Ag Treatment Research Articles

Motor and behavioral changes in rats with adenine-induced chronic renal failure: influence of acacia gum treatment

Chronic renal failure (CRF) either occurring naturally in humans or induced surgically in rats causes alterations in behavior and motor functions. However, the effect of chemically induced CRF in rats on behavior is not known. We induced CRF in rats by feeding adenine (0.75% w/w, four weeks) and investigated the effect of the ensuing CRF on a depression model (forced swimming test, FST), analgesia (mechanical nociception), neuromuscular coordination (Rota-rod test) and motor activity (activity meter test). Further, we investigated the effect of giving acacia gum (AG, 10% w/v) in the drinking water concomitantly with adenine using the above models. AG has been previously shown to ameliorate the severity of CRF in humans and rats. Adenine-induced CRF significantly increased the plasma concentrations of urea and creatinine, and reduced creatinine clearance. Additionally, it significantly reduced motor activity and increased immobility time in the FST, suggesting a depressant-like effect. Both of these actions were significantly antagonized by AG treatment. Adenine insignificantly reduced the mechanical nociceptive threshold by 15%. The results of the tests for neuromuscular coordination were inconclusive. In conclusion, adenine-induced CRF caused motor and behavioral alterations, and these were significantly mitigated by administration of AG.

Ultraviolet Protection, Flame Retardancy and Antibacterial Properties of Treated Polyester Fabric Using Plasma-Nano Technology

Nanotechnology provides the ability to engineer the properties of materials. The possibility of using dielectric barrier discharge (DBD) air plasma treatment for fibre surface activation to facilitate deposition of aluminum oxide (Al2O3), nano-silver (Ag) and nano-titanium dioxide (TiO2) onto polyester fabric is investigated. It is aimed to study the possibility of engineering the multifunctional of polyester fabric. The treated fabric is evaluated through measuring the whiteness index (WI), wettability, surface roughness, surface morphology, flame retardancy, ultraviolet protection factor (UPF), thermo-gravimetric analysis (TGA), antibacterial activity, mechanical properties, and coloration behavior as well as fastness properties. Scan electron microscopy (SEM) and transmission electron microscopy (TEM) graphs show deposition of Al2O3 and nano particles (NPs) of TiO2 and Ag onto the fibre after washing several times. Air plasma-Al2O3 treatment improves the flame retarding, UPF, the thermal stability and whiteness of polyester fabric; whereas air plasma-nano Ag treatment affects positively the antibacterial activity of the fibre and air plasma-nano TiO2 enhances the fibre protection against ultraviolet rays. The colouration behaviour of the treated samples is unchanged or slightly improved.

Patterning of Polystyrene by Scanning Electrochemical Microscopy. Biological Applications to Cell Adhesion

Polystyrene surfaces may be patterned by Ag(II), NO(3)(•), and OH(•) electrogenerated at the tip of a scanning electrochemical microscope. These electrogenerated reagents lead to local surface oxidation of the polymer. The most efficient surface treatment is obtained with Ag(II). The patterns are evidenced by XPS and IR and also by the surface wettability contrast between the hydrophobic virgin surface and the hydrophilic pattern. Such Ag(II) treatment of a polystyrene Petri dish generates discriminative surfaces able to promote or disfavor the adhesion of proteins and also the adhesion and growth of adherent cells. The process is also successfully applied to a cyclo-olefin copolymer and should be suitable to pattern any hydrogenated polymer.

ChemInform Abstract: Solar Energy Conversion at the p-InP/Vanadium3+/2+ Semiconductor/ Electrolyte Contact. A Study Based on Differential Capacitance and Current-Voltage Data.

Previously unachieved values are obtained for the open-circuit voltage (0.7 to 0.8 V) and the fill-factor (76%) at the illuminated p-InP/V[sup 3+/2+]-HCl semiconductor/electrolyte contact ( face) coated with a submonolayer amount of silver. Photoelectrochemical solar cell efficiency is 11%, despite significant optical reflection and electrolyte absorption losses. Differential capacitance measurements demonstrate a semiconductor/surface energy barrier height of up to [psi][sub B] = 1.2 eV, independent of the Ag treatment. This value is considerably larger than typically found at solid-state p-InP/Ag contacts. Barrier heights derived from Mott-Schottky data are compared to photovoltages; results indicate that interface recombination and a slow charge-transfer (bare p-InP) and thermionic emission from the metal (Ag-treated p-InP) are important factors limiting the cell efficiency. Flatband potential shifts owing to a slow charge-transfer under photocurrent flow are reduced by the Ag treatment. In a finite potential range of about 400 mV (0 to [minus]400 mV/SCE), both photovoltages and Mott-Schottky data reveal an unpinned Fermi level at bare and Ag-treated electrodes. The unpinned barrier follows the ideal Schottky barrier model for an absolute SCE potential of [minus]5.0 eV/SCE. Reference to related work at InP and GaAs is made.

