Determination of free malonaldehyde formed in liver microsomes upon CCl4 oxidation

Free malonaldehyde formed in the microsomes prepared from livers of monkey, rat, rabbit, mouse, cow, pig, dog, sheep and horse upon CCl4 oxidation was derivatized by reaction with N-methylhydrazine to form 1-methylpyrazole which was subsequently analyzed by capillary gas chromatography. Among the livers from animals tested, the monkey and rat livers produced the most malonaldehyde upon CCl4 treatment. Horse liver showed the greatest resistance to CCl4 oxidation. The gas chromatography method used in the present study exhibited an accurate and specific measurement of free malonaldehyde that might provide an understanding of the biochemical process of in vitro lipid peroxidation.     

Increase in histamine synthesis by liver macrophages in CCl4-injured mast cell-deficient W/Wv mice

This study set out to examine the possible role of liver macrophages in histamine synthesis in the injured liver. The effects of the hepatotoxins Escherichia coli lipopolysaccharide (LPS) and CCl4 on histamine synthesis in the liver of mice were evaluated. C3H/HeJ mice were resistant to LPS in including histidine decarboxylase (HDC) in the liver compared with C3H/HeN mice and mast cell-deficient W/Wv mice. However, C3H/HeJ mice did respond strongly to another hepatotoxin, CCl4, leading to a significant increase in HDC activity. CCl4 also caused a marked increase in HDC activity and histamine levels in the liver of W/Wv mice. In addition, injection of CCl4 produced a large increase in the activity of HDC in the spleen and lung of W/Wv mice. HDC activity was confined to the nonparenchymal cells, with parenchymal cells expressing essentially no HDC activity. The CCl4-induced increase in HDC activity was confined, at least in part, to the liver macrophages. These results indicate that the macrophages are responsible for the increase in HDC-dependent histamine production in the liver caused by the injection of hepatotoxins. The possible role of histamine in liver regeneration after injury is discussed.     

A potential experimental model for the study of osteopenia in CCl4 liver cirrhotic rats

In the present study we have examined the regulation of the polyamine biosynthetic pathway in a cell line deficient in ornithine decarboxylase (ODC) activity. These cells were unable to grow unless polyamines were provided in their growth medium. Seeding the cells in the absence of polyamines rapidly resulted in a cellular depletion of putrescine and spermidine. Although the cells were devoid of ODC activity they were demonstrated to express an inactive ODC which was feedback regulated by polyamines in a normal manner. Cells seeded in the absence of polyamines exhibited a marked increase in ODC synthesis rate which was not correlated with an equal change in the ODC mRNA level. The synthesis of S-adenosylmethionine decarboxylase (AdoMetDC) was also increased in the cells seeded in the absence of polyamines. However, this increase was essentially explained by a change in the amount of AdoMetDC mRNA. The addition of putrescine to the growth medium appeared to stimulate the conversion of AdoMetDC proenzyme into its two subunits, indicating a physiological role of putrescine in the regulation of AdoMetDC expression.     

Number of Purkinje cells and Bergmann astrocytes in rats with CCl4--induced liver disease

The nuclei of Purkinje cells and Bergmann astrocytes were counted on sagittal sections from cerebellum and the length of stratum gangliosum was measured in rats with CCl4-induced liver disease, using an electronic image analyzer. After 8 weeks of CCl4-administration a reduction was found in the number of Purkinje cells, many of which showed homogenizating changes. Ten weeks after termination of the administration period the number of Purkinje cells was reduced by 12 percent. The number of Bergmann astrocytes remained significantly increased after 8 weeks of CCl4-administration (max. 20 per cent). The changes of Purkinje cell and Bergmann astrocyte density developed during the period of severe liver necrosis, whereas only minor changes were found in the ensuing period of liver "cirrhosis". In the perfusion fixed specimens, the Bergmann astrocyte nuclei increased in volume up to 65 per cent and immersion fixed brains showed typical Alzheimer type II nuclear changes. The impact of the increased plasma ammonia concentration on the astrocytes is discussed.     

