Synergistic effect of Se-methylselenocysteine and vitamin E in ameliorating the acute ethanol-induced oxidative damage in rat

The present study was conduced to investigate the synergistic effects of combined treatments with Se-methylselenocysteine (SeMSC) and vitamin E (Vit E) in reversing oxidative stress induced by ethanol in serum and different tissues of rats. Sixty female rats were randomly divided into six groups for 30 days’ consecutive pretreatments as followed: control (I), physiological saline (II), 2.8 μg kg⁻¹ Se as SeMSC (III), 2.8 μg kg⁻¹ Se as sodium selenite (Na₂SeO₃, IV), 5 mg kg⁻¹ α-tocopherol as α-tocopherol acetate (Vit E, V), 5 mg kg⁻¹ α-tocopherol as α-tocopherol acetate and 2.8 μg kg⁻¹ Se as SeMSC (VI). All animals in groups II–VI were treated by ethanol treatment to cause oxidative stress. After 6 h of ethanol treatment, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), the contents of total antioxidant capacity (T-AOC), malondialdehyde (MDA), glutathione (GSH) and carbonyl protein (CP) in the serum, liver, heart and kidney were measured. The result showed that the individual SeSMC, Na₂SeO₃ and vitamin E could effectively increase the SOD, T-AOC, GSH-Px and GSH contents as well as significantly decrease the MDA and CP concentrations in the tissues of ethanol-induced rats. At the same dose on different forms of Se, SeMSC showed greater antioxidant activity than Na₂SeO₃. Moreover, group VI (SeMSC and α-tocopherol acetate) showed much better antioxidant activity than individual group III (SeMSC) and V (α-tocopherol acetate) due to the synergistic effect.     

Serum cytokines and muscle strength after anterior cruciate ligament surgery are not modulated by high-doses of vitamins E (α- and γ-tocopherol’s) and C

The purpose of this investigation was to identify if supplemental vitamin E (consisting of α- and γ-tocopherol’s) and C modulate serum cytokine and muscle strength following an ACL injury and surgery. Subjects were randomly assigned to one of two groups: (1) placebo (n = 14) or (2) vitamins E (α-[600 mg RRR-α-tocopherol, αT] and γ-[600 mg of RRR-γT]) and C (1000 mg ascorbic acid, AA) (EC; n = 15). Supplements were taken daily starting ∼2-wk prior to and concluding 16-wk after surgery. Fasting blood samples were obtained and single-leg peak isometric force measurements were performed at baseline (prior to supplementation), before surgery (∼120-min – blood draw only), and 8-wk, 12-wk, and 16-wk after surgery. αT, γT, AA, and cytokines were measured in each blood sample, and peak isometric force was measured on the injured and non-injured legs separately at each testing session. An exercise protocol consisting of repetitive knee and hip extension and flexion contractions to exhaustion was performed on the injured limb at 16-wk. Vitamin E and C supplementation significantly (all p < 0.05) increased plasma αT (∼40%), γT (∼160%), and AA (∼50%) concentrations. Serum cytokine concentrations, peak isometric force, and time to exhaustion during the exercise protocol were not significantly different between groups. Based on these findings, we conclude that vitamin E and C supplementation increases their endogenous levels without minimizing muscular weakness or modulating serum cytokine concentrations after ACL surgery.     

