐GaIN. The tissue and blood samples of animals were collected for morphological and biochemical evaluations. Histopathological injury in kidney tissues was observed together with a significant increase in tissue lipid peroxidation (LPO) level, myeloperoxidase (MPO), lactate dehydrogenase, catalase and superoxide dismutase (SOD) activities, and serum creatinine and urea levels, and a significant decrease in glutathione level and glutathione peroxidase activity in D‐GaIN injected rats. However, a decrease in the degenerative changes was detected in the kidney tissue of D‐GaIN + antioxidant group, and biochemical results showed reversed effects. In conclusion, it seems reasonable to conclude that the treatment of the antioxidant combination has a protective effect on D‐GaIN‐induced kidney injury of rats. Copyright © 2010 John Wiley & Sons, Ltd.     

Neonatal exposure to bisphenol A advances pubertal development in female rats

Neonatal exposure to bisphenol A (BPA) is hypothesized to advance pubertal development. However, the effects of neonatal BPA exposure on pubertal development has not been described. In this study, female Sprague‐Dawley rats were exposed to 0.05, 0.5, 5, or 10 mg·kg^?1·day^?1 BPA, or corn oil vehicle alone from postnatal day 1 (PND1) to PND10 via subcutaneous injection. We evaluated day of vaginal opening (DVO), ovarian morphology, serum hormone concentrations, and hypothalamic expression of Gnrh1 and Kiss1 in female rats at PND35. DVO was significantly advanced in rats exposed to 5 and 10 mg·kg^?1·day^?1 BPA. Serum hormone concentrations increased as BPA dose increased. Additionally, hypothalamic Gnrh1 and Kiss1 expression were increased with BPA exposure; rats exposed to 10 mg·kg^?1·day^?1 BPA had significantly upregulated hypothalamic Gnrh1 and Kiss1 expressions in terms of both messenger RNA and protein levels. Our results suggest that exposure to a 10 mg·kg^?1·day^?1 dose of BPA might advance pubertal development significantly. In addition, within the range of 0 to 10 mg·kg^?1·day^?1, neonatal exposure to BPA may affect pubertal development in a dose‐dependent manner.     

Influence of kolaviron and vitamin E on ethylene glycol monoethyl ether‐induced haematotoxicity and renal apoptosis in rats

The present study investigated the protective effects of kolaviron, a biflavonoid from the seed of Garcinia kola, and vitamin E on ethylene glycol monoethyl ether (EGEE)‐induced haematotoxicity and renal apoptosis in male rats. EGEE was administered at a dose of 200 mg kg^?1 alone or simultaneously administered with kolaviron (100 and 200 mg kg^?1) and vitamin E (50 mg kg^?1) for 14 days. Results of haematological examination showed that white blood cells, platelets, neutrophils and mean corpuscular haemoglobin concentration were significantly lower, whereas lymphocytes were increased in EGEE‐exposed rats compared with those in the control. Administration of EGEE caused a significant decrease in the superoxide dismutase and catalase activities as well as in the glutathione level but significantly increased glutathione Stransferase activity and levels of hydrogen peroxide and lipid peroxidation in kidneys of rats compared with those in the control. Also, EGEE‐treated rats showed significant elevation in the serum urea and creatinine with marked increase in the frequency of terminal deoxynucleotidyl transferase‐mediated dUTP nick end labelling assay‐positive apoptotic cells in the tubular epithelial cells in comparison with the control. Co‐administration with kolaviron or vitamin E exhibited chemoprotective effects against EGEE‐mediated haematotoxicity, augmented renal antioxidant status and prevented the induction of renal apoptosis. Copyright © 2013 John Wiley & Sons, Ltd.     

