Fatty acid synthesis in fetal lung

De novo fatty acid synthesis in lung is significant during fetal growth and development. Specific activity and relative rate of synthesis of fatty acid synthetase increase with the days of gestational age and drop significantly after birth. Fetal lungs contain thyroid hormone receptors and binding capacities of this hormone to the fetal lungs also increase with the days of gestational age. Our results suggest that de novo fatty acid synthesis in fetal lungs may make a significant contribution towards surfactant synthesis.     

Structure of the d-galactan isolated from aloe barbadensis miller

Hot-water extraction of the pulp obtained by dehydrating the jelly of the fleshy leaves of Aloe barbadensis furnished a mixture of polysaccharides containing mainly pectic acid, along with a d-galactan, a glucomannan, and an arabinan. The pectic acid was partly removed by treatment with calcium chloride, and the resulting, hexose-enriched, polysaccharide mixture was fractionated through a column of DEAE-cellulose to yield a d-galactan containing d-galactose (92.9% and d-galacturonic acid (3.8%). Hydrolysis of the permethylated d-galactan furnished 2,3,4,6-tetra-, 2,3,6-tri-, and 2,3-di-O-methylgalactose in the molar ratios of 1:26:1. On periodate oxidation, the d-galactan reduced 0.95 molar equivalent of the oxidant per hexosyl residue, and liberated one molar equivalent of formic acid per 26 galactosyl residues. Smith degradation of the d-galactan afforded mainly threitol. From these results, a structure has been assigned to the repeating unit of the d-galactan. The number-average, molecular weight of the peracetylated galactan has been found to be 3.74 x 10⁴.     

Tissue difference in gamma-glutamyl transpeptidase attributed to sialic acid content.

Gamma-glutamyl transpeptidase (GGT) was extracted from the microsomal fraction of various bovine tissues and partially purified. Purified enzymes demonstrated different mobilities toward the anode in polyacrylamide gel electrophoresis in 0.5% Emulphogene BC720, pH 7.5. The ciliary-body GGT migrated fastest, while the brain enzyme was electrophoresed most slowly. The apparent Km values (Km′) of GGT for L-gamma-glutamyl-p-nitroanilide were 1.4–2.0 mM when assayed with glycylglycine as the gamma-glutamyl acceptor. After neuraminidase treatment, electrophoretic mobility was decreased considerably for all enzyme preparations, compatibly with the removal of negatively charged sialic-acid residues. The Km′ values of the enzyme were not affected by the hydrolytic treatment. Electrophoresis of digested enzymes showed essentially identical mobilities. From these results we conclude that tissue differences in GGT are attributable to the varying extent of sialylation of enzyme.     

Antiulcerogenic and anti-inflammatory effects of emodin, isolated from Rhamnus triquerta wall

Emodin, an anthraquinone derivative, isolated from the whole plant of R. triquerta, in 15 mg/kg dose (ip) exhibited anti-inflammatory activity against carrageenin-induced pedal inflammation in rats. In the same dosage it also showed antiulcer activity against 4 hr pylorus-ligated, aspirin and immobilization stress-induced gastric ulcers in rats. It decreased acid and pepsin output and augmented mucus secretion in terms of total carbohydrate: protein ratio in the gastric juice of aspirin treated pylorus-ligated rats, indicating that the antiulcerogenic effect of emodin may be due to its effect on gastric secretion.     

A 14-kilodalton inner membrane protein of Vibrio cholerae biotype e1 tor confers resistance to group IV choleraphage infection to classical vibrios.

Choleraphage phi 149 differentiates the two biotypes, classical and el tor, of Vibrio cholerae. This phage cannot replicate in V. cholerae biotype el tor cells because the concatemeric DNA intermediates produced are unstable and cannot be chased to mature phage DNA. A V. cholerae biotype el tor gene coding for a 14,000-Da inner membrane protein which destabilizes the concatemeric DNA intermediates by hindering their binding to the cell membrane has been identified. Presumably, a 22,000-Da V. cholerae biotype el tor protein might also have a role in conferring phage phi 149 resistance to cells belonging to the biotype el tor. A nucleotide sequence homologous to the 1.2-kb V. cholerae biotype el tor DNA coding for both the 14,000- and 22,000-Da proteins is present in all strains of classical vibrios but is not transcribed. The nucleotide sequence of the gene coding for the 14,000-Da protein has been determined.     

The v-src oncogene may not be responsible for the increased radioresistance of hematopoietic progenitor cells expressing v-src.

Infection of the IL-3-dependent, myeloid progenitor cell line 32D cl 3 with murine retroviruses that contain either the wild-type or a temperature-sensitive mutant v-src can render these cells growth-factor independent. These cells also became resistant to gamma irradiation administered at the low-dose rate of 0.05 Gy/min, which is used clinically. The v-src-dependent nature of resistance to gamma irradiation was examined by studying four clones of 32D cl 3 cells that had been infected with a retrovirus carrying the tsLA31A mutant of v-src. The tyrosine-specific kinase activity of this mutant is dramatically reduced at the nonpermissive temperature of 39 degrees C. Cells transformed by v-src and grown at either 34 or 39 degrees C, in the presence or absence of IL-3, demonstrated a significantly higher D0 compared to parental cells examined under identical conditions. In addition, expression of v-src abrogated the synergistic killing effect of heat and gamma irradiation. The D0 of parental 32D cl 3 cells kept at 39 degrees C after gamma irradiation was reduced significantly compared to the D0 of these cells kept at 34 degrees C. This contrasts with data from 32D cl 3 cells infected with either the wild-type v-src or the temperature-sensitive mutant, neither exhibited a synergistic effect in the D0 at either 34 or 39 degrees C. Therefore, while continuous expression of a v-src gene product is required for maintenance of the growth-factor-independent state, v-src does not appear to be responsible for the increased gamma-radiation resistance of these cells at low dose rate.     