Composition of α-tocopherol and fatty acids in porcine tissues after dietary supplementation with vitamin E and different fat sources

The present study evaluated the effect of increasing supplementation of all-rac-α-tocopheryl acetate and dietary fatty acid composition during a four week period after weaning on porcine tissue composition of α-tocopherol stereoisomers and fatty acids, and on hepatic expression of genes involved in transfer of α-tocopherol, and oxidation and metabolism of fatty acids. From day 28 to 56 of age, pigs were provided 5% of tallow, fish oil or sunflower oil and 85, 150, or 300 mg/kg of all-rac-α-tocopheryl acetate. Samples of liver, heart, and adipose tissue were obtained from littermates at day 56. Tissue fatty acid composition was highly influenced by dietary fat sources. Dietary fatty acid composition (P<0.001) and vitamin E supplementation (P<0.001) influenced the α-tocopherol stereoisomer composition in liver, i.e. less proportion of the RRR-α-tocopherol was observed in pigs provided fish oil and the highest dose of vitamin E in comparison with other dietary treatments. In addition, the stereoisomer composition of α-tocopherol in heart, and adipose tissue was influenced by dietary treatments. Expression of genes in liver involved in the regulation of FA conversion, SCD (P=0.002) and D6D (P=0.04) were lower in pigs fed fish oil compared to other treatments, whereas the fatty acid oxidation, as indicated by the expression of PPAR-α, was higher when sunflower and fish oil was provided (P=0.03). Expression of α-TTP in liver was higher in pigs fed fish oil (P=0.01). Vitamin E supplementation did not influence significantly the hepatic gene expression.     

Protective effect of Piper betle leaf extract against cadmium-induced oxidative stress and hepatic dysfunction in rats

The present study was undertaken to examine the attenuative effect of Piper betle leaf extract (PBE) against cadmium (Cd) induced oxidative hepatic dysfunction in the liver of rats. Pre-oral supplementation of PBE (200 mg/kg BW) treated rats showed the protective efficacy against Cd induced hepatic oxidative stress. Oral administration of Cd (5 mg/kg BW) for four weeks to rats significantly (P > 0.05) elevated the level of serum hepatic markers such as serum aspartate transaminase (AST), serum alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma-glutamyl transpeptidase (GGT), bilirubin (TBRNs), oxidative stress markers viz., thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH), protein carbonyls (PC) and conjugated dienes (CD) and significantly (P > 0.05) reduced the enzymatic antioxidants viz., superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (G6PD) and non-enzymatic antioxidants Viz., reduced glutathione (GSH), total sulfhydryls (TSH), vitamin C and vitamin E in the liver. Pre-oral supplementation of PBE (200 mg/kg BW) in Cd intoxicated rats, the altered biochemical indices and pathological changes were recovered significantly (P > 0.05) which showed ameliorative effect of PBE against Cd induced hepatic oxidative stress. From the above findings, we suggested that the pre-administration of P. betle leaf extract exhibited remarkable protective effects against cadmium-induced oxidative hepatic injury in rats.     

Synthesis and characterization of a fluorescent probe for α-tocopherol suitable for fluorescence microscopy

Previously prepared fluorescent derivatives of α-tocopherol have shown tremendous utility in both in vitro exploration of the mechanism of ligand transfer by the α-tocopherol transfer protein (α-TTP) and the intracellular transport of α-tocopherol in cells and tissues. We report here the synthesis of a 4,4-difluoro-4-bora-3a,4a-diaza-s-indacene (BODIPY) containing α-tocopherol analog having extended conjugation with an alkenyl thiophene group that extends the absorption and emission maxima to longer wavelengths (λ_ex = 571 nm and λ_em = 583 nm). The final fluorophore thienyl-ene-BODIPY-α-tocopherol, 2, binds to recombinant human α-TTP with a K_d = 8.7 ± 1.1 nM and is a suitable probe for monitoring the secretion of α-tocopherol from cultured Mcf7#189 cells.     

