Neuroprotective effect of rough aster butanol fraction against oxidative stress in the brain of mice challenged with kainic acid

The neuroprotective effect of the butanol fraction from the methanol extract of Aster scaber Thunb. (rough aster butanol fraction) on oxidative damage in the brain of mice challenged with kainic acid was examined using behavioral signs and biochemical parameters of oxidative stress. The rough aster butanol fraction (0.4-1.0 g/kg) was administered to ICR male mice, 6-8 weeks, through a gavage for 4 days consecutively, and on the third day, kainic acid (50 mg/kg) was ip administered. When compared to the vehicle-treated control, no significant changes in body and brain weight were observed in mice administered the rough aster butanol fraction. Administration of kainic acid only, causing a lethality of approximately 54%, resulted in a significant decrease of total glutathione level and an increase of the thiobarbituric acid-reactive substances (TBARS) value in brain tissue. When the rough aster butanol fraction was examined for neuroprotective action, the rough aster butanol fraction (0.4 g/kg) alleviated the lethality (25%) of kainic acid and the behavioral sign of its neurotoxicity. Moreover, administration of the rough aster butanol fraction at a dose of 0.4 g/kg restored the glutathione level in the cytosolic portion of brain homogenate to approximately 80% (p < 0.05). Also, the rough aster butanol fraction (0.4 g/kg) led to a significant reduction of kainic acid-induced increase of TBARS value. In addition, the glutathione peroxidase activity was restored significantly (p < 0.05) in the cytosolic portion of brain homogenate, whereas glutathione reductase activity was not. On the basis of these results, the rough aster butanol fraction is suggested to contain a functional agent to prevent oxidative stress in the brain of mice.     

Effect of antioxidant flavanone, naringenin, from Citrus junoson neuroprotection

Amyloid beta protein (Abeta)-induced free radical-mediated neurotoxicity is known as a leading hypothesis for a cause of Alzheimer's disease. Abeta increased free radical production and lipid peroxidation in PC12 nerve cells, resulting in apoptosis and cell death. The protective effect of naringenin, a major flavanone constituent isolated from Citrus junos, against Abeta-induced neurotoxicity was investigated using PC12 cells. Pretreatment with isolated naringenin and vitamin C prevented the generation of the Abeta-induced reactive oxygen species. Naringenin resulted in the decrease of Abeta toxicity in a manner of concentration dependence, which was assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. However, treatment with these antioxidants inhibited the Abeta-induced neurotoxic effect. The antiamnestic activity of naringenin in vivo was also evaluated using ICR mice with amnesia induced by scopolamine (1 mg/kg body weight). Naringenin, when administered to ICR mice at 4.5 mg/kg body weight, significantly ameliorated scopolamine-induced amnesia as measured in the passive avoidance test. Therefore, these results indicate that micromolecular Abeta-induced in vitro oxidative cell stress is reduced by naringenin and naringenin may be a useful chemopreventive agent against a neurodegenerative disease such as Alzheimer's disease.     

Toxic dose of a simple phenolic antioxidant, protocatechuic acid, attenuates the glutathione level in ICR mouse liver and kidney.

It has previously been reported that a toxic dose of protocatechuic acid (PA), a naturally occurring simple phenolic antioxidant in dietary plant foodstuff, has a potential to enhance tumorigenesis and induce contact hypersensitivity in mouse skin. In this study, the modifying effect of a toxic dose of PA on the glutathione (GSH) level in mouse liver and kidney was examined. Intraperitoneal administration of PA (500 mg/kg) caused significant hepatic and nephrotic GSH depletion. Interestingly, slight but significant hepatotoxicity and nephrotoxicity, characterized by the enhancement of plasmic alanine aminotrasferase (ALT) activity and urea level, respectively, were also observed. The subchronic administration of PA (0.1% in drinking water) for 60 days showed not only a significant decrease in the GSH level in kidney but also a significant enhancement of ALT activity in plasma. The protective role of GSH for acute hepatotoxicity using GSH-depleted mice administered a GSH synthesis inhibitor buthionine sulfoximine was also demonstrated. Thus, it is suggested that overdoses of PA can disturb the detoxification of other electrophilic toxicants including ultimate carcinogens.     

