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Z X Xu

Publications and source records attributed to Z X Xu.

At least 37 records · Page 2Linked to original sources
PubMed1995

Glucocorticoid stimulation of fatty-acid synthase gene transcription in fetal lung: antagonism by retinoic acid.

Glucocorticoid hormones are known to stimulate the rate of fatty acid biosynthesis and to increase the activity and mRNA level of fatty-acid synthase (FAS) in late gestation fetal lung. We have now examined the effect of dexamethasone on FAS transcription in fetal rat lung. Explants of 19-day fetal rat lung cultured for 48 h in serum-free medium were exposed to dexamethasone (10(-7) M) for various time periods. Nuclei were isolated, and the rate of [32P]UTP incorporation into FAS and gamma-actin RNA transcripts was measured by transcription-elongation assay. Dexamethasone increased FAS transcription but had no effect on that of actin. The maximum effect of the hormone, approximately threefold increase, was observed 1-2 h after addition of the hormone but was still apparent up to 48 h. FAS transcription but not that of actin was inhibited by cycloheximide and puromycin in both control and dexamethasone-treated cultures. However, the stimulatory effect of the hormone was not significantly reduced by the inhibitors. Retinoic acid antagonized the stimulatory effects of dexamethasone on FAS activity, mRNA content as measured by Northern analysis, mass as measured by Western blotting, and rate of transcription. The effect of retinoic acid was dependent on concentration in the relatively narrow range of 5 x 10(-6) to 5 x 10(-4) M. These data show that glucocorticoids stimulate transcription of the FAS gene in late gestation fetal rat lung, that normal transcription of the FAS gene is dependent on ongoing protein synthesis, and that glucocorticoid stimulation of FAS gene expression is antagonized by retinoic acid.

Animals↗
PubMed1994

P2u purinoceptor stimulation of surfactant secretion coupled to phosphatidylcholine hydrolysis in type II cells.

ATP is known to stimulate surfactant phospholipid secretion in type II cells, and there is evidence that this effect is mediated by a P2 purinoceptor. At least five subtypes of the P2 receptor have been reported, but it is not clear which one exists on the type II cell. To determine whether it is the P2u subtype, at which UTP is equipotent with ATP, we have compared the effects of ATP and UTP on phosphatidylcholine secretion and second messenger formation in primary cultures of rat type II cells. ATP and UTP were equally potent in stimulating phosphatidylcholine secretion and phospholipase D activation. The potency order, UTP = ATP > ADP > 2-methylthio-ATP, was the same as that reported for the P2u receptor. UTP stimulated diacylglycerol and phosphatidic acid formation to the same extent as ATP. ATP also increased choline formation. Formation of diacylglycerol was biphasic, and the first peak in response to ATP was previously shown to be associated with inositol trisphosphate formation. Northern analysis showed that the P2u receptor gene was expressed to a greater extent in type II cells than in whole lung. These data suggest that ATP and UTP act via a P2u receptor that is coupled to phosphoinositide-specific phospholipase C with subsequent activation of phospholipase D acting on phosphatidylcholine. ATP has also been reported to act at an additional type II cell receptor coupled to adenylate cyclase. In contrast, UTP did not promote adenosine 3',5'-cyclic monophosphate formation and therefore does not act at that receptor.

Adenosine Triphosphate↗
PubMed1994

[Clinical effect and experimental study of xijian tongshuan pill].

Xijian Tongshuan pill (XJTS), consisted of Siegesbeckia orientalis, Moschus moschiferus, Hirudo nipponica, Prunus Persicae, Carthamus tinctoruis, Ligusticum wallichi, Panax notoginseng, Angelica Sinensis, Borneolum, etc, were used in treating 70 patients with cerebral thrombosis. The marked effective rate was 82.9%, total effective rate was 96.7%. In control group A, Dextranum and Venoruton were used, in control group B cyclandelate capsule were used. The marked effective rate was 61.7% and 61.1% respectively, the total effective rate was 81.7% and 83.3%. The differences were significant (P < 0.01). The improvement of blood rheology and CT of brain were also significant (P < 0.01). The experiment proved that XJTS pill could inhibit and delay the thrombosis of rabbit, inhibit the platelet aggregation. Acute and subacute toxicity tests proved that XJTS pill was safe and effective.

Adult↗
PubMed1993

Glucocorticoid regulation of fatty acid synthase gene expression in fetal rat lung.