Involvement of advanced glycation end-products, pentosidine and N ɛ-(carboxymethyl)lysine, in doxorubicin-induced cardiomyopathy in rats

In the pathogenesis of doxorubicin (DXR)-induced cardiomyopathy, oxidative stress appears to play an important role. It has been reported that pentosidine and N ɛ-(carboxymethyl)lysine (CML), advanced glycation end-products (AGEs), are formed by the combined processes of glycation and oxidation and play a significant role in the process of complications of diabetic mellitus. We investigated the potential involvement of AGE formation in DXR-induced cardiomyopathy in rats. Male Crl:CD(SD) rats received intravenous injection of DXR at 2 mg/kg or saline once weekly for 8 weeks, with or without daily treatment with the AGE formation inhibitors, aminoguanidine (AG, 25 mg/kg/day, i.p.) and pyridoxamine (PM, 60 mg/kg/day, i.p.). Time-course experiments revealed significantly increased pentosidine and CML in the heart in the DXR group from Week 6. These findings coincided with a decrease in fractional shortening (FS), an index of cardiac function, and the development of cardiomyopathy characterized by vacuolated hypertrophic myocardial fibers. There was a significant correlation between the myocardial AGEs and FS or plasma cardiac troponin-I. Immunohistochemical staining showed localization of pentosidine to the cytoplasm of vacuolated myocardial cells. In DXR-treated rats, oxidative stress was enhanced prior to any observed increase in pentosidine and CML levels in the heart. Hyperglycemia was not observed throughout the study period. Intervention by AG or PM treatment ameliorated the functional and morphological changes induced by DXR in the heart, in addition to lowered myocardial pentosidine and CML levels. These results suggested that DXR accelerates the formation of pentosidine and CML in the heart through enhanced oxidative stress and that AGE formation is involved in DXR-induced cardiomyopathy. The findings may enable development of novel preventive therapies and predictive biomarkers of DXR-induced cardiomyopathy.

Impaired Mast Cell Activation in Gene-Targeted Mice Lacking the Serum- and Glucocorticoid-Inducible Kinase SGK1

The PI3K pathway plays a pivotal role in the stimulation of mast cells. PI3K-dependent kinases include the serum- and glucocorticoid-inducible kinase 1 (SGK1). The present study explored the role of SGK1 in mast cell function. Mast cells were isolated from bone marrow (BMMC) of SGK1 knockout mice (sgk1(-/-)) and their wild-type littermates (sgk1(+/+)). The BMMC number as well as CD117, CD34, and FcepsilonRI expression in BMCCs were similar in both genotypes. Upon Ag stimulation of the FcepsilonRI receptor, Ca(2+) entry but not Ca(2+) release from intracellular stores was markedly impaired in sgk1(-/-) BMMCs. The currents through Ca(2+)-activated K+ channels induced by Ag were significantly higher in sgk1(+/+) BMMCs than in sgk1(-/-) BMMCs. Treatment with the Ca(2+) ionophore ionomycin (1 microM) led to activation of the K+ channels in both genotypes, indicating that the Ca(2+)-activated K+ channels are similarly expressed and sensitive to activation by Ca(2+) in sgk1(+/+) and sgk1(-/-) BMMCs, and that blunted stimulation of Ca(2+)-activated K+ channels was secondary to decreased Ca(2+) entry. Ag-IgE-induced degranulation and early IL-6 secretion were also significantly blunted in sgk1(-/-) BMMCs. The decrease in body temperature following Ag treatment, which reflects an anaphylactic reaction, was substantially reduced in sgk1(-/-) mice, pointing to impaired mast cell function in vivo. Serum histamine levels measured 30 min after induction of an anaphylactic reaction were significantly lower in sgk1(-/-) than in sgk1(+/+)mice. The observations reveal a critical role for SGK1 in ion channel regulation and the function of mast cells, and thus disclose a completely novel player in the regulation of allergic reaction.