Anti-inflammatory activity of an orange peel polymethoxylated flavone, 3',4',3,5,6,7,8-heptamethoxyflavone, in the rat carrageenan/paw edema and mouse lipopolysaccharide-challenge assays

The anti-inflammatory properties of 3',4',3,5,6,7,8-heptamethoxyflavone (HMF), a citrus polymethoxylated flavone, were studied in the bacterial lipopolysaccharide (LPS)-challenge/tumor necrosis factor-alpha (TNFalpha) response in mice and in the carrageenan/paw edema assay in rats. In each of these trials, HMF administered by intraperitoneal (ip) injection exhibited anti-inflammatory activity, whereas HMF administered orally (po) produced no effects. The inhibition observed in the LPS-challenge/TNFalpha assay correlated with the HMF levels in the blood sera of mice dosed (ip) with either 33 or 100 mg/kg body weight. Low levels of HMF (0.035 +/- 0.024 ppm) were detected in the blood sera of mice dosed orally [100 mg of HMF (suspended in vegetable oil)/kg], whereas ip injection led to higher levels (0.517 +/- 0.051 ppm). This may account for the different levels of anti-inflammatory effects observed in mice following ip vs oral HMF administration. HMF metabolites, including a number of mono- and di-demethylated HMF metabolites and their glucuronic acid conjugates, were also detected, but results of these studies suggest that the glucuronidated metabolites of HMF are inactive in these inflammation models.     

Neuroprotective Effects of Longan ( Dimocarpus longan Lour.) Flower Water Extract on MPP(+)-Induced Neurotoxicity in Rat Brain

In this study, the neuroprotective effect of Dimocarpus longan Lour. flower water extract (LFWE) was investigated. First, an in vitro study showed that LFWE concentration-dependently inhibited lipid peroxidation of brain homogenates incubated at 37 °C. The antioxidative activity of LFWE was more potent than that of glutathione or Trolox. Furthermore, an ex vivo study found that the basal lipid peroxidation (0 °C) and lipid peroxidation incubated at 37 °C were lower in the brain homogenates of LFWE-treated (500 mg/day) rats, indicating that the brain of LFWE-treated rats was more resistant to oxidative stress. Moreover, a Parkinsonian animal model was employed to demonstrate that oral administration of LFWE (125-500 mg/kg/day) dose-dependently attenuated 1-methyl-4-phenylpyridinium (MPP(+))-induced neurotoxicity in the nigrostriatal dopaminergic system of rat brain. In conclusion, this study suggests that LFWE is antioxidative, anti-inflammatory, and anti-apoptotic. Furthermore, oral administration of LFWE appears to be useful in preventing and/or treating central nervous system neurodegenerative diseases, including Parkinsonism.     

Effects of dietary supplementation with Yucca schidigera Roezl ex Ortgies and its saponin and non-saponin fractions on rat metabolism.

Yucca schidigera Roezl ex Ortgies, family Lillaceae, was fractionated with butan-1-ol to yield a butanol extractable fraction (BE; saponin fraction) and a non-butanol fraction (NBE; non-saponin fraction). Four groups of eight male rats were allowed ad libitum access to diets supplemented with water (control) or 200 mg x kg(-1) total Y. schidigera (TOT) or 200 mg x kg(-1) of each of the fractions (NBE or BE). The effects of dietary supplementation with the fractions and their interactions in TOT were analyzed according to the factorial experimental design by two-way analysis of variance. All three supplementation groups displayed significantly reduced serum urea levels (P < 0.05). The TOT and NBE fractions were found to significantly increase serum insulin levels (P < 0.01) in the absence of any fluctuations in serum glucose levels. Urea cycle enzyme activities, namely, arginase (EC 3.5.3.1) and argininosuccinate lyase (EC 4.3.2.1), were significantly decreased (P < 0.05) in vivo, although no effect was observed in vitro. Both fractions displayed effects, indicating that the active constituents are present in both fractions.     