Biodegradation of nicotine by newly isolated Pseudomonas sp. CS3 and its metabolites

Aims: Isolation and characterization of nicotine‐degrading bacteria with advantages suitable for the treatment of nicotine‐contaminated water and soil and detection of their metabolites. Methods and Results: A novel nicotine‐degrading bacterial strain was isolated from tobacco field soil. Based on morphological and physiochemical properties and sequence of 16S rDNA, the isolate was identified as Pseudomonas sp., designated as CS3. The optimal culture conditions of strain CS3 for nicotine degradation were 30°C and pH 7·0. However, the strain showed broad pH adaptability with high nicotine‐degrading activity between pH 6·0 and 10·0. Strain CS3 could decompose nicotine nearly completely within 24 h in liquid culture (1000 mg L^?1 nicotine) or within 72 h in soil (1000–2500 mg kg^?1 nicotine) and could endure up to 4000 mg L^?1 nicotine in liquid media and 5000 mg kg^?1 nicotine in soil. Degradation tests in flask revealed that the strain had excellent stability and high degradation activity during the repetitive degradation processes. Additionally, three intermediates, 3‐(3,4‐dihydro‐2H‐pyrrol‐5‐yl) pyridine, 1‐methyl‐5‐(3‐pyridyl) pyrrolidine‐2‐ol and cotinine, were identified by GC/MS and NMR analyses. Conclusions: The isolate CS3 showed outstanding nicotine‐degrading characteristics such as high degradation efficiency, strong substrate endurance, broad pH adaptability, and stability and persistence in repetitive degradation processes and may serve as an excellent candidate for applications in the bioaugmentation process to treat nicotine‐contaminated water and soil. Also, detection of nicotine metabolites suggests that strain CS3 might decompose nicotine via a unique nicotine‐degradation pathway. Significance and Impact of the Study: The advantage of applying the isolated strain lies in broad pH adaptability and stability and persistence in repetitive use, the properties previously less focused in other nicotine‐degrading micro‐organisms. The strain might decompose nicotine via a nicotine‐degradation pathway different from those of other nicotine‐utilizing Pseudomonas bacteria reported earlier, another highlight in this study.     

Effects of nicotine and vitamin E on 6-phosphogluconate dehydrogenase activity in some rat tissues in vivo and in vitro

The aim of this study was to investigate whether nicotine affects 6-phosphogluconate dehydrogenase (6PGD) enzyme activity in some rat tissues, and to see the modulatory effects of vitamin E on this effect in vivo. In addition, the effects of nicotine and vitamin E on 6PGD activity were also tested in vitro. The groups were: nicotine [0.5 mg/kg/day, intraperitoneal (i.p.)]; nicotine + vitamin E [75 mg/kg/day, intragastric (i.g.)]; and control group (receiving only vehicles). There were eight rats per group and supplementation period was 3 weeks. The results of in vivo study showed that nicotine activated the muscle, lungs, and testicular 6PGD enzyme activity but had no effect on heart and liver 6PGD activity. Also, nicotine + vitamin E activated the muscle, testicle, and liver 6PGD enzyme activity, while this combination had no effect on heart, and lungs in vivo. When nicotine is administered with vitamin E the increase in 6PGD enzyme activity in muscle and testicles were lower. On the other hand the increase in 6PGD enzyme activity was eliminated by vitamin E in lungs, while 6PGD enzyme activity was increased by vitamin E, which was not affected by nicotine only. In vitro results correlated well with in vivo experimental results. Our results suggest that vitamin E may favourably increase 6PGD enzyme activity in liver in nicotine treated rats, while it has negligible effects on this enzyme activity in other tissues.     

Effect of feeding supplemental copper on performance,fatty acid profile and on cholesterol contents and oxidative stability of meat of rabbits