Subunit a Facilitates Aqueous Access to a Membrane-embedded Region of Subunit c in Escherichia coli F1F0 ATP Synthase

Rotary catalysis in F(1)F(0) ATP synthase is powered by proton translocation through the membrane-embedded F(0) sector. Proton binding and release occurs in the middle of the membrane at Asp-61 on transmembrane helix 2 of subunit c. Previously, the reactivity of cysteines substituted into F(0) subunit a revealed two regions of aqueous access, one extending from the periplasm to the middle of the membrane and a second extending from the middle of the membrane to the cytoplasm. To further characterize aqueous accessibility at the subunit a-c interface, we have substituted Cys for residues on the cytoplasmic side of transmembrane helix 2 of subunit c and probed the accessibility to these substituted positions using thiolate-reactive reagents. The Cys substitutions tested were uniformly inhibited by Ag(+) treatment, which suggested widespread aqueous access to this generally hydrophobic region. Sensitivity to N-ethylmaleimide (NEM) and methanethiosulfonate reagents was localized to a membrane-embedded pocket surrounding Asp-61. The cG58C substitution was profoundly inhibited by all the reagents tested, including membrane impermeant methanethiosulfonate reagents. Further studies of the highly reactive cG58C substitution revealed that NEM modification of a single c subunit in the oligomeric c-ring was sufficient to cause complete inhibition. In addition, NEM modification of subunit c was dependent upon the presence of subunit a. The results described here provide further evidence for an aqueous-accessible region at the interface of subunits a and c extending from the middle of the membrane to the cytoplasm.

Higher accumulation of γ-aminobutyric acid induced by salt stress through stimulating the activity of diamine oxidases in Glycine max (L.) Merr. roots

Polyamines (PAs) are assumed to perform their functions through their oxidative product such as γ-aminobutyric acid (GABA) formation. However, there is only limited information on the interrelation between PA degradation and GABA accumulation under salt stress. In order to reveal a quantitative correlation between PA oxidation and GABA accumulation, the effects of treatments with different NaCl concentrations, along with aminoguanidine (AG, a specific inhibitor of diamine oxidases (DAO; EC: 1.4.3.6)) and a recovery test from salt stress on endogenous free PAs, γ-aminobutyric acid (GABA) accumulation and DAO activity were determined in roots of soybean [ Glycine max (L.) Merr.] cultivar Suxie-1. The results showed that the levels of putrescine (Put), cadaverine (Cad), and spermidine (Spd) decreased significantly with increasing salt concentrations. This occurred because salt stress strongly promoted DAO activity to stimulate PA degradation. GABA accumulation increased with growing NaCl concentrations, about an 11- to 17-fold increase as compared with the control plants. AG treatment increased the accumulation of endogenous free PAs as a result of a strong retardation of DAO activity, but decreased GABA accumulation. The recovery for 6 days in 1/2 Hoagland solution from 100 mM NaCl stress resulted in a decrease in DAO activity, a rebound of PA levels and a simultaneous reduction of GABA content. A close correlation was observed between the changes in DAO activity and GABA accumulation. The results indicated that higher GABA accumulation (about 39%) induced by salt stress could come from PA degradation, suggesting that PAs might perform their functions through GABA formation under salt stress.

Peroxisome proliferator-activated receptor α-independent effects of peroxisome proliferators on cysteinyl leukotriene production in mast cells