Neuroprotective effects of resveratrol on MPTP-induced neuron loss mediated by free radical scavenging

Resveratrol is a natural polyphenol and possesses many biological functions such as anti-inflammatory activity and protection against atherosclerosis and myocardial infraction. Parkinson's disease is a common progressive neurodegenerative disease. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is the most useful neurotoxin to induce Parkinsonism. The present study was carried out to elucidate the neuroprotective effect and possible mechanism of resveratrol on MPTP-induced striatal neuron loss. Sixty adult Balb/c mice were divided into four groups: sham operation, MPTP treatment (30 mg/kg, i.p.), MPTP combined with resveratrol administration (20 mg/kg, i.v.), and resveratrol treatment alone. Microdialysis and high-performance liquid chromatography were used to analyze dihydroxybenzoic acid (DHBA) that reflected the hydroxyl radical level. In the present study, we found MPTP chronic administration significantly induced motor coordination impairment in mice. After MPTP administration, the hydroxyl radical levels in substantia nigra were also significantly elevated and animals displayed severe neuronal loss. Resveratrol administration significantly protected mice from MPTP-induced motor coordination impairment, hydroxyl radical overloading, and neuronal loss. Our results demonstrated that resveratrol could elicit neuroprotective effects on MPTP-induced Parkinsonism through free radical scavenging.     

Absorption, tissue distribution, excretion, and metabolism of clothianidin in rats

Absorption, distribution, excretion, and metabolism of clothianidin [(E)-1-(2-chloro-1,3-thiazol-5-ylmethyl)-3-methyl-2-nitroguanidine] were investigated after a single oral administration of [nitroimino-(14)C]- or [thiazolyl-2-(14)C]clothianidin to male and female rats at a dose of 5 mg/kg of body weight (bw) (low dose) or 250 mg/kg of bw (high dose). The maximum concentration of carbon-14 in blood occurred 2 h after administration of the low oral dose for both labeled clothianidins, and then the concentration of carbon-14 in blood decreased with a half-life of 2.9-4.0 h. The orally administered carbon-14 was rapidly and extensively distributed to all tissues and organs within 2 h after administration, especially to the kidney and liver, but was rapidly and almost completely eliminated from all tissues and organs with no evidence of accumulation. The orally administered carbon-14 was almost completely excreted into urine and feces within 2 days after administration, and approximately 90% of the administered dose was excreted via urine. The major compound in excreta was clothianidin, accounting for >60% of the administered dose. The major metabolic reactions of clothianidin in rats were oxidative demethylation to form N-(2-chlorothiazol-5-ylmethyl)-N'-nitroguanidine and the cleavage of the carbon-nitrogen bond between the thiazolylmethyl moiety and the nitroguanidine moiety. The part of the molecule containing the nitroguanidine moiety was transformed mainly to N-methyl-N'-nitroguanidine, whereas the thiazol moiety was further metabolized to 2-(methylthio)thiazole-5-carboxylic acid. With the exception of the transiently delayed excretion of carbon-14 at the high-dose level, the rates of biokinetics, excretion, distribution, and metabolism of clothianidin were not markedly influenced by dose level and sex.     

Pharmacokinetics of cycloalliin, an organosulfur compound found in garlic and onion, in rats

Cycloalliin, an organosulfur compound found in garlic and onion, has been reported to exert several biological activities and also to remain stable during storage and processing. In this study, we investigated the pharmacokinetics of cycloalliin in rats after intravenous or oral administration. Cycloalliin and its metabolite, (3R,5S)-5-methyl-1,4-thiazane-3-carboxylic acid, in plasma, urine, feces, and organs was determined by a validated liquid chromatography-mass spectrometry method. When administered intravenously at 50 mg/kg, cycloalliin was rapidly eliminated from blood and excreted into urine, and its total recovery in urine was 97.8% +/- 1.3% in 48 h. After oral administration, cycloalliin appeared rapidly in plasma, with a tmax of 0.47 +/- 0.03 h at 25 mg/kg and 0.67 +/- 0.14 h at 50 mg/kg. Orally administered cycloalliin was distributed in heart, lung, liver, spleen, and especially kidney. The Cmax and AUC0-inf values of cycloalliin at 50 mg/kg were approximately 5 times those at 25 mg/kg. When administered orally at 50 mg/kg, cycloalliin was excreted into urine (17.6% +/- 4.2%) but not feces. However, the total fecal excretion of (3R,5S)-5-methyl-1,4-thiazane-3-carboxylic acid was 67.3% +/- 5.9% (value corrected for cycloalliin equivalents). In addition, no (3R,5S)-5-methyl-1,4-thiazane-3-carboxylic acid was detected in plasma (<0.1 microg/mL), and negligible amounts (1.0% +/- 0.3%) were excreted into urine. In in vitro experiments, cycloalliin was reduced to (3R,5S)-5-methyl-1,4-thiazane-3-carboxylic acid during anaerobic incubation with cecal contents of rats. These data indicated that the low bioavailability (3.73% and 9.65% at 25 and 50 mg/kg, respectively) of cycloalliin was due mainly to reduction to (3R,5S)-5-methyl-1,4-thiazane-3-carboxylic acid by the intestinal flora and also poor absorption in the upper gastrointestinal tract. These findings are helpful for understanding the biological effects of cycloalliin.     