(ADP-ribosyl)ation pattern of chromosomal proteins during ageing.

(ADP-ribosyl)ation of chromosomal proteins was studied by incubating the nuclei of brain and liver of young and old rats with 14C-NAD+. In brain as well as in liver histone proteins show approximately 2-3 fold higher (ADP-ribosyl)ation than that of non-histone chromosomal (NHC) proteins of both the age groups. H1 seems to be the major target for (ADP-ribosyl)ation. Amongst nucleosomal histones H2B is the main acceptor of 14C-labelled ADP-ribose moieties. A sharp age related decline of (ADP-ribosyl)ation of chromosomal proteins was observed in both the tissues.     

cDNA sequence of the long mRNA for human glutamine synthase.

Screening a human liver cDNA library in lambda ZAP revealed several clones for the mRNA of glutamine synthase. The longest clone was completely sequenced and consists of a 109 bp 5' untranslated region, a 1119 bp protein coding region, a 1498 bp 3' untranslated region and a poly(A) tract of 12 bp.     

Interaction of benzanthrone with cytochrome P450: altered patterns of hepatic xenobiotic metabolism in rats

Benzanthrone, an anthraquinone dye intermediate, is commonly used for the synthesis of a number of polycyclic vat and disperse dyes. Our prior studies have shown that benzanthrone can be metabolized by rat hepatic microsomal cytochrome P450 (P450) (Biochem. Int., 18, 1989, 1237). In this study, the interaction of benzanthrone with rat hepatic microsomal P-450 and its effect on xenobiotic metabolism have been investigated. Parenteral administration of benzanthrone (40 mg/kg body weight) for 3, 7, or 21 days caused no change in the relative body weight or organ weight of rats. The levels of P450 were found to be reduced (33%-50%) in all the benzanthrone-exposed animals at all the time periods. In vitro addition of benzanthrone caused a spectral change with oxidized P450 and concentration-dependent reduction in the carbon monoxide spectrum of dithionite-reduced P450. The addition of benzanthrone to hepatic microsomes prepared from phenobarbital-treated rats resulted in spectral changes characterized by an absorbance maximum at 397 nm indicative of type I binding. In vitro addition of benzanthrone showed a concentration-dependent inhibition of hepatic aminopyrine N-demethylase (APD) and ethoxyresorufin-O-deethylase (ERD) activities with respective I50 values of 9.5 x 10(-4) and 8.0 x 10(-5) M. However, the inhibition of aryl hydrocarbon hydroxylase (AHH) even at the highest concentration of benzanthrone (10(-2) M), was of the order of only 29%. In vivo administration of benzanthrone also led to the inhibition of APD, AHH, and ERD activities at all treatment times although the magnitude of inhibition was of a lower order.(ABSTRACT TRUNCATED AT 250 WORDS)     

Modulation of lymphoproliferation and oxidative burst by herpes-transformed tumors.

In this study, herpes simplex virus Type 2 (HSV-2)-transformed cells (H238) and conditioned medium (CM) from H238 cell cultures were studied with respect to their effects on lymphoproliferation and the chemiluminescent oxidative burst of phagocytic cells. The H238 cells expressed a nuclear antigen detectable by fluorescent antibody testing using pooled sera from tumor-bearing mice, but no HSV-1 or HSV-2 cell membrane antigens could be found using specific monoclonal antibodies. BALB/c mice subcutaneously injected with 1 X 10(6) H238 cells developed progressively growing fibrosarcomas and depressed T lymphocyte blastogenesis in response to phytohemagglutinin (PHA) by 6 weeks post-injection when compared to non-injected controls. In contrast, oxygen radical production was increased by nearly 28-fold in the tumor-bearing subjects at this time. Incubation of normal mouse spleen cells in 100 microliters to 500 microliters of CM/ml resulted in significant dose-dependent suppression of PHA-induced lymphoproliferation. This was seen when the total spleen cell population was used, as well as after removal of the adherent cells, thereby suggesting that the inhibitory effect was not due to activation of adherent suppressor cells by the CM. However, the oxidative burst of total and adherent spleen cells from normal mice was significantly enhanced by the presence of either the H238 cells or their CM. In contrast, oxygen radical production by J774A.1 cells (a BALB/c mouse macrophage cell line) was depressed by H238 cells. Our results show that H238 tumors can alter lymphocyte as well as phagocytic cell functions both in vivo and in vitro. These tumor-induced modulations may occur via secretion of soluble factors or direct cell-to-cell interactions and, thus, may influence the outcome of immunotherapy in the tumor-bearing host.