There are developmental and glucocorticoid-induced increases in the rate of fatty acid biosynthesis and in the activity of fatty acid synthase in late gestation fetal lung. We have now measured mRNA levels of fatty acid synthase and of two other enzymes of fatty acid biosynthesis, ATP citrate lyase and acetyl-CoA carboxylase, in developing fetal and postnatal rat lung and in fetal lung explants cultured with and without dexamethasone. There was a developmental increase in the mRNA for fatty acid synthase with the maximum level being reached on fetal day 21 (term is fetal day 22). This profile was similar to that reported for de novo fatty acid synthesis and fatty acid synthase activity. There was a similar but less pronounced developmental increase in the mRNA for ATP citrate lyase and a corresponding increase in its activity. There was no developmental change in the mRNA for acetyl-CoA carboxylase. Dexamethasone increased the level of fatty acid synthase mRNA approximately threefold but had no effect on those for ATP citrate lyase and acetyl-CoA carboxylase. The effect of dexamethasone on fatty acid synthase mRNA was rapid, biphasic, and partly inhibited by actinomycin D and cycloheximide. We conclude that glucocorticoids increase expression of the gene for fatty acid synthase in fetal lung. The effect of the hormone appears to be due to increased transcription and post-transcriptional events and is dependent on protein synthesis.

Animals↗
PubMed1992

Kinetics of aluminum in rats. III: Effect of route of administration.

Male Fischer rats received 0.1 mg/kg (bolus) of elemental aluminum as the sulfate salt via the portal (n = 4) or systemic (n = 4) route of administration. Blood and bile were serially sampled over an 8-h period, postadministration. Aluminum was determined by flameless atomic absorption spectrophotometry. Blood aluminum concentrations declined in a monoexponential fashion, with half-lives of 0.7 h (portal) and 1.08 h (systemic) (p less than 0.05). The corresponding systemic clearances were 48.9 +/- 10.6 and 35.1 +/- 3.64 mL/(h.kg) (p less than 0.05). The systemic availability following portal administration was 0.66, indicating a significant "first-pass" effect. Biliary aluminum recovery (% dose) was negligible following both routes [0.83 +/- 0.062% (portal) versus 1.3 +/- 0.22% (systemic), p less than 0.05]. Bile flow decreased approximately 40% (p less than 0.05) immediately upon injection of aluminum via the portal route only; flow remained suppressed throughout the study. This decrease in bile flow was most likely responsible for the lower biliary recovery with this route. In contrast, liver recovery of aluminum at 8-h postadministration was higher with the portal route (65.4 +/- 4.1 versus 39.4 +/- 2.52%). These results show that reported values for oral "bioavailability" of aluminum, often calculated by the standard AUC ratio method, underestimate the true extent of absorption. One mechanism of aluminum-related jaundice observed clinically may be due to cholestasis.

Aluminum↗
PubMed1992

Aluminum-induced acute cholinergic neurotoxicity in rat.

In the present study the acute effect of intravenous aluminum chloride (1 mg/kg) on choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities of rats was investigated. Aluminum was found to cross the blood-brain barrier (BBB) as indicated by the detection of aluminum in the cerebrospinal fluid (CSF) 30 min after femoral vein injection. Two hours following aluminum injection, ChAT activity in the basal forebrain and hippocampus was significantly reduced by 30% and 22%, respectively, whereas no change was observed in the caudate nuclei. On the other hand, AChE activity was significantly increased by 45% in the caudate nuclei, whereas little change was observed in other brain areas. This report demonstrates that rapid transport of Al across the BBB, and the acute nature of Al neurotoxicity in rats.

Acetylcholinesterase↗
PubMed1992

Kinetics of aluminum in rats. IV: Blood and cerebrospinal fluid kinetics.

Aluminum causes central nervous system (CNS) toxicities in both humans and various animal species. Although blood aluminum concentrations are monitored in the clinic, very little is known regarding the relationship between such concentrations and corresponding CNS aluminum content. As a first step in that direction, this study was undertaken to simultaneously determine blood and CSF kinetics of this element. Following intravenous injection of aluminum (1 mg/kg), there was a rapid (within 30 min, post injection) increase in CSF aluminum; peak concentrations (38-45 ng/ml) were achieved between 2-3 h. While peak blood aluminum concentrations increased about 58-fold from the pre-dose value (from 256 +/- 120 to 14,730 +/- 388 ng/ml), corresponding increases in CSF aluminum were only about 20-fold. Blood and CSF aluminum concentrations declined monoexponentially with half-lives of 2.77 and 3.45 h, respectively (P < 0.05). Results from these showed that blood and CSF compartments achieve equilibrium and indicated the feasibility of determining brain aluminum content using blood concentrations.

Aluminum↗
PubMed1991

Kinetics of aluminum in rats. II: Dose-dependent urinary and biliary excretion.