Chemical composition, antioxidant properties, and thermal stability of a phytochemical enriched oil from Acai (Euterpe oleracea Mart.)

Phenolic compounds present in crude oil extracts from acai fruit ( Euterpe oleracea) were identified for the first time. The stability of acai oil that contained three concentrations of phenolics was evaluated under short- and long-term storage for lipid oxidation and phenolic retention impacting antioxidant capacity. Similar to acai fruit itself, acai oil isolates contained phenolic acids such as vanillic acid (1,616 +/- 94 mg/kg), syringic acid (1,073 +/- 62 mg/kg), p-hydroxybenzoic acid (892 +/- 52 mg/kg), protocatechuic acid (630 +/- 36 mg/kg), and ferulic acid (101 +/- 5.9 mg/kg) at highly enriched concentrations in relation to acai pulp as well as (+)-catechin (66.7 +/- 4.8 mg/kg) and numerous procyanidin oligomers (3,102 +/- 130 mg/kg). Phenolic acids experienced up to 16% loss after 10 weeks of storage at 20 or 30 degrees C and up to 33% loss at 40 degrees C. Procyanidin oligomers degraded more extensively (23% at 20 degrees C, 39% at 30 degrees C, and 74% at 40 degrees C), in both high- and low-phenolic acai oils. The hydrophilic antioxidant capacity of acai oil isolates with the highest phenolic concentration was 21.5 +/- 1.7 micromol Trolox equivalents/g, and the total soluble phenolic content was 1252 +/- 11 mg gallic acid equivalents/kg, and each decreased by up to 30 and 40%, respectively, during long-term storage. The short-term heating stability at 150 and 170 degrees C for up to 20 min exhibited only minor losses (<10%) in phenolics and antioxidant capacity. Because of its high phenolic content, the phytochemical-enriched acai oil from acai fruit offers a promising alternative to traditional tropical oils for food, supplements, and cosmetic applications.     

Profiling and characterization antioxidant activities in Anoectochilus formosanus hayata

Phytochemical characteristics and antioxidant activities of the crude and fractionated plant extracts of Anoectochilus formosanus were evaluated using five different assay systems. An acid-treatment (2 N HCl in 95% ethanol) was employed to treat a butanol fraction (BuOH), creating an acid-hydrolyzed BuOH fraction. The IC(50) values for DPPH radicals in the BuOH and acid-hydrolyzed BuOH fractions were 0.521 and 0.021 mg/mL, respectively. The acid-hydrolyzed BuOH exhibited approximately 5-fold higher activity in scavenging superoxide anion than catechin. The acid-hydrolyzed BuOH fraction also effectively protected phi x174 supercoiled DNA against strand cleavage induced by H(2)O(2) and reduced oxidative stress in HL-60 cells. Metabolite profiling showed that the aglycones of flavonoid glycosides in BuOH were produced after acid hydrolytic treatment, and this resulted in a significant increase in antioxidant activities of acid-hydrolyzed BuOH. One new diarylpentanoid, kinsenone, and three known flavonoid glycosides and their derivatives were identified for the first time from A. formosanus, with strong antioxidant properties.     