One hundred and four rabbits, five weeks old at the beginning of the experiment, were divided into four groups according to a feed additive treatment. Rabbits of the 1st, 2nd, 3rd and 4th group were fed a basal granulated feed (control), basal feed supplemented with CuSO₄ · 5H₂O at 50mg Cu · kg^‐1, basal feed supplemented with 150mg Cu · kg^‐1, and the latter feed supplemented with 100mg · kg^‐1 vitamin E, respectively. The duration of the experiment was 42 days. Addition of Cu at 150mg · kg.^‐1 increased weight gain non‐significantly by 9.1%. This effect was the most pronounced in the first two weeks of fattening. The lowest mortality was observed in rabbits fed the highest amount of additives (7.7% vs. 19.2% in the control). Rabbits were slaughtered at the age of 11 weeks. Neither treatment influenced proportions of saturated, monounsaturated and polyunsaturated fatty acids in lipids extracted from the loin and hindleg muscles. In rabbits fed the highest amount of copper and vitamin E, the cholesterol concentration was significantly decreased by 13.6% and 17.9% in the loin and hindleg meat, respectively. Effects of Cu added at 50mg · kg^‐1 were marginal. Copper had no effect on the oxidative stability of meat, measured as thiobarbituric acid‐reactive substances in meat stored at 4°C for 0, 3 and 8 days. Vitamin E added in excess of nutritional requirement improved the oxidative stability of meat. In copper‐fed rabbits, Cu accumulated in the liver, but not in muscles. Feeding of the basal feed for 7 days to rabbits previously fed copper sulphate decreased the hepatic Cu concentration by 14.0 to 24.4%     

Effects of varying levels of dietary vitamin E (α‐tocopherol) on growth performance,proximate and fatty acid composition of juvenile silver pomfret (Pampus argenteus Euphrasen, 1788)

This study investigated the effects of elevated dietary levels of vitamin E (α‐tocopherol) on growth performance, proximate composition and fatty acid profiles of juvenile silver pomfret, Pampus argenteus. Three semi‐purified experimental diets were formulated to contain 49% protein and 16% lipid. High docosahexaenoic acid (DHA) tuna oil was added to the diets to supplement DHA. A graded level of vitamin E (0‐, 50‐, and 100 mg kg^?1) was added to experimental diets 1 to 3, respectively. Analyzed vit. E levels were 155.2, 195.3 and 236.4 mg kg^?1 in diets 1, 2 and 3, respectively. The experiment was conducted for 12 weeks with juvenile silver pomfret (29.6 ± 7.6 g) using a flow‐through system consisting of nine 1‐m³ tanks. Each treatment had three replicates and fish were stocked at the rate of 20 m^?3. Growth performance and feed utilization parameters of fish fed diets 2 and 3 were significantly (P < 0.05) higher than in fish fed diet 1, but the parameters in diets 2 and 3 did not differ significantly (P > 0.05). Although whole body protein levels were not influenced by the dietary vit. E levels, whole body lipid in fish fed diet 2 was significantly higher than in fish fed the other diets. The whole body vit. E levels in fish fed diet 2 (22.6 mg kg^?1) and diet 3 (24.1 mg kg^?1) were significantly (P < 0.05) higher than in those fed diet 1 (18.2 mg kg^?1). Whole body total saturated fatty acids were significantly lower, and DHA levels higher in fish fed diets 2 and 3 than those fed diet 1. The results of the present study suggest that increasing dietary supplementation of vit. E in high lipid diets enhances the growth performance of fish and that a dietary level of 196 mg kg^?1 vit. E is suitable for the growth of silver pomfret.     

Effects of dietary l‐carnitine supplements on growth and body composition in beluga sturgeon (Huso huso) juveniles

The effects of dietary l ‐carnitine on growth performance, whole body composition and feed utilization were studied in beluga, Huso huso. Fish were randomly allocated in 15 tanks (30 fish per tank) and triplicate groups were fed to satiety during 84 days one of five isonitrogenous (41% CP) and isoenergetic (20 MJ kg^?1) diets, each differing in l ‐carnitine content [0 (control), 300, 600, 900 and 1200 mg kg^?1 diet]. At the end of the trial, fish grew from 19‐ to 23‐fold in weight, from 8.4 g to a maximum of 191 g. Fish fed 300–600 mg l ‐carnitine had the highest specific growth rate (SGR, 3.69 and 3.72% day^?1) and protein efficiency ratio (PER, 0.95 and 0.99), and the lowest feed conversion ratio (FCR, 1.4 and 1.3) than the other groups (P < 0.0001). SGR, PER and FCR were the poorest for fish fed 1200 mg l ‐carnitine, while fish fed the unsupplemented and 900 mg l ‐carnitine supplemented diet showed intermediate performance. Body lipid concentration decreased significantly from 5.8 to 5.1% (P < 0.0001) with dietary l ‐carnitine supplementation increasing from 0 to 300 mg. Energy content was significantly lower in fish fed the 900 and 1200 mg l ‐carnitine diet (5.8 MJ kg^?1), when compared with the other treatment groups (6.4–6.6 MJ kg^?1). The results indicated that feeding sturgeon on diets supplemented with 300 mg l ‐carnitine kg^?1 diet improved growth performance, and stimulated protein‐sparing effects from lipids.     