The effects of peroxisome proliferators, the ligands of a nuclear receptor peroxisome proliferator-activated receptor (PPAR) α, on cysteinyl leukotriene production were investigated in rodent mast cells. Peroxisome proliferators Wy-14,643 (30 μM) and fenofibrate (100 μM) significantly inhibited the cysteinyl leukotriene production that was induced by antigen (Ag) treatment after overnight sensitization to Ag specific immunoglobulin E (IgE) in a rat basophilic leukemia (RBL)-2H3 mast cell line. Similar inhibition by these drugs was observed in IgE and Ag-treated mouse bone marrow-derived mast cells, A23187-treated RBL-2H3 and A23187-treated mouse peritoneal macrophages. Wy-14,643 (30 μM) and fenofibrate (100 μM) did not affect the release of radioactivity from RBL-2H3 pre-incubated with [ 3H]-arachidonic acid, which is considered an index of phospholipase A 2 activity. Wy-14,643 (30 μM) and fenofibrate (100 μM) did not directly inhibit 5-lipoxygenase activity. Troglitazone was found to directly inhibit the activity of 5-lipoxygenase. The PPARα mRNA level was at less than the limit of detection for the realtime polymerase chain reaction both in RBL-2H3 and bone marrow-derived mast cells. Wy-14,643 (30 μM) and fenofibrate (100 μM) did not induce acyl-CoA oxidase mRNA in RBL-2H3, which was reported to be induced by peroxisome proliferators via PPARα in hepatocytes. Wy-14,643 (30 μM) and fenofibrate (100 μM) inhibited the cysteinyl leukotriene production in bone marrow-derived mast cells from PPARα-null mice. It was concluded that the inhibitory effects of these peroxisome proliferators on cysteinyl leukotriene production are independent of PPARα in mast cells.

Inhibitory effect of inducible nitric oxide synthase inhibitors on DMBA-induced hamster buccal–pouch squamous-cell carcinogenesis

We investigated the effects of two NOS inhibitors (AG and l-NAME) on DMBA-induced hamster buccal-pouch carcinogenesis. Six hundred Syrian golden hamsters were split into two divisions (I and II); divisions split into three groups (experimental groups A and B, control group C); and each group into subgroups of 20 (A1-A6, B1-B6 and C1-C3). The pouches of animals in groups A1-A3 were painted first with AG of differing concentrations (10, 20, and 30 micromol/ml) and then 30 min later with DMBA (0.5%), thrice weekly for 9 weeks. Subgroups A4-A6 only received AG treatment. Groups B1 to B6 were similarly treated with l-NAME. Animals in division II were treated in the same manner for 13 weeks. Post-mortem analysis revealed that both inhibitors can suppress the development of epithelial dysplasias and squamous-cell carcinomas. An associated increase in the numbers of epithelial hyperplasias was paralleled by a decrease in iNOS protein expression. This animal model can be employed to evaluate the potential use of iNOS inhibitors as novel therapeutic tools for oral squamous-cell carcinogenesis.

Chronic administration of aminoguanidine reduces vascular nitric oxide production and attenuates liver damage in bile duct‐ligated rats

Nitric oxide (NO) has been implicated in the pathogenesis of liver cirrhosis. This study investigated the activity of nitric oxide synthase (NOS) in cirrhosis induced by bile duct-ligation (BDL) with NOS inhibitors. Three days after operation, rats were randomized to receive aminoguanidine (AG, 25 mg/kg/day) or L-N(G)-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg/day) for 21 days. Vascular NO production, which was increased in BDL cirrhotic rats, was reduced by 75% with AG but not L-NAME chronic administration. AG treatment attenuated liver damage, while L-NAME aggravated it. AG significantly suppressed inducible NOS (iNOS) expression in aorta of BDL rats at both mRNA and protein level, but much less efficient in reducing it in liver. In contrast, endothelial NOS (eNOS) expression was not markedly affected. Calcium-independent NOS activity, which was dramatically increased in aorta of BDL rats, was abolished by AG treatment. In liver, however, both calcium-dependent and -independent NOS activity were increased by AG treatment. Chronic administration of AG could reduce systemic NO levels as well as suppress iNOS expression and activity in aorta of BDL rats. It also improved liver function, possibly because of its ability to increase hepatic NOS activity, and to correct the systemic hemodynamic disorders by decreasing vascular NO production.

Adverse Effect of Ag Treatment on the Electrochemical Performance of the 5 V Nanometric Spinel LiNi[sub 0.5]Mn[sub 1.5]O[sub 4] in Lithium Cells

The effect of coating the nanometric spinel with Ag on its rate capability was studied. The X-ray photoelectron spectroscopy (XPS) concentration depth profiles obtained reveal that the intensity of the Ag 3d peak remains unchanged for a long sputtering time, so the spinel particles do not seem to be coated by an Ag layer. The effect is detrimental at high charge/discharge rates and the addition of silver significantly degrades the rate capability of the spinel. Ag oxide nanoclusters formed in the first charge process possibly establish a barrier that hinders transfer of the high ion flux between the electrolyte and electrode.