Chronic vitamin E deficiency promotes vitamin C deficiency in zebrafish leading to degenerative myopathy and impaired swimming behavior

We hypothesized that zebrafish (Danio rerio) undergoing long-term vitamin E deficiency with marginal vitamin C status would develop myopathy resulting in impaired swimming. Zebrafish were fed for 1 y a defined diet without (E ?) and with (E +) vitamin E (500 mg α-tocopherol/kg diet). For the last 150 days, dietary ascorbic acid concentrations were decreased from 3500 to 50 mg/kg diet and the fish sampled periodically to assess ascorbic acid concentrations. The ascorbic acid depletion curves were faster in the E ? compared with E + fish (P < 0.0001); the estimated half-life of depletion in the E ? fish was 34 days, while in it was 55 days in the E + fish. To assess swimming behavior, zebrafish were monitored individually following a “startle-response” stimulus, using computer and video technology. Muscle histopathology was assessed using hematoxylin and eosin staining on paramedian sections of fixed zebrafish. At study end, E ? fish contained 300-fold less α-tocopherol (p < 0.0001), half the ascorbic acid (p = 0.0001) and 3-fold more malondialdehyde (p = 0.0005) than did E + fish. During the first minute following a tap stimulus (p < 0.05), E + fish swam twice as far as did E ? fish. In the E ? fish, the sluggish behavior was associated with a multifocal, polyphasic, degenerative myopathy of the skeletal muscle. The myopathy severity ranged from scattered acute necrosis to widespread fibrosis and was accompanied by increased anti-hydroxynonenal staining. Thus, vitamin E deficiency in zebrafish causes increased oxidative stress and a secondary depletion of ascorbic acid, resulting in severe damage to muscle tissue and impaired muscle function.     

Selenoproteins protect against avian nutritional muscular dystrophy by metabolizing peroxides and regulating redox/apoptotic signaling

Nutritional muscular dystrophy (NMD) of chicks is induced by dietary selenium (Se)/vitamin E (Vit. E) deficiencies and may be associated with oxidative cell damage. To reveal the underlying mechanisms related to the presumed oxidative cell damage, we fed four groups of 1-day-old broiler chicks (n = 40/group) with a basal diet (BD; 10 μg Se/kg; no Vit. E added, −Se −Vit. E) or the BD plus all-rac-α-tocopheryl acetate at 50 mg/kg (−Se +Vit. E), Se (as sodium selenite) at 0.3 mg/kg (+Se −Vit. E), or both of these nutrients (+Se +Vit. E) for 6 weeks. High incidences of NMD (93%) and mortality (36%) of the chicks were induced by the BD, starting at week 3. Dietary Se deficiency alone also induced muscle fiber rupture and coagulation necrosis in the pectoral muscle of chicks at week 3 and thereafter, with increased (P < 0.05) malondialdehyde, decreased (P < 0.05) total antioxidant capacity, and diminished (P < 0.05) glutathione peroxidase activities in the muscle. To link these oxidative damages of the muscle cells to the Se-deficiency-induced NMD, we first determined gene expression of the potential 26 selenoproteins in the muscle of the chicks at week 2 before the onset of symptoms. Compared with the +Se chicks, the −Se chicks had lower (P < 0.05) muscle mRNA levels of Gpx1, Gpx3, Gpx4, Sepp1, Selo, Selk, Selu, Selh, Selm, Sepw1, and Sep15. The −Se chicks also had decreased (P < 0.05) production of 6 selenoproteins (long-form selenoprotein P (SelP-L), GPx1, GPx4, Sep15, SelW, and SelN), but increased levels (P < 0.05) of the short-form selenoprotein P in muscle at weeks 2 and 4. Dietary Se deficiency elevated (P < 0.05) muscle p53, cleaved caspase 3, cleaved caspase 9, cyclooxygenase 2 (COX2), focal adhesion kinase (FAK), phosphatidylinositol 3-kinase (PI3K), phospho-Akt, nuclear factor-κB (NF-κB), p38 mitogen-activated protein kinase (p38 MAPK), phospho-p38 MAPK, phospho-JNK, and phospho-ERK and decreased (P < 0.05) muscle procaspase 3, procaspase 9, and NF-κB inhibitor α. In conclusion, the downregulation of SelP-L, GPx1, GPx4, Sep15, SelW, and SelN by dietary Se deficiency might account for induced oxidative stress and the subsequent peroxidative damage of chick muscle cells via the activation of the p53/caspase 9/caspase 3, COX2/FAK/PI3K/Akt/NF-κB, and p38 MAPK/JNK/ERK signaling pathways. Metabolism of peroxides and redox regulation are likely to be the mechanisms whereby these selenoproteins prevented the onset of NMD in chicks.     