Occurrence of the free and Peptide forms of pyroglutamic acid in plasma from the portal blood of rats that had ingested a wheat gluten hydrolysate containing pyroglutamyl peptides

In order to determine pyroglutamic acid levels in plasma, we developed a method based on precolumn derivatization of the carboxyl group of pyroglutamic acid with 2-nitrophenylhydrazine. Eight-week-old male SD strain rats were administered 200 mg of an acidic peptide fraction obtained from a commercial wheat gluten hydrolysate containing 0.63 mmol/g pyroglutamyl peptide. After administration, significant amounts of free pyroglutamic acid were observed in the ethanol-soluble fraction of the plasma from the portal vein. In addition, pyroglutamate aminopeptidase digestion of the ethanol-soluble fraction liberated significant amounts of pyroglutamic acid, which indicated the presence of the pyroglutamyl peptide. The presence of the pyroglutamyl peptide in the plasma was further confirmed by size exclusion chromatography. The levels of free and peptide forms of pyroglutamic acid increased significantly and reached a maximum (approximately 40 nmol/mL) at 15 and 30 min after administration, respectively.     

Direct in vivo evidence of protective effects of grape seed procyanidin fractions and other antioxidants against ethanol-induced oxidative DNA damage in mouse brain cells

Ethanol is a principle ingredient of alcoholic beverages with potential neurotoxicity and carcinogenicity, and the ethanol-associated oxidative DNA damage in the central nervous system is well documented. The present work studied the possible protective effects of grape seed oligomer and polymer procyanidin fractions against ethanol-induced toxicity and compared these with resveratrol and other well-known antioxidants (ascorbic acid and vitamin E). By using the single cell gel electrophoresis (comet assay), a simple and sensitive technique for genotoxicity studies, the potential genotoxicity of acute and chronic ethanol administration in the different brain regions was investigated. Acute ethanol administration, at the dose of 2.5 or 5.0 g kg(-1) i.p., could induce significant DNA damage in cerebellum and hippocampus. Chronic administration of ethanol at the dose of 2.5 or 5.0 g kg-1 p.o. for 30 days could induce significant DNA damage in cerebellum, hippocampus, hypothalamus, and cortex, which could be auto-repaired at least 3 days after ethanol withdrawal. Oral administration of grape seed oligomer and polymer procyanidins and resveratrol (25, 50, and 100 mg kg(-1)) for 3 days before acute ethanol (5.0 g kg(-1), i.p.) or repeated administration of these substances together with ethanol (5.0 g kg(-1), p.o.) for 30 consecutive days could significantly inhibit DNA damage in brain cells induced by ethanol. As compared, ascorbic acid (50, 100, and 200 mg kg(-1)) and vitamin E (100, 200, and 400 mg kg(-1)) could also present protective effects on ethanol-induced DNA damage. Furthermore, the concentrations of ethanol and acetaldehyde in brain regions of the mice were detected by gas chromatography after administration of ethanol plus antioxidants. All of the results indicated that ethanol could induce region-specific oxidative DNA damage in which the cerebellum and hippocampus were more vulnerable, but intake of grape seed procyanidins or other natural antioxidants could protect the brain against ethanol-induced genotoxicity.     