Effects of Nitric Oxide Synthase Inhibition on Intestinal Damage in Rats with Experimental Necrotizing Enterocolitis

In the inflamed intestinal mucosa of necrotizing enterocolitis (NEC), nitric oxide (NO) generated by inducible nitric oxide synthase (iNOS) may contribute to the pathogenesis of local intestinal damage. To study the importance of iNOS for the pathogenesis of NEC, the effects of selective (aminoguanidine, AG) and nonselective (L-nitroarginine methyl ester, L-NAME) iNOS inhibitors on intestinal morphologic changes were assessed in neonatal rats with experimental NEC. The neonatal rats were randomized into one of the five treatment groups. The control group consisted of rats that were breast-fed. The NEC group, consisting of neonates separated from their mothers, were gavaged with a special rodent formula to produce NEC. Rats in the sham, the AG, and the L-NAME groups were gavaged in a similar fashion to those in the NEC group; in addition, they were treated with 0.9 % saline, 10 mg/kg/day AG, and 10 mg/kg/day L-NAME, respectively. The rats were sacrificed on day 4, and the last 4 cm of terminal ileum was harvested for morphological studies and detection of nitrite and nitrate levels in tissue. The animals in the NEC and sham groups showed various degrees of intestinal inflammatory changes and increased tissue levels of nitrite and nitrate compared to those in the control group. Both AG and L-NAME treatment decreased the tissue levels of these nitrogen oxides, but the inflammatory changes of the intestine appeared to be attenuated only in the AG treated animals. L-NAME treatment did not improve the intestinal damage and increased mortality. These results may indicate that NO synthesized by iNOS plays a pathogenic role in formula-fed induced NEC and that inhibition of iNOS improves intestinal inflammatory damage.

Reversal by aminoguanidine of the age-related increase in glycoxidation and lipoxidation in the cardiovascular system of Fischer 344 rats

Non-enzymatic glycoxydation and lipoxidation of proteins continues to stimulate great interest in gerontology as both markers and promoters of aging. The first aim of the study was to determine the age-related changes in levels of N ɛ-(carboxymethyl)lysine (CML) and 4-hydroxy-2-nonenal (HNE) present on proteins of the cardiovascular system of Fischer 344 rats and identify the particular polypeptides being modified. The second objective was to evaluate whether pharmacological administration of aminoguanidine (1 g/L in the drinking water) could reverse protein glycoxidation and lipoxidation. CML content in serum, aorta, and heart proteins from 28-month-old rats was double of that found in 4-month-old animals. AG administration to old rats for 3 months from the age of 25 months lowered CML content by 15 ( P = .2275), 44 ( P < .0001), and 28% ( P = .0072) in serum, aorta, and heart, respectively. Serum albumin, transferrin and immunoglobulins were most prominently adducted by both CML and HNE. While the extent of albumin and transferrin modification was comparable between age groups, CML and HNE bound to immunoglobulins increased in the sera of old rats as a result of the accumulation of immunoglobulin heavy and light chains. AG treatment prevented immunoglobulin accumulation in serum, suggesting a beneficial action on renal filtration. Lipoxidation of heart mitochondrial proteins was prevalent over glycoxidation, either as CML or pentosidine. Although AG prevented HNE-induced inactivation of the α-ketoglutarate dehydrogenase complex in vitro, it had no effect in rat hearts, suggesting AG could not reach the mitochondrial matrix.

Influence of abomasal carbohydrates on small intestinal sodium-dependent glucose cotransporter activity and abundance in steers1