Rapid quantitative determination of fat-soluble vitamins and coenzyme Q-10 in human serum by reversed phase ultra-high pressure liquid chromatography with UV detection

We are presenting the first ultra-high pressure LC (UHPLC) method for rapid quantitative measurement of vitamin A, E (α- and γ-tocopherol), β-carotene and CoQ₁₀ from human serum. The chromatography was performed on Shield RP₁₈ UHPLC column with UV detection. The method was validated based on linearity, accuracy, matrix effects study, precision and stability. The calibration was linear over the following range: 0.09–10.0 for retinol and γ-tocopherol, 0.05–5 for β-carotene, 0.9–100 for α-tocopherol and 0.14–15 mg/L for CoQ₁₀. The limit of detection and quantitation for retinol, γ-tocopherol, β-carotene, α-tocopherol and CoQ₁₀ were as follows 0.07/0.024, 0.018/0.06, 0.004/0.12, 0.078/0.261, 0.008/0.028 mg/L. The recoveries were above 85%. The inter- and intra-assay precision was below 10%. Reference intervals were established for children and adults. Because of its low cost, extremely short analysis time (2 min) and excellent chromatographic reproducibility this UHPLC method can easily be adopted for high-throughput clinical and pharmacokinetics studies.     

A combination of ascorbic acid and α-tocopherol or a combination of Mg and Zn are both able to reduce the adverse effects of lindane-poisoning on rat brain and liver

The purpose of this study, carried out on male Wistar rats, was to evaluate the beneficial effects of supplementation with ascorbic acid (Vit C) and α-tocopherol (Vit E) or with Mg and Zn upon lindane-induced damages in liver and brain. Under our experimental conditions, lindane poisoning (5 mg/kg body weight per day for 3 days) resulted in (1) an increased level of plasma glucose, cholesterol and triglycerides, (2) an increased activity of LDH, ALP, AST, ALT, (3) an oxidative stress in liver and brain as revealed by an increased level of lipids peroxidation (TBARS) and a decrease of glutathione-peroxidase, superoxide dismutase and catalase activities in liver and brain. In conclusion, both Vit C + E or Mg + Zn treatments display beneficial effects upon oxidative stress induced by lindane treatment in liver and brain.     

α-tocopherol β-oxidation localized to rat liver mitochondria

Approximately 40% of Americans take dietary supplements, including vitamin E (α-tocopherol). Unlike other fat-soluble vitamins, α-tocopherol is not accumulated to toxic levels. Rather tissue levels are tightly regulated, in part via increased hepatic metabolism and excretion that could, theoretically, alter metabolism of drugs, environmental toxins, and other nutrients. To date, in vivo subcellular location(s) of α-tocopherol metabolism have not been identified. The proposed pathway of α-tocopherol metabolism proceeds via ω-hydroxylation to 13′-OH-α-tocopherol, followed by successive rounds of β-oxidation to form α-CEHC. To test the hypothesis that α-tocopherol ω-hydroxylation occurs in microsomes while β-oxidation occurs in peroxisomes, rats received daily injections of vehicle, 10 mg α-tocopherol, or 10 mg trolox/100 g body wt for 3 days, and then microsomes, mitochondria, and peroxisomes were isolated from liver homogenates. Homogenate α-tocopherol levels increased 16-fold in α-tocopherol-injected rats, while remaining unchanged in trolox- or vehicle-injected rats. Total α-tocopherol recovered in the three subcellular fractions represented 93 ± 4% of homogenate α-tocopherol levels. In α-tocopherol-injected rats, microsome α-tocopherol levels increased 28-fold, while mitochondria and peroxisome levels increased 8- and 3-fold, respectively, indicating greater partitioning of α-tocopherol to the microsomes with increasing liver α-tocopherol. In α-tocopherol-injected rats, microsome 13′-OH-α-tocopherol levels increased 24-fold compared to controls, and were 7-fold greater than 13′-OH-α-tocopherol levels in peroxisome and mitochondrial fractions of α-tocopherol-injected rats. An unexpected finding was that α-CEHC, the end product of α-tocopherol metabolism, was found almost exclusively in mitochondria. These data are the first to indicate a mitochondrial role in α-tocopherol metabolism.     