水肥一体化施磷对滴灌玉米磷素、磷素营养及磷肥利用效率的影响

【目的】在新疆大规模的节水滴灌农业生产中,根据作物不同生育阶段对磷素营养吸收特性,按比例通过水肥一体化以水施磷是满足作物磷素营养需求、减少磷的固定及提高磷肥利用效率的有效途径。【方法】本文在田间条件下设置不施磷 (CK)、固体磷酸二铵60%基施+40%追施(T1)、液体磷酸60%基施+40%追施(T2)、液体磷酸全部追施(T3)处理,研究了不同磷肥及施肥方式对滴灌玉米磷素吸收、产量及磷肥利用率的影响。【结果】液体磷酸全部追施处理可显著提高玉米的生物量、穗粒数和千粒重 (P0.05),玉米产量达20622 kg/hm2,其产量比CK、磷酸二铵60%基施+40%追施和液体磷酸60%基施+40%追施处理分别提高了37%、25%、10%;在抽雄期和成熟期不施磷对照、T1、T2、T3处理的玉米吸磷量分别为14.0、22.7、21.0、18.3 kg/hm2 和 68.4、77.8、87.2、91.9 kg/hm2,在成熟期全部追肥处理植株的吸磷量显著高于其他处理,说明磷肥随水追施可显著改善玉米磷素营养(P0.05);T1、T2、T3处理磷肥利用率（REP）和农学效率（AEP）分别为16.6%、32.6%、40.6% 和 7.9 kg/kg、22.7 kg/kg、40.6 kg/kg,T3处理的REP和AEP分别比其它处理提高了8个百分点~24个百分点和17.9~32.7 kg/kg,液体磷酸全追可显著提高磷肥利用效率 (P0.05)。【结论】液体磷肥100%以追肥的方式随水滴施可显著改善玉米生育中后期的磷素营养并提高产量。提高石灰性土壤玉米对磷肥的吸收利用效率,磷肥利用率可达40.6%。     

Fresh green tea and gallic acid ameliorate oxidative stress in kainic acid-induced status epilepticus

Green tea is one of the most-consumed beverages due to its taste and antioxidative polyphenols. However, the protective effects of green tea and its constituent, gallic acid (GA), against kainic acid (KA)-induced seizure have not been studied. We investigated the effect of fresh green tea leaf (GTL) and GA on KA-induced neuronal injury in vivo and in vitro. The results showed that GTL and GA reduced the maximal seizure classes, predominant behavioral seizure patterns, and lipid peroxidation in male FVB mice with status epilepticus (SE). GTL extract and GA provided effective protection against KA-stressed PC12 cells in a dose-dependent manner. In the protective mechanism study, GTL and GA decreased Ca(2+) release, ROS, and lipid peroxidation from KA-stressed PC12 cells. Western blot results revealed that mitogen-activated protein kinases (MAPKs), RhoA, and COX-2 expression were increased in PC12 cells under KA stress, and expression of COX-2 and p38 MAPK, but not RhoA, was significantly reduced by GTL and GA. Furthermore, GTL and GA were able to reduce PGE(2) production from KA-stressed PC12 cells. Taken together, the results showed that GTL and GA provided neuroprotective effects against excitotoxins and may have a clinical application in epilepsy.     

Phenolic compounds of barley grain and their implication in food product discoloration

Barley grains contain significant amounts of phenolic compounds that may play a major role in the discoloration of food products. Phenolic acid and proanthocyanidin (PA) composition of 11 barley genotypes were determined, using high-performance liquid chromatography and liquid chromatography-mass spectrometry, and their significance on food discoloration was evaluated. Abraded grains contained 146-410 microg/g of phenolic acids (caffeic, p-coumaric, and ferulic) in hulled barley and 182-282 microg/g in hulless barley. Hulled PA-containing and PA-free genotypes had comparable phenolic acid contents. Catechin and six major barley PAs, including dimeric prodelphinidin B3 and procyandin B3, and four trimers were quantified. PAs were quantified as catechin equivalents (CE). The catechin content was higher in hulless (48-71 microg/g) than in hulled (32-37 microg/g) genotypes. The total PA content of abraded barley grains ranged from 169 to 395microg CE/g in PA-containing hulled and hulless genotypes. Major PAs were prodelphinidin B3 (39-109 microg CE/g) and procyanidin B3 (40-99 microg CE/g). The contents of trimeric PAs including procyanidin C2 ranged from 53 to 151 g CE/g. Discoloration of barley flour dough correlated with the catechin content of abraded grains (r = -0.932, P < 0.001), but not with the content of individual phenolic acids and PAs. Discoloration of barley flour dough was, however, intensified when total PA extracts and catechin or dimeric PA fractions were added into PA-free barley flour. The brightness of dough also decreased when the total PA extract or trimeric PA fraction was added into heat-treated PA-free barley flour. Despite its low concentration, catechin appears to exert the largest influence on the discoloration of barley flour dough among phenolic compounds.     