Most animals adapt readily to increased supplies of carbohydrate in the intestinal lumen by increasing enzymes for degradation and increasing glucose transporter activity. However, the extent of upregulation of Na+-dependent glucose cotransporter 1 (SGLT1) activity and content in response to increased delivery of carbohydrate to the small intestinal lumen of ruminants is unclear. Therefore, an experiment was conducted to determine the effect of glucose and starch hydrolysate on the activity and abundance of SGLT1 in the small intestine of steers. In a randomized complete block design, 40 crossbred beef steers (243+/-2 kg BW) were fed 0.163 Mcal of ME/(kg BW0.75(d; W), 0.215 Mcal of ME/(kg BW0.75 x d; 2M), or 0.163 Mcal ME/(kg BW0.75 x d) and infused for 35 d into the rumen (R) or abomasum (A) with 12.6 g/(kg BW0.75 x d) of starch hydrolysate (S) or into the abomasum with 14.4 g/(kg BW0.75 x d) of glucose (G). Steers were slaughtered, and brush-border membrane vesicles were prepared from the small intestinal samples obtained from five equidistant sites along the intestine. Maltase activity in vesicles and homogenates differed with intestinal sampling site (quadratic, P < 0.001). Steers on the AG treatment yielded a greater intestinal maltase activity (38 nmol glucose x mg protein(-1) x min(-1)) compared with the AS, RS, W, or 2M treatments (34, 26, 23, and 23 nmol glucose x mg protein(-1) x min(-1) respectively [SEM = 3; P = 0.02]). Sodium-dependent glucose uptake averaged 18.4+/-3.94 pmol glucose/(mg protein x s) and was not affected by treatment, but uptake decreased distally along the intestine (P < 0.001). There was no effect of treatment on SGLT1 protein abundance, but SGLT1 protein abundance increased linearly from the duodenum to the ileum (P = 0.05). The inverse relationship between glucose uptake and SGLT1 abundance suggests that the regulation of brush border Na+-dependent glucose transport capacity is complex, involving factors other than the presence of luminal carbohydrate.

The value of fludarabine in addition to ARA-C and G-CSF in the treatment of patients with high-risk myelodysplastic syndromes and AML in elderly patients

AbstractFludarabine in addition to cytosine-arabinoside (ARA-C) increases the accumulation of ARA-C–5′-triphosphate (ARA-CTP), which is responsible for the cytotoxic effect in leukemic blasts. In a randomized phase 3 trial, patients with high-risk myelodysplastic syndrome (MDS) (n = 91) or elderly patients with acute myeloid leukemia (AML) (n = 43) were randomized to receive 2 induction courses consisting of ARA-C (2 g/m2days 1 through 5) and granulocyte colony-stimulating factor (G-CSF) (filgrastim, 5μg/kg) during and after chemotherapy with or without fludarabine (25 mg/m2, days 1 through 5) (FLAG versus AG). Consolidation consisted of daunorubicin (45 mg/m2, days 1 through 3) and ARA-C (200 mg/m2, days 1 through 7). Complete remission (CR) rate following AG was 65% versus 71% with FLAG (P= .49). Overall survival (OS) at 24 months was 24% for AG treatment and 39% for FLAG (P= .32). Event-free survival (EFS) at 2 years was 10% and 19% (P= .31) for the AG and FLAG treatments, respectively. Platelet and granulocyte recovery times after the second cycle were prolonged in the FLAG treatment group. Grades 3 to 4 neurotoxicities were more often reported in the FLAG arm (14% versus 3%,P= .03), whereas no significant differences in other toxicities were observed. In a cohort of patients, the in vivo accumulation of ARA-CTP in leukemic cells was determined. Although ARA-CTP accumulation in leukemic cells after FLAG was enhanced, clinical outcome in terms of CR rate, OS, EFS, and disease-free survival (DFS) was not significantly improved by combining fludarabine with ARA-C. (Blood. 2004;103:2908-2913)

Enhancement of tanshinone production in Salvia miltiorrhiza hairy root culture by Ag+ elicitation and nutrient feeding.

Ag (+) was employed as an abiotic elicitor to stimulate the secondary metabolite production in hairy root culture of Salvia miltiorrhiza, a valuable herbal plant. The addition of Ag (2)S (2)O (3) at 15 - 40 microM to the culture between 12 and 22 days post inoculation resulted in more than 2-fold increase in the yields of the three diterpenoid tanshinones, tanshinone I, tanshinone IIA and cryptotanshinone. This stimulating effect was dependent on the Ag (+) dose, the day of Ag (+) addition to the culture and the tanshinone species, while the total yield of the three tanshinones (TT) was mainly dependent on the Ag (+) dose, with the highest being attained at 30 microM. The Ag (+) treatment also caused a dose-dependent inhibition of hairy root growth. Sucrose feeding or medium renewal before the addition of Ag (+) to the culture effectively prevented the growth inhibition, and significantly increased the biomass concentration and volumetric tanshinone yield. With combined medium renewal and Ag (+) treatment, in particular, the TT yield was increased 6.6-fold relative to that of the control (55.7 mg/L versus 7.3 mg/L). The elicitor function of Ag (+) in the hairy root culture was validated by its ability to induce the characteristic elicitor responses of plants, the increase in cross-cell membrane ion fluxes and the production of reactive oxygen species.