Simple GC-FID method development and validation for determination of α-tocopherol (vitamin E) in human plasma

This paper describes the development and validation of a novel GC-FID method for the determination of α-tocopherol concentration in human plasma which does not requires derivatization. The standard solutions and the plasma working solutions were prepared in absolute ethanol. To determine the concentration of α-tocopherol in human plasma, an aliquot of the plasma sample was deproteinized with ethanol. α-tocopherol was extracted with a mixture of hexane and dichloromethane (9:1). GC separation was performed using a HP-5 capillary column. Nitrogen was used as carrier gas at a flow-rate of 2 ml min^− 1. Calibration curves were linear over the concentration range 1–30 μg ml^− 1 (for standard solutions and solutions without endogenous α-tocopherol in plasma) and 5–34 μg ml^− 1 (for solutions with endogenous α-tocopherol in plasma). Absolute recovery, precision, sensitivity and accuracy assays were carried out. The analytical recovery of α-tocopherol from plasma averaged 97.44%. The limit of quantification (LOQ) and the limit of detection (LOD) of method for standard samples were 0.35 μg.ml^− 1 and 0.30 μg.ml^− 1, respectively. Within-day and between-day precision, expressed as the relative standard deviation (RSD) were less than 4%, and accuracy (relative error) was better than 8%. This novel method, developed and validated in our laboratory, could be successfully applied to the in-vivo determination of α-tocopherol. The endogenous α-tocopherol amounts in blood of twelve healthy volunteers with no vitamin drug usage were measured with this method.     

Physiological effects of transport duration on stress biomarkers and meat quality of medium-growing Yellow broiler chickens

Pre-slaughter transport exerts negative effects on broilers’ welfare, meat yield, and meat quality, but little is known about the effect of transport on medium-growing broiler chickens. This study aimed at evaluating the effects of different durations of transport (0, 0.5, 1, 2, and 3 h) on stress biomarkers and meat quality of medium-growing Yellow-feathered broiler chickens. One hundred and eighty Chinese Yellow-feathered broilers aged 75 days (marketing age), of 2.02 kg average BW, were allotted into five groups; each group contained six replicates (six birds/replicate (crate)). Each crate with dimensions 74 × 55 × 27 cm (length × width × height) was loaded with six birds, that is, 30 kg live BW/m² crate. The tested transport durations increased BW loss (linear, P < 0.01), plasma concentrations of ACTH (linear, P < 0.10), cortisol and corticosterone (quadratic, P < 0.05), and activity of glutathione peroxidase (linear, P < 0.05), whereas plasma glucose was not affected. In breast muscle, contents of glycogen, lactic acid, malondialdehyde, and reduced glutathione were not affected (P > 0.05), but total antioxidant capacity decreased (linear, P < 0.01). The drip loss of breast muscle increased (linear, P < 0.01), whereas shear force, pH at 24 h postmortem, and breast meat color lightness (L*), redness (a*), and yellowness (b*) scores were not affected. In conclusion, the tested transport durations (from 0.5 to 3 h) increased BW loss and some plasma stress biomarkers in 75-day-old Yellow-feathered broiler chickens, but the effect on meat quality attributes was minor.     