淹水对石灰性土壤无机磷形态转化的影响

  【目的】  磷肥施入土壤后大部分转化为与铁氧化物关系密切的Fe-P和O-P,而淹水后土壤中铁的氧化还原过程可能影响与铁氧化物结合的磷的形态及有效性的变化。研究不同施磷处理下淹水土壤Fe (II) 、无机磷组分等的变化,以期明确淹水后土壤无机磷形态及磷有效性变化及其与铁氧化还原过程的关系。  【方法】  用不施磷土壤 (P0) 和连续6年施用P 180 kg/hm2的土壤 (P180) 进行室内模拟培养试验。将土壤装于西林瓶内,加水模拟淹水条件,西林瓶密封后,分别在避光或者光照条件下,于 (30 ± 1)℃恒温培养40天。测定供试土壤以及淹水培养土壤中的速效磷、无机磷以及不同形态无机磷组分含量,测定培养过程Fe (II) 的动态变化,以探讨磷形态转化与铁氧化还原过程的关系。  【结果】  施用磷肥显著增加土壤中的速效磷含量和无机磷总量,P0处理土壤速效磷含量为 (7.65 ± 1.65) mg/kg,P180处理土壤速效磷含量高达 (33.5 ± 2.01) mg/kg。施入土壤中的磷只有很小部分以Ca₂-P存在,主要以Ca₁₀-P、Ca₈-P、Al-P和Fe-P形态存在。避光淹水培养后,土壤速效磷含量增加,P0和P180处理土壤速效磷含量的增量分别为8.44、2.95 mg/kg。淹水培养降低了土壤Ca₈-P含量,提升了Fe-P、O-P、Al-P含量。光照和避光条件下P180处理土壤中Ca₈-P含量分别降低106.8、156.2 mg/kg,Fe-P含量分别增加23.4、47.0 mg/kg,O-P含量分别增加64.1、92.9 mg/kg,Al-P含量分别增加38.8、34.7 mg/kg,避光时Ca₈-P降幅以及Fe-P和O-P的增量均大于光照条件下。避光条件下,铁还原量和还原最大速率与Ca₈-P变化量之间存在显著负相关关系,与Fe-P、O-P增量之间存在显著正相关关系。  【结论】  淹水条件下,石灰性土壤中的Fe (Ⅲ) 还原形成Fe (Ⅱ) 和Fe (Ⅲ) 混合物,增加了铁氧化物的比表面积和磷吸附点,可促进Ca₈-P向O-P、Fe-P和Al-P转化。光照降低了Fe (Ⅲ) 的还原量,可能是Ca₈-P向O-P、Fe-P和Al-P转化率低的原因之一。     

仿刺参肠多糖对免疫功能的影响及抗肿瘤研究

多糖能参与机体的免疫调节,具有抗肿瘤等多种功能。本实验采用灌胃不同剂量仿刺参(Apostichopus japonicus)肠多糖的方法,研究了多糖对小鼠(Mus musculus)免疫功能的影响及其对小鼠的抗肿瘤作用。结果显示,仿刺参肠多糖对接种的H22肿瘤具有剂量依赖性的抑制作用,高剂量组(400mg/kg/d)抑瘤效果最好;胸腺指数高剂量肿瘤组最高(P<0.05),而其他各组差异不明显,脾脏指数在肿瘤组内随着剂量的增大表现为先升高再降低,而空白组呈一直上升的趋势;高剂量多糖可以显著提高荷瘤小鼠和空白小鼠的白介素2(IL-2)含量(P<0.05),对荷瘤小鼠的肿瘤坏死因子(TNF-α)含量也具有显著提升作用(P<0.05),但对空白组小鼠的TNF-α含量影响不显著;荷瘤小鼠的自然杀伤(NK)细胞活力普遍低于空白小鼠,随灌胃剂量的提升空白小鼠NK细胞活力具有上升趋势,荷瘤小鼠的NK细胞活力在中剂量组达到最高后开始下降。实验表明,仿刺参肠多糖可以促进小鼠的免疫功能,并且对小鼠体内肿瘤在一定剂量范围内具有浓度依赖性的抑制作用。     