Tissue chemistry and morphology affect root decomposition of perennial bioenergy grasses on sandy soil in a sub‐tropical environment

Second‐generation biofuels and bio‐based products derived from lignocellulosic biomass are likely to replace current fuels derived from simple sugars and starch because of greater yield potential and less competition with food production. Besides the high aboveground biomass production, these bioenergy grasses also exhibit extensive root systems. The decomposition of root biomass greatly influences nutrient cycling and microbial activity and subsequent accumulation of carbon (C) in the soil. The objective of this research was thus to characterize root morphological and chemical differences in six perennial grass species in order to better understand root decomposition and belowground C cycling of these bioenergy cropping systems. Giant reed (Arundo donax), elephantgrass (Pennisetum purpureum), energycane (Saccharum spp.), sugarcane (Saccharum spp.), sweetcane (Saccharum arundinaceum), and giant miscanthus (Miscanthus × giganteus) were established in Fall 2008 in research plots near Gainesville, Florida. Root decomposition rates were measured in situ from root decomposition bags over 12 months along with initial and final root tissue composition. Root potential decomposition rate constant (K) was higher in elephantgrass (3.64 g kg^?1 day^?1) and sweetcane (2.77 g kg^?1 day^?1) than in sugarcane (1.62 g kg^?1 day^?1) and energycane (1.48 g kg^?1 day^?1). Notably, K was positively related to initial root tissue total C (Total C), total fiber glucose (TFG), total fiber xylose (TFX), and total fiber carbohydrate (TFC) concentrations, but negatively related to total fiber arabinose (TFA) and lignin (TL) concentrations and specific root volume (SRV). Among the six species, elephantgrass exhibited root traits most favorable for fast decomposition: high TFG, high TFX, high TFC, high specific root length (SRL), and a low SRV, whereas giant reed, sugarcane, and energycane exhibited slow decomposition rates and the corresponding root traits. Thus, despite similar aboveground biomass yields in many cases, these species are likely to differentially affect soil C accumulation.     

Soil nitrogen transformations under Populus tremuloides, Betula papyrifera and Acer saccharum following 3 years exposure to elevated CO2 and O3

Increases in atmospheric CO₂ and tropospheric O₃ may affect forest N cycling by altering plant litter production and the availability of substrates for microbial metabolism. Three years following the establishment of our free‐air CO₂–O₃ enrichment experiment, plant growth has been stimulated by elevated CO₂ resulting in greater substrate input to soil; elevated O₃ has counteracted this effect. We hypothesized that rates of soil N cycling would be enhanced by greater plant productivity under elevated CO₂, and that CO₂ effects would be dampened by O₃. We found that elevated CO₂ did not alter gross N transformation rates. Elevated O₃ significantly reduced gross N mineralization and microbial biomass N, and effects were consistent among species. We also observed significant interactions between CO₂ and O₃: (i) gross N mineralization was greater under elevated CO₂ (1.0 mg N kg^?1 day^?1) than in the presence of both CO₂ and O₃ (0.5 mg N kg^?1 day^?1) and (ii) gross NH₄⁺ immobilization was also greater under elevated CO₂ (0.8 mg N kg^?1 day^?1) than under CO₂ plus O₃ (0.4 mg N kg^?1 day^?1). We used a laboratory ¹⁵N tracer method to quantify transfer of inorganic N to organic pools. Elevated CO₂ led to greater recovery of NH₄⁺‐¹⁵N in microbial biomass and corresponding lower recovery in the extractable NO₃^? pool. Elevated CO₂ resulted in a substantial increase in NO₃^?‐¹⁵N recovery in soil organic matter. We observed no O₃ main effect and no CO₂ by O₃ interaction effect on ¹⁵N recovery in any soil pool. All of the above responses were most pronounced beneath Betula papyrifera and Populus tremuloides, which have grown more rapidly than Acer saccharum. Although elevated CO₂ has increased plant productivity, the resulting increase in plant litter production has yet to overcome the influence of the pre‐existing pool of soil organic matter on soil microbial activity and rates of N cycling. Ozone reduces plant litter inputs and also appears to affect the composition of plant litter in a way that reduces microbial biomass and activity.     