Previous iv studies from our laboratories have shown that the disappearance half-life of blood aluminum increased with dose. Experiments were initiated to determine if saturation of biliary and/or urinary excretion could be responsible for this dose-dependent behavior. Biliary aluminum excretion (0-12 h) accounted for less than 1% of the injected amount at 0.1- and 1.0-mg/kg doses. During the same interval, urinary excretion accounted for 16.7 +/- 2.66 and 8.85 +/- 2.2% of administered dose at the low and high doses, respectively (p less than 0.05); corresponding long term (0 to 13 or 22 days) urinary recoveries were 37.6 +/- 3.67 and 28.4 +/- 1.88% of the injected dose (p less than 0.05), with most (66-70%) of the excretion occurring in the first 24 h. This is consistent with many previous reports showing that urinary excretion is one major elimination pathway for aluminum. Both biliary and urinary clearances decreased with increasing blood aluminum concentration; the biliary and urinary clearance values at low concentrations (500-900 ng/mL) were approximately four- and threefold higher than the corresponding values at higher concentrations (10,000-12,000 ng/mL), respectively. It appears that this apparent saturability of biliary clearance may be due to concentration-dependent of transfer from blood to liver, rather than from liver to bile. In vitro ultrafiltration studies support the hypothesis that decreases in urinary clearance were due to decreased filterability of aluminum at the glomerulus as its blood concentration was increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗
PubMed1991

Changes in pulmonary Cu-Zn contents in superior mesenteric artery occlusion shock of rabbit.

Contents of Cu and Zn of into-pulmonary blood (IPB), out-pulmonary blood (OPB), Lung tissue, and supernatant and macrophages of Lung Lavage were determined in superior mesenteric artery occlusion (SMAO) shock of rabbits. Zn of pulmonary tissue was 11.42 +/- 0.60 and 14.52 +/- 1.78 (micrograms/g wet wt) in SMAO shock and control groups, respectively. Content of Zn was found to be lower, Cu was not changed, and Cu/Zn ratio increased in lung tissue in SMAO shock. Contents of Cu and Zn in other samples were not changed. The results suggest that lower Zn in lung tissue related to acute lung injury.

Animals↗
PubMed1990

Glucocorticoid induction of fatty-acid synthase mediates the stimulatory effect of the hormone on choline-phosphate cytidylyltransferase activity in fetal rat lung.

Fetal lung fatty-acid synthase and choline-phosphate cytidylyltransferase activities are increased by glucocorticoids. There is evidence that the hormone increases synthesis of fatty-acid synthase but only increases the catalytic activity of the cytidylyltransferase. Free fatty acids and a number of phospholipids have been reported to stimulate cytidylyltransferase activity in several organs, including the lung. We have addressed the question of whether glucocorticoid induction of fatty-acid synthase mediates the stimulatory effect of the hormone on choline-phosphate cytidylyltransferase activity. Explants of 18-day fetal rat lung were cultured for 48 h with dexamethasone and inhibitors of de novo fatty acid biosynthesis (agaric acid and hydroxycitric acid) being included in the medium for the final 20 h. Dexamethasone increased the activities of fatty acid synthase and choline-phosphate cytidylyltransferase by 84% and 60%, respectively. Agaric acid and hydroxycitric acid completely abolished the stimulatory effect of the hormone on cytidylyltransferase but not on fatty-acid synthase. The inhibitors had no effect on cytidylyltransferase activity in control cultures. Fetal lung choline-phosphate cytidylyltransferase can be maximally stimulated by inclusion of phosphatidylglycerol in the assay mixture and under this condition, cytidylyltransferase activity in control and dexamethasone-treated cultures in the presence and absence of the inhibitors were all increased to the same level. Therefore, the inhibitors did not diminish the capacity of cytidylyltransferase to be fully activated. We suggest that the glucocorticoid induction of fatty-acid synthase in fetal lung results in increased synthesis of fatty acids which in turn, either as free acids or after incorporation into phospholipids, activate choline-phosphate cytidylyltransferase.

Animals↗
PubMed1990

Simultaneous sampling of blood, bile, and urine in rats for pharmacokinetic studies.

A method for simultaneous serial sampling of blood, bile, and urine from rats is described. Techniques for cannulation of jugular and femoral veins, bile duct, and bladder are described that make serial sampling of these three fluids possible. A saline infusion regimen was developed that prevents dehydration and maintains constant hematocrit values throughout the experiment. Accuracy of timed-samples can be easily controlled along with complete collection of voided urine. This method also allows for economy in terms of cost (number of animals used) and time in pharmacokinetic investigations involving the rat where extensive sampling of blood, bile, and urine are needed. In addition, interanimal variability, which can be quite high in such studies, is avoided by sampling all these three fluids in a single rat. While the kinetic parameters of blood aluminum obtained from this anesthetized animal model compare well with those in unanesthetized rats reported from this laboratory, this method is most useful for comparative studies.