Influence of R genome on the nutritional value of triticale for broiler chicks

The following grain characteristics: protein, arabinoxylan and dietary fibre content, viscosity and water holding capacity of wheat, rye and triticale of different ploidy levels were studied as to their effect on body weight gain (BWG), feed to gain ratio (FCR), apparent metabolizable energy (AME_n), dry matter digestibility (DMD) and apparent protein retention (APR) in young broiler chicks fed isograin and isoprotein diets based on these cereals. Highly significant correlations (p≤0.01) were found between physicochemical and biological quality indicators when all cereals were taken into account. A negative response of chicks to triticale was obtained only when chicks were fed diets containing the tetraploid forms, while the nutrition parameters of chicks fed diets containing the octo- and hexaploid triticale, with rye genome shares of 1 : 3 and 1 : 2, did not differ (p≥0.05) from those fed a wheat diet. Rye diets yielded the lowest BWG, AME_n and DMD and the poorest FCR. The results indicate that as long as the share of the R genome is a minor component of the total triticale genome pool, its antinutritional effect is masked by the wheat genome. The results also indicate that hexaploid triticale can constitute the sole cereal component in the diets of young broiler chicks.     

MGMT Ile143Val polymorphism,dietary factors and the risk of breast,colorectal and prostate cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk study

O⁶-Methylguanine-DNA methyltransferase (MGMT) repairs DNA damage caused by alkylating agents including N-nitroso compounds from diet. MGMT Ile143Val polymorphism may lead to less DNA damage repair and increased cancer risk depending on the environmental exposures. We investigated interactions between dietary factors and the MGMT Ile143Val polymorphism in relation to breast, colorectal and prostate cancer risk. There were 276/1498, 273/2984 and 312/1486 cases/controls for the breast, colorectal and prostate cancer studies respectively; all nested within the EPIC-Norfolk study, a prospective cohort of approximately 25,000 men and women aged 40–79. Baseline 7-day food diary data were collected for dietary assessment. MGMT Ile143Val polymorphism was not overall associated with breast, colorectal and prostate cancer risk. There was a significant interaction between this polymorphism and intake of red and processed meat on colorectal cancer risk (P_interaction = 0.04) suggesting an increased risk among carriers of the variant genotype compared to the MGMT Ile143Ile common genotype. A lower colorectal cancer risk was seen with higher intake of vitamin E and carotene among the variant genotype group but not in the common genotype group (P_interaction = 0.009 and P_interaction = 0.005 for vitamin E and carotene, respectively). A higher prostate cancer risk was seen with higher alcohol intake among the variant genotype (OR = 2.08, 95% CI = 1.21–3.57, P_interaction = 0.0009) compared to the common genotype with lower alcohol intake. In this UK population, the MGMT Ile143Val polymorphism was not overall associated with breast, colorectal and prostate cancer risk. There was evidence for this polymorphism playing a role in modulating the risk of prostate cancer in presence of alcohol. For colorectal cancer, the MGMT Ile143Val polymorphism may confer increased or decreased risk depending on the dietary exposure.     

Relative bioavailabilities of organic zinc sources with different chelation strengths for broilers fed diets with low or high phytate content