L‐NAME co‐treatment prevent oxidative damage in the lung of adult Wistar rats treated with vitamin A supplementation

Based on the fact that vitamin A in clinical doses is a potent pro‐oxidant agent to the lungs, we investigated here the role of nitric oxide (NO^?) in the disturbances affecting the lung redox environment in vitamin A‐treated rats (retinol palmitate, doses of 1000–9000 IU·kg^?1·day^?1) for 28 days. Lung mitochondrial function and redox parameters, such as lipid peroxidation, protein carbonylation and the level of 3‐nytrotyrosine, were quantified. We observed, for the first time, that vitamin A supplementation increases the levels of 3‐nytrotyrosine in rat lung mitochondria. To determine whether nitric oxide (NO ?) or its derivatives such as peroxynitrite (ONOO‐) was involved in this damage, animals were co‐treated with the nitric oxide synthase inhibitor L‐NAME (30 mg·kg^?1, four times a week), and we analysed if this treatment prevented (or minimized) the biochemical disturbances resulting from vitamin A supplementation. We observed that L‐NAME inhibited some effects caused by vitamin A supplementation. Nonetheless, L‐NAME was not able to reverse completely the negative effects triggered by vitamin A supplementation, indicating that other factors rather than only NO? or ONOO‐ exert a prominent role in mediating the redox effects in the lung of rats that received vitamin A supplementation. Copyright © 2011 John Wiley & Sons, Ltd.     

EFFECT OF VITAMIN E SUPPLEMENTATION AND PARTIAL SUBSTITUTION OF POLY- WITH MONO-UNSATURATED FATTY ACIDS IN PIG DIETS ON MUSCLE,AND MICROSOME EXTRACT a-TOCOPHEROL CONCENTRATION AND LIPID OXIDATION

The experiment was organized in a 3×2 factorial arrangement with three dietary fat blends and a basal (20 mg kg^?1 diet) or supplemented (220 mg kg^?1) level of α-tocopheryl acetate. Dietary vitamin E and monounsaturated to polyunsaturated fatty acid ratio (dietary MUFA/PUFA) affected muscle α-tocopherol concentration (α-tocopherol [log μg g^?1]=0.18 (±0.105)+0.0034 (±0.0003)·dietary α-tocopherol [mg kg^?1 diet] (P<0.0001)+0.39 (±0.122)·dietary MUFA/PUFA (P<0.0036)). An interaction between dietary α-tocopherol and dietary MUFA/PUFA exists for microsome α-tocopherol concentration (α-tocopherol [log μg g^?1]=1.14 (±0.169) (P<0.0001)+0.0056 (±0.00099)·dietary α-tocopherol [mg kg^?1 diet] (P<0.0001)+0.54 (±0.206)·dietary MUFA/PUFA (P<0.0131)?0.0033 (±0.0011)·dietary α-tocopherol [mg kg^?1)]×dietary MUFA/PUFA (P<0.0067)), and hexanal concentration in meat (hexanal [ng·g^?1]=14807.9 (±1489.8)?28.8 (±10.6) dietary α-tocopherol [mg·kg^?1] (P<0.01)?8436.6 (±1701.6)·dietary MUFA/PUFA (P<0.001)+24.0 (±11.22)·dietary α-tocopherol·dietary MUFA/PUFA (P<0.0416)). It is concluded that partial substitution of dietary PUFA with MUFA lead to an increase in the concentration of α-tocopherol in muscle and microsome extracts. An interaction between dietary α-tocopherol and fatty acids exists, in which at low level of dietary vitamin E inclusion, a low MUFA/PUFA ratio leads to a reduction in the concentration of α-tocopherol in microsome extracts and a concentration of hexanal in meat above the expected values.     