Selective inhibition of hepatic collagen accumulation in experimental liver fibrosis in rats by a new prolyl 4-hydroxylase inhibitor

In order to detect and characterize allergen-specific T cells in the airways of atopic asthmatics, we measured proliferation and cytokine production by bronchoalveolar lavage (BAL) T cells isolated from Dermatophagoides pteronyssinus (Der p)-sensitive asthmatics and nonatopic control subjects, and compared the results with those generated using peripheral blood (PB) T cells. BAL and PB mononuclear cells were collected 24 h after segmental allergen challenge by fibreoptic bronchoscopy and venepuncture, respectively. T cells purified from BAL and PB were stimulated with autologous, irradiated antigen-presenting cells and D. pteronyssinus extract or a control, nonallergen antigen (M. tuberculosis purified protein derivative [PPD]). IL-5 and IFN-gamma concentrations were measured in culture supernatants by ELISA, and T-cell proliferation by 3H-thymidine uptake. D. pteronyssinus-induced proliferation of T cells derived from both BAL and PB was elevated in asthmatics when compared with control subjects (p < 0.05), whereas PPD-induced proliferation was equivalent in both compartments. In the asthmatics, D. pteronyssinus-induced proliferative responses of equivalent numbers of BAL and PB T cells obtained after allergen challenge were statistically equivalent. Nevertheless, BAL T cells stimulated with D. pteronyssinus produced significantly greater amounts of IL-5 than did PB T cells (p < 0.05). Allergen-induced proliferation and IL-5 production by BAL T cells in the asthmatics after segmental allergen challenge correlated with the percentages of eosinophils in the BAL fluid (p < 0.01). Further, BAL T cells from asthmatic patients produced significantly higher amounts of IL-5 than did the same number of cells from nonatopic control subjects (p < 0.05). We conclude that, in D. pteronyssinus-sensitive asthmatics, allergen-specific T cells can be detected in the bronchial lumen after allergen challenge and that allergen-induced proliferation and IL-5 production by these cells correlates with local eosinophil influx. Although bronchial luminal T cells show an equivalent proliferative response to allergen stimulation as compared with PB T cells, they do produce more IL-5, consistent with the hypothesis that local differentiation or priming of these cells within the bronchial mucosal environment results in upregulation of allergen-induced IL-5 secretion.     

Curative effects of mandur bhasma on liver and kidney of albino rats after induction of acute hepatitis by CCl(4)

Hepatocurative effects of mandur bhasma were studied in albino rats after induction of acute hepatitis by CCl4 liquid paraffin and CCl4 + liquid param. Recovery of the liver was studied with reference to histological architecture and differential counts of degenerated, recovering and recovered hepatocytes. Alterations in the kidney were also studied histologically. Hepatotoxins were given (s.c.) daily for 11 days. Mandur bhasma was given (po) for 7 days to normal, CCl4, liquid paraffin and CCl4 + liquid paraffin treated rats from day 12 to day 18. There were no spontaneous liver and kidney recoveries within a week after the cessation of the treatments of hepatotoxins. Mandur bhasma treatment showed conspicuous recoveries of liver and kidney within a week and total recoveries were noticed after two weeks. Biochemical alterations in lipid peroxidation, glucose-phosphatase and total proteins were studied during present work. The alterations in the histology and biochemical parameters of liver and kidney show hepatocurative potency of mandur bhasma.     

二苯硫脲-泡沫塑料富集碘-四氯化碳萃取光度法测定矿石中痕量金

研究了叠装已被二苯硫脲丙酮液浸润后的泡沫塑料片的色层柱富集金。灰化泡沫塑料后。采用12-CC14萃取光度法测定矿石中的痕显金。通过方法的回收率试验测定金的回收率为94％-104％。与其他测定方法进行比较。此测定方法效果较好。     

Localization and mRNA steady-state level of cellular fibronectin in rat liver undergoing a CCl4-induced acute damage or fibrosis

Sequence similarity between a translated nucleotide sequence and a known biological protein can provide strong evidence for the presence of a homologous coding region, even between distantly related genes. The computer program BLASTX performed conceptual translation of a nucleotide query sequence followed by a protein database search in one programmatic step. We characterized the sensitivity of BLASTX recognition to the presence of substitution, insertion and deletion errors in the query sequence and to sequence divergence. Reading frames were reliably identified in the presence of 1% query errors, a rate that is typical for primary sequence data. BLASTX is appropriate for use in moderate and large scale sequencing projects at the earliest opportunity, when the data are most prone to containing errors.     