A six-day experiment was conducted to estimate the relative bioavailability values (RBV) of zinc (Zn) in three organic sources (oZn) with different chelation strengths compared to inorganic ZnSO₄ (iZn) for broilers fed a low or high phytate diet. A total of 1080, one-d-old male broiler chicks were randomly assigned to one of 18 dietary treatments (six replicates cages of ten chicks per cage) in a completely randomized design involving a 2 × 2 × 4 factorial arrangement with two levels of added phytate (0 or 10 g phytate as sodium phytate/kg), two levels of added Zn (30 or 60 mg/kg) and four Zn sources (iZn and three oZn sources) plus one low and one high phytate control treatments without Zn addition. The three oZn sources consisted of (1) Zn amino acid with weak chelation strength (ZnAA-L, formation quotient Q_f = 6.6, containing 119 g Zn/kg), (2) Zn proteinate with moderate chelation strength (ZnPRO-M, Q_f = 30.7, containing 133 g Zn/kg) or (3) Zn proteinate with strong chelation strength (ZnPRO-H, Q_f = 944.0, containing 186 g Zn/kg). Chicks were harvested at 6 days of age and pancreas metallothionein (MT) mRNA expression was used to estimate Zn RBV. Pancreas MT mRNA expression increased (P<0.01) as dietary Zn level increased. Chicks fed high phytate diets had lower (P<0.05) MT mRNA expression than chicks fed low phytate diets. Based on multiple linear regression slope ratios with ZnSO₄ set at 1.00, the RBV of ZnAA-L, ZnPRO-M and ZnPRO-H were 1.01, 1.28 and 0.70, respectively, for low phytate diets, and 1.05, 1.39 and 0.92, respectively, for high phytate diets. The slope for the oZn source with moderate chelation strength differed (P<0.05) from iZn and the other two oZn sources. The RBV of ZnAA-L, ZnPRO-M and ZnPRO-H under the high phytate diet increased by 0.04, 0.11 and 0.22, respectively, compared to those under the low phytate diet. Results indicate that the oZn sources with moderate or strong chelation strength offer partial or complete resistance to interference from high dietary phytate during digestion; and the oZn with moderate chelation strength had a greater RBV with both low and high phytate diets than iZn or oZn sources with weak or strong chelation strength.     

Effect of dietary cobalt supplementation on plasma and rumen metabolites in Mehraban lambs

Two experiments were conducted to study the effects of different levels of dietary cobalt on performance, plasma and rumen metabolites and nutrient digestibility in Mehraban male lambs. Experiment 1: 28, 8–9-month-old lambs were randomly divided into four groups. Animals were fed a basal diet containing 0.088 mg Co/kg DM and were supplied with 0 (control), 0.25, 0.50, or 1.00 mg Co/kg DM as reagent grade CoSO₄·7H₂O. The experiment lasted for 70 days. Experiment 2: four lambs from each group in Experiment 1 were randomly allocated to the individual metabolic crates to measure the effects of dietary Co on nutrient digestibility. Final body weight, average daily gain and gain efficiency were higher (p < 0.05) in the group supplemented with 0.50 mg Co/kg DM compared to other groups. Plasma glucose and vitamin B₁₂ concentrations increased (p < 0.05) at all levels of Co supplementation on day 68 of the experiment and for vitamin B₁₂ were higher (p < 0.05) at 0.50 and 1.00 mg Co/kg DM compared to 0.25 mg Co/kg DM. There was no significant difference among treatments for TVFA and ruminal fluid pH. Digestibility of dry matter, organic matter, crude protein and neutral detergent fiber increased (p < 0.05) by Co supplementation, but did not differ among Co supplied treatments. The obtained results showed that lambs fed the control diet containing 0.088 mg Co/kg DM had a reduced appetite and gained less than the supplemented animals, suggesting that the level of 0.088 mg Co/kg DM was inadequate for normal growth of Mehraban male lambs, and a total level of 0.58 mg Co/kg DM might be optimum level for enhancing performance.     

Sea buckthorn (Hippophae rhamnoides L.) vegetative parts as an unconventional source of lipophilic antioxidants

The profile of lipophilic antioxidants in different vegetative parts (leaves, shoots, buds and berries) was studied in sea buckthorn (Hippophae rhamnoides L.) male and female plants collected in the end of spring. Five lipophilic compounds, i.e. three tocopherol homologues (α, β and γ), plastochromanol-8 and β-carotene, were identified in each vegetative part of male and female sea buckthorn plants at the following concentrations: 7.25–35.41, 0.21–2.43, 0.41–1.51, 0.19–1.79 and 4.43–24.57 mg/100 g dry weight basis. Additionally, significant amounts of α-tocotrienol (1.99 mg/100 g dry weight basis) were detected in buds. The α-tocopherol and β-carotene were predominant lipophilic antioxidants in each vegetative part, accounting for 78.3–97.0% of identified compounds. The greatest amounts of lipophilic antioxidants were found in leaves, especially of female plants. Nevertheless, apart from leaves, also shoots of plants of both sexes seem to be a good source of α-tocopherol and β-carotene.     