High‐fat diet and hydrochlorothiazide increase oxidative stress in brain of rats

This study evaluated the effect of possible synergic interaction between high fat diet (HF) and hydrochlorothiazide (HCTZ) on biochemical parameters of oxidative stress in brain. Rats were fed for 16 weeks with a control diet or with an HF, both supplemented with different doses of HCTZ (0.4, 1.0, and 4.0 g kg⁻¹ of diet). HF associated with HCTZ caused a significant increase in lipid peroxidation and blood glucose levels. In addition, HF ingestion was associated with an increase in cerebral lipid peroxidation, vitamin C and non‐protein thiol groups (NPSH) levels. There was an increase in vitamin C as well as NPSH levels in HCTZ (1.0 and 4.0 g kg⁻¹ of diet) and HF plus HCTZ groups. Na⁺–K⁺‐ATPase activity of HCTZ (4.0 g kg⁻¹ of diet) and HCTZ plus HF‐fed animals was significantly inhibited. Our data indicate that chronic intake of a high dose of HCTZ (4 g kg⁻¹ of diet) or HF change biochemical indexes of oxidative stress in rat brain. Furthermore, high‐fat diets consumption and HCTZ treatment have interactive effects on brain, showing that a long‐term intake of high‐fat diets can aggravate the toxicity of HCTZ. Copyright © 2009 John Wiley & Sons, Ltd.     

Effects of nicotine and Vitamin E on Carbonic anhydrase activity in some rat tissues In Vivo and In Vitro

Effects of nicotine, nicotine+vitamin E and nicotine+Hippophea rhamnoides L. extract (HRe-1) on muscle, heart, lungs, testicle, kidney, stomach, brain and liver carbonic anhydrase (CA; EC 4.2.1.1.) enzyme activities were investigated in vivo. Groups of rats were given nicotine (0.5?mg/kg/day, i.p.), nicotine+vitamin E (75?mg/kg/day, i.g.), nicotine+HRe-1 (250?mg/kg/day, i.g.) and a control group vehicle only. The results showed that nicotine inhibited the heart, lung, stomach and liver CA enzyme activities by ～80% (p?<?0.001), ～94% (p?<?0.001), ～47% (p?<?0.001) and ～81% (p?<?0.001) respectively, and activated muscle and kidney, but had no effects on the testicle and brain CA activities. Nicotine+vitamin E inhibited the heart and liver CA enzyme activities by ～50% (p?<?0.001), and ～50% (p?<?0.001), respectively, and nicotine+vitamin E activated the muscle CA activity. However, nicotine+vitamin E had no effect on lung, testicle, kidney, stomach and brain CA activities. Nicotine+HRe-1 inhibited the heart and stomach CA enzyme activities by ～51% (p?<?0.001), and ～32% (p?<?0.002), respectively, and activated the muscle and brain CA activities, but had no effects on the lung, testicle, kidney, and liver CA activities. In vitro CA inhibition results for similar experiments correlated well with the in vivo experimental results in lungs, testicles, kidney, stomach, brain and liver tissues.     