黑土累积磷的释放动力学特征及主要影响因素

  【目的】  长期大量施用磷肥致使农田土壤磷快速累积,磷肥增产效率和利用率下降。研究不同施肥措施下土壤累积磷的释放动力学特征及其机制,为累积磷的活化利用和磷肥高效施用提供理论依据。  【方法】  黑土长期定位试验位于黑龙江省哈尔滨市,在5个不同处理采集土样,分别标记为P1、P2、P3、P4和P5,其Olsen-P含量依次为15.5、20.2、93.2、199和216 mg/kg。采用0.5 mol/L NaHCO₃连续浸提法测定5个土壤样品中有效磷的释放量,以5个动力学方程拟合或描述有效磷的释放动力学。采用Hedley法测定了浸提前后土壤活性磷(Resin-P、NaHCO₃-P_i、NaHCO₃-P_o)、中活性磷(NaOH-P_i、NaOH-P_o、DilHCl-P)和稳性磷(ConcHCl-P_i、ConcHCl-P_o、Residual-P)含量。  【结果】  连续浸提过程中,供试5个土壤的Olsen-P释放均呈先快后慢的趋势,在浸提1400 min (10次)时基本达到平衡。以米氏方程(Michaelis)、一级方程、Elovich方程、抛物线方程和幂函数方程描述有效磷的释放动力学特征,拟合方程的决定系数(R2)均在0.964及以上(P<0.01),其中又以米氏方程和一级方程为佳,其R2分别为0.9955和0.9922。由米氏方程可知,供试5个土壤的有效磷最大释放量分别为59.8、60.9、332.6、589.7和717.0 mg/kg,随Olsen-P含量的增加而增加,Olsen-P每增加1 mg/kg,磷释放量平均增加3.12 mg/kg;5个土壤有效磷的最大释放量占土壤全磷的比例分别为13.68%、14.86%、45.44%、60.67%和66.45%,也随Olsen-P含量的增加而增加,但土壤浸提残留磷(全磷与可提取有效磷之差)均为373.99 mg/kg左右,说明施磷对土壤残留磷的影响较小,长期施肥累积的磷具有较高的活性。一级方程和Elovich方程表明,黑土有效磷的释放是以扩散为主的动力学过程。连续浸提后,土壤活性磷平均减少了82.9% (67.8%～93.5%),中活性磷平均减少了34.6% (17.2%～52.0%),稳定性磷无显著变化。活性磷中的Resin-P和NaHCO₃-P_i显著降低了89.8% (78.5%～96.0%)和84.5% (72.9% ～91.3%),这表明Resin-P和NaHCO₃-P_i的有效性最高。土壤活性磷库、中稳态磷库、磷释放的动力学方程参数与土壤有机质、Olsen-P、全磷呈显著正相关,与pH呈显著负相关,说明土壤累积磷的释放过程主要受到土壤活性磷、中活性磷、土壤有机质、pH和全磷含量的影响。  【结论】  黑土固定的残留磷量受施肥的影响较小,施肥累积的磷大部分可以释放,尤其Resin-P和NaHCO₃-P_i的有效性最高。黑土中磷的释放符合米氏方程和一级方程,磷释放量随Olsen-P水平的增加而增加。土壤有机质、pH和全磷含量是磷释放过程的主要影响因素。     

Dose and duration effect of alpha-tocopheryl acetate supplementation on chicken meat fatty acid composition, tocopherol content, and oxidative status

The effects of dietary alpha-tocopheryl acetate (alpha-TA) doses (75, 150, and 225 mg/kg) and the duration of this supplementation (0, 10, 21, 32, and 43 days prior to slaughter) on fatty acid composition, alpha-tocopherol content, and oxidative status were studied either in raw or in cooked dark chicken meat with its skin. With regard to fatty acid composition, raw meat was affected by both dietary factors. Various polyunsaturated fatty acids decreased as a result of higher alpha-TA doses, whereas these fatty acids increased with longer supplementation periods. Cooked meat showed similar trends for the duration of alpha-TA supplementation. On the other hand, alpha-tocopherol content in raw and cooked meat increased as a result of the dose and duration of alpha-TA supplementation. Formation of lipid hydroperoxides and thiobarbituric acid values of these meats were also influenced by these two dietary factors, and the dietary combination of 150 mg/kg of alpha-TA during the last 32 days was optimal in terms of supplementation costs and meat oxidative stability.