Aluminum↗
PubMed1990

Mechanism of aluminum-induced inhibition of hepatic glycolysis: inactivation of phosphofructokinase.

Aluminum, an abundant element in the earth's crust, has been implicated in various pathological disorders and low concentrations of this element have recently been shown to inhibit brain glycolysis. However, despite the fact that aluminum accumulates in high concentrations in the liver, potential effects of this metal on hepatic intermediary metabolism have not been explored. In perfused livers from untreated rats, maximal rates of production of lactate plus pyruvate (glycolysis) were 93 +/- 15 mumols/g/hr. Glycolysis was severely inhibited in livers from aluminum-treated rats (0.5 mg/kg, 6 hr before experiment) with maximal rates of only 23 +/- 4 mumols/g/hr. In contrast, glucose production (glycogenolysis) and hepatic oxygen uptake were not altered significantly by prior treatment with aluminum. In livers from fasted rats, pretreatment with aluminum did not influence gluconeogenesis or production of lactate and pyruvate from fructose (5 mM). This finding indicates that pyruvate kinase is not inhibited by aluminum and implicates phosphofructokinase, hexokinase and/or glucokinase as sites for the inhibitory effect of aluminum on glycolysis. In liver homogenates from untreated rats, increasing concentrations of aluminum did not show any appreciable effect on hexokinase or glucokinase activity but did cause progressive decreases in phosphofructokinase activity. Therefore, aluminum-induced inhibition of liver phosphofructokinase, an important control site in the glycolytic pathway, is most likely responsible for aluminum-induced inhibition of hepatic glycolysis.

Adenosine Triphosphate↗
PubMed1989

Influence of dexamethasone on the lipid distribution of newly synthesized fatty acids in fetal rat lung.

There is a developmental increase in fatty acid biosynthesis and surfactant production in late-gestation fetal lung and both are accelerated by glucocorticoids. We have examined the distribution of the newly synthesized fatty acids to determine whether they are preferentially incorporated into surfactant. Explants of 18 day fetal rat lung were cultured with and without dexamethasone for 48 h and then with [3H]acetate for 4 h after which labeled fatty acids were measured. Incorporation of radioactivity from acetate was considered a measure of newly synthesized fatty acids. Phospholipids contained 86% of the newly synthesized fatty acids of which approx. 80% were in phosphatidylcholine. Phosphatidylcholine and disaturated phosphatidylcholine contained a much greater percentage of the labeled fatty acids than of the phospholipid mass determined by phosphorus assay while phosphatidylethanolamine, phosphatidylserine and sphingomyelin contained less. Dexamethasone increased the rate of acetate incorporation into total lipid fatty acids but it had little effect on fatty acid distribution, except that it increased the percentages in phosphatidylglycerol and disaturated phosphatidylcholine. The hormone also increased the mass of these two phospholipids to a greater extent than that of the total. These data suggested that the newly synthesized fatty acids are preferentially incorporated into surfactant phospholipids and that this process is accelerated by dexamethasone. However, since phosphatidylcholine and phosphatidylglycerol are not exclusive to surfactant, we compared isolated lamellar bodies with a residual fraction not enriched in surfactant. The rate of acetate incorporation into fatty acids in lamellar body phosphatidylcholine as well as its specific activity (radioactivity per unit phosphorus) were both increased by dexamethasone. Specific activity, however, was no greater in the lamellar bodies than in the residual fraction in both control and dexamethasone-treated cultures. Therefore, there is no preferential incorporation of newly synthesized fatty acids into phospholipids in surfactant as opposed to those in other components of the lung.

Acetates↗
PubMed1989

[Studies on the fine structure of Toxoplasma gondii tachyzoite].

Toxoplasma gondii tachyzoite was crescent-shaped. The pellicle of the parasite consisted of two membranes. The anterior end contained the polar ring and conoid, the former being the thickened inner membrane and the latter a cylindrical organelle which was made up of about 10 filaments arranged in an oblique row. The subpellicular microtubules numbering 22 originated at the polar ring and extended to the posterior end. The rhoptries extended from the conoid and terminated anterior to the nucleus with a narrow dense neck and an enlarged posterior portion with a glandular structure. The rhoptries perhaps had a secretory function and the conoid might be related to the invasion of the tachyzoite into the host cell.

Animals↗