Stimulation of asialoglycoprotein uptake by recombinant human hepatocyte growth factor in normal and damaged rat liver

BACKGROUND: Hepatocyte growth factor (HGF) is a strong mitogen of hepatocytes. However, little is known about the effect of HGF on the asialoglycoprotein receptors (ASGPR) of hepatocytes. The aim of this study was to identify alterations in binding of ligand to ASGPR by recombinant human HGF (rhHGF) infusion. METHODS: RhHGF was administered to rats with either normal or dimethylnitrosamine (DMN)-damaged livers. Technetium-99m-diethylenetriaminepentaacetic acid-galactosyl-human serum albumin (GSA) blood clearance was used to measure ASGPR activity. RESULTS: In normal and damaged rats, liver weight, hepatocyte nuclear size, and number of hepatocytes (cells/mm2) were not altered by rhHGF, but GSA blood clearance after rhHGF infusion was significantly increased over the preinfusion rate. CONCLUSIONS: Independent of proliferation of hepatocytes, rhHGF stimulates a hepatocytic function of the receptor-mediated uptake of ASGP.     

Differential expression of transforming growth factor-beta and its receptors in hepatocytes and nonparenchymal cells of rat liver after CCl4 administration

BACKGROUND/AIMS: Transforming growth factor-beta (TGF-beta) is a family of multifunctional proteins that regulate hepatocyte proliferation, and biosynthesis of the extracellular matrix. In this study we examined whether modulation of TGF-beta receptor expression contributes to the liver diseases. METHODS: The mRNA expression of TGF-beta1, TGF-beta type I receptor (TGFbetaRI), TGF-beta type II receptor (TGFbetaRII) and TGF-beta type III receptor (TGFbetaRIII) in rat livers injured by CCl4 administration was studied by Northern blotting. The mRNA expression patterns were confirmed by in situ hybridization. RESULT: The peak of TGF-beta1 mRNA expression was observed 48 h after acute intoxication with CCl4 in nonparenchymal cells. However, the levels of TGFbetaRI and TGFbetaRII mRNA expression decreased from 24 h to 48 h and from 12 h to 48 h, respectively, and returned to the normal level by 72 h. TGFbetaRII mRNA expression was depressed more and for longer than that of TGFbetaRI mRNA. Analysis in separated hepatocytes and nonparenchymal cells from the injured livers indicated that the mRNA changes occurred in hepatocytes. Nonparenchymal cells expressed TGFbetaRI and TGFbetaRII mRNAs at constant levels during liver regeneration. TGFbetaRIII mRNA, which also decreased after 12 h, was not apparent in hepatocytes but only in nonparenchymal cells. CONCLUSIONS: These observations suggest that: (i) whenever TGF-beta1 is increased in CCl4-treated livers, it may induce liver fibrogenesis via nonparenchymal cells; (ii) the mitoinhibitory effect of TGF-beta1 on hepatocytes is transiently relieved by down-regulation of TGF-beta receptors for 72 h post-damage; and (iii) the resistance to TGF-beta growth inhibition between 24 to 48 h may be predominantly due to down-regulation of the expression of TGFbetaRII.     

巯基树脂富集I2-CCl4萃取光度法测定矿石中的铂

研究了矿样分解后利用巯基树脂富集铂，洗脱分离后转化为氰铂酸与碘化钾反应析出碘，采用I2—CCl4萃取光度法测定矿石中铂的方法。通过方法的回收率实验，并与其它测定方法进行比较，得到了较为满意的结果。     

螯合树脂富集I2-CCl4萃取光度法测定矿石中的金

利用NK8310鳌合树脂富集金，用硫脲-盐酸解脱液解脱后，采用I2-CCl4萃取光度法测定矿石中的金．取得了较为满意的结果。