Using CO2 to enhance carbon capture and biomass applications of freshwater macroalgae

A major limiting factor in the development of algae as a feedstock for the bioenergy industry is the consistent production and supply of biomass. This study is the first to access the suitability of the freshwater macroalgal genus Oedogonium to supply biomass for bioenergy applications. Specifically, we quantified the effect of CO₂ supplementation on the rate of biomass production, carbon capture, and feedstock quality of Oedogonium when cultured in large‐scale outdoor tanks. Oedogonium cultures maintained at a pH of 7.5 through the addition of CO₂ resulted in biomass productivities of 8.33 (±0.51) g DW m^?2 day^?1, which was 2.5 times higher than controls which had an average productivity of 3.37 (±0.75) g DW m^?2 day^?1. Under these productivities, Oedogonium had a carbon content of 41–45% and a higher heating value of 18.5 MJ kg^?1, making it an ideal biomass energy feedstock. The rate of carbon fixation was 1380 g C m^?2 yr^?1 and 1073.1 g C m^?2 yr^?1 for cultures maintained at a pH of 7.5 and 8.5, and 481 g C m^?2 yr^?1 for cultures not supplemented with CO₂. This study highlights the potential of integrating the large‐scale culture of freshwater macroalgae with existing carbon waste streams, for example coal‐fired power stations, both as a tool for carbon sequestration and as an enhanced and sustainable source of bioenergy.     

Taurine supplementation decreases oxidative stress in skeletal muscle after eccentric exercise

Infrequent exercise, typically involving eccentric actions, has been shown to cause oxidative stress and to damage muscle tissue. High taurine levels are present in skeletal muscle and may play a role in cellular defences against free radical‐mediated damage. This study investigates the effects of taurine supplementation on oxidative stress biomarkers after eccentric exercise (EE). Twenty‐four male rats were divided into the following groups (n = 6): control; EE; EE plus taurine (EE + Taurine); EE plus saline (EE + Saline). Taurine was administered as a 1‐ml 300 mg kg^?1 per body weight (BW) day^?1 solution in water by gavage, for 15 consecutive days. Starting on the 14th day of supplementation, the animals were submitted to one 90‐min downhill run session and constant velocity of 1·0 km h^?1. Forty‐eight hours after the exercise session, the animals were killed and the quadriceps muscles were surgically removed. Production of superoxide anion, creatine kinase (CK) levels, lipoperoxidation, carbonylation, total thiol content and antioxidant enzyme were analysed. Taurine supplementation was found to decrease superoxide radical production, CK, lipoperoxidation and carbonylation levels and increased total thiol content in skeletal muscle, but it did not affect antioxidant enzyme activity after EE. The present study suggests that taurine affects skeletal muscle contraction by decreasing oxidative stress, in association with decreased superoxide radical production. Copyright © 2010 John Wiley & Sons, Ltd.     

Hesperidin regresses cardiac hypertrophy by virtue of PPAR‐γ agonistic,anti‐inflammatory,antiapoptotic, and antioxidant properties

Hesperidin (HES), a flavanone glycoside, predominant in citrus fruits, has an agonistic activity on peroxisome proliferator‐activated receptor gamma (PPAR‐γ). PPAR‐γ is an inhibitor of cardiac hypertrophy (CH) signaling pathways. In this study, we investigated the cardioprotective effect of HES in isoproterenol (ISO)‐induced CH through PPAR‐γ agonistic activity. For this, male albino Wistar rats were divided into six groups (n = 6), that is, normal, ISO‐control, HES treatment group (200 mg kg^?1; p.o.), HES per se (200 mg kg^?1; p.o.), enalapril treatment group (30 mg kg^?1; p.o.), and combination group (HES 200 mg kg^?1; p.o.+enalapril 30 mg kg^?1; p.o.). ISO (3 mg kg^?1; s.c.) was administered to all groups except normal and per se to induce CH. HES or enalapril treatment of 28 days significantly attenuated pathological changes, improved cardiac hemodynamics, suppressed oxidative stress, and apoptosis along with an increased PPAR‐γ expression. The combination of enalapril with HES exhibited an effect similar to that of HES or enalapril alone on all the aforementioned parameters. Therefore, HES may be further evaluated as a promising molecule for the alleviation of CH.