Effects of iNOS inhibitor on IFN-γ production and apoptosis of splenocytes in genetically different strains of mice infected with Toxoplasma gondii

To evaluate the role of nitric oxide (NO) in IFN-gamma production and apoptosis of splenocytes in genetically different strains of mice with toxoplasmosis, BALB/c (a toxoplasmosis resistant strain) and C57BL/6 (a toxoplasmosis susceptible strain) mice were infected with Toxoplasma gondii cysts orally and subsequently injected intraperitoneally with aminoguanidine, an iNOS inhibitor (AG; 35 mg/kg per mouse daily for 14 days). When BALB/c or C57BL/6 mice were infected with T. gondii without AG treatment, number of brain cysts, NO and IFN-gamma production by splenocytes, and percentages of apoptotic splenocytes were increased compared to uninfected control mice without AG treatment. AG treatment increased the number of brain cysts, and reduced NO and IFN-gamma production in T. gondii-infected C57BL/6 mice. In contrast, in T. gondii-infected BABL/c mice, the number of brain cysts, and NO and IFN-gamma production of splenocytes was not altered by treatment with AG. However, the percentages of apoptotic splenocytes in T. gondii-infected BALB/c or C57BL/6 mice were not affected by AG treatment. These results suggest that NO modulates IFN-gamma production in T. gondii-infected C57BL/6 mice, and that NO is involved in mediating a protective response in toxoplasmosis susceptible, but not resistant, mice strain during acute infection.

Desempenho e características de carcaça de novilhos alimentados com dietas contendo diferentes fontes de lipídios

Este trabalho foi realizado para se avaliar o desempenho animal, as características da carcaça e a maciez da carne de 36 novilhos mestiços, apresentando, ao início do experimento, média de 14 meses de idade e aproximadamente 320 kg de peso vivo. Os animais foram confinados e receberam dietas com alto teor de concentrado: uma controle (CO), sem adição de lipídios; outra contendo 5% de sais de cálcio de ácidos graxos (AG); e outra com 21% de caroço de algodão (CA). A ingestão de matéria seca no tratamento AG foi menor que no CA, mas não diferiu da ingestão do CO. O ganho médio diário e a eficiência alimentar não apresentaram diferenças significativas entre os tratamentos. Os valores encontrados para a análise de uréia sangüínea foram significativamente maiores no tratamento CA em relação ao AG. O rendimento de carcaça, a área de olho de lombo, a espessura de gordura, as gorduras renal e pélvica, o peso do fígado, o pH e a temperatura não foram significativamente diferentes. Não houve diferença também para o índice de perda de água por cozimento e maciez, verificada pela força de cisalhamento nos diferentes tempos de maturação. Os sais de cálcio de ácidos graxos a 5% e o caroço de algodão a 21% podem ser empregados nas rações para confinamento, sem causarem alterações no desempenho animal ou nas características de carcaça.

The mechanisms and costs of physiological and toxicological acclimation to waterborne silver in juvenile rainbow trout (Oncorhynchus mykiss).

Juvenile rainbow trout were exposed to 0, 0.1, 1, 3, and 5 micro g/l silver (Ag, as AgNO3) for 23 days. Specific growth rate, cumulative food consumption, food-conversion efficiency, and critical swimming speed (U(crit)) were significantly reduced during 5 micro g/l Ag exposure, demonstrating a physiological cost of silver acclimation. Only the 5 microg/l Ag treatment had significant cumulative mortality (5.2%). Fish were most susceptible to silver on days 5 and 15. Exposure to 5 microg/l Ag significantly lowered plasma Na+ and Cl- on days 5 and 10, but plasma ion concentration recovered thereafter. Unidirectional Na+ uptake and gill Na/K-ATPase activity were significantly inhibited by 3 and 5 microg/l Ag exposure. Na+ uptake was inhibited by 3 micro g/l Ag at day 5 alone, whereas the effects at the highest Ag exposure persisted until day 15. Gill Na/K-ATPase was inhibited on day 5 in both the 3 and 5 microg/l Ag treatments but increased to approx. 1.5 times of control levels by day 23. Only the 3 and 5 microg/l Ag treatments produced toxicological acclimation (at least twofold elevations in 168-h LC50 values in fish subsampled on days 15 and 23). We conclude that physiological acclimation results from compensatory changes in Na+ transport at the gills, and that these changes may eventually lead to toxicological acclimation.