Alteration of lung lipids in ozone exposed rats.

Exposure of adult male rats to 1.1 ± 0.3 ppm of ozone gave a 10-fold elevation of arachidonic acid in the lipid of the endobronchial washings. Arachidonate and linoleate increased in the cholesteryl esters from 6.5% to 55.5% and 4.7% to 20.4%, respectively. Similar changes also occurred in the composition of phosphatidyl choline. Serum lecithin:cholesterol acyl transferase (LCAT) activity was increased by exposure to ozone and returned to normal levels upon reexposure to an atmosphere of uncontaminated air. The results suggest that the lipid enzyme systems are strongly influenced by ozone exposure.     

Two novel gene orders and the role of light-strand replication in rearrangement of the vertebrate mitochondrial genome

Two novel mitochondrial gene arrangements are identified in an agamid lizard and a ranid frog. Statistical tests incorporating phylogeny indicate a link between novel vertebrate mitochondrial gene orders and movement of the origin of light-strand replication. A mechanism involving errors in light-strand replication and tandem duplication of genes is proposed for rearrangement of vertebrate mitochondrial genes. A second mechanism involving small direct repeats also is identified. These mechanisms