Meat quality in goats as influenced by dietary protein and energy levels,and postmortem aging

The objectives of this study were to determine effects of different dietary treatments and postmortem aging on meat quality characteristics in goats. Twenty castrated dairy goats (BW = 30.7 ± 6.80 kg, age 10 months) were subjected to one of four dietary treatments for 82 days (treatment): (i) 2.5 Mcal/kg DM DE and 12% CP, (ii) 2.5 Mcal/kg DM DE and 18% CP, (iii) 2.9 Mcal/kg DM DE and 12% CP, or (iv) 2.9 Mcal/kg DM DE and 18% CP. At the end of the feeding trial, the animals were slaughtered to evaluate meat quality. Longissimus muscle pH and temperature were measured at 0, 3, 6, 9, 12, 15, 18, and 24 h postmortem (time). Sarcomere length (1.65 μm), total collagen (4.17 mg/g), and heated calpastatin (44.7 units) measured at 24 h postmortem were not influenced by treatment (P > 0.05). Warner–Bratzler shear force values, collagen solubility, and cooking losses of loin/rib chops (2.5 cm thick) aged for 1, 3, or 6 days postmortem were not influenced by treatment (P > 0.05) or aging time (P > 0.05). Postmortem sampling time affected muscle pH and temperature decline (P < 0.01), but there was no effect of treatment. There was a trend toward a treatment × time interaction (P < 0.06) in muscle pH. Temperature and pH declines followed cubic (P < 0.01) and linear (P < 0.01) trends, respectively. Average muscle temperature declined rapidly and reached 14.5 ± 2.0 °C at 3 h postmortem, while the pH was still high (6.60 ± 0.087). In conclusion, diet did not influence meat quality characteristics, and shear force values of chevon did not decrease due to postmortem aging. Rapid heat dissipation from goat carcasses during too rapid chilling may have caused cold shortening of muscles resulting in meat that did not respond to aging.     

Newcastle disease virus (NDV) induces protein oxidation and nitration in brain and liver of chicken: Ameliorative effect of vitamin E

The present study was aimed at investigating the therapeutic efficacy of vitamin E on oxidative injury in brain and liver of Newcastle disease virus (NDV) challenged chickens. We have analyzed the xanthine oxidase (XOD) activity; uric acid (UA) levels and superoxide radical generation by using electron spin resonance spectroscopy. Further, protein oxidation, nitration and apoptosis were evaluated in the brain and liver of the control, NDV-infected and NDV + Vit. E treated groups. A significant elevation was observed in XOD activity and UA levels in brain (p < 0.001) and liver (p < 0.05) of NDV infected birds when compared to controls. Further, significant increase in the production of superoxides, enhanced intracellular protein carbonyls and nitrates were observed in the brain and liver of NDV-infected birds over healthy subjects. Apoptosis studies also suggested that a larger number of TUNEL positive cells were observed in brain and a moderately in liver of NDV-infected chickens. However, all these perturbations were significantly ameliorated in NDV + Vit. E treated chickens as compared to NDV-infected birds. Taken together, our results suggested that NDV-induced neuronal and hepatic damage at least in part mediates oxidative stress and on the other hand, supplementation of vitamin E mitigates NDV-induced oxidative damage thereby protects brain and liver of chickens. These findings could provide new insights into the understanding of NDV pathogenesis and therapeutic effects of dietary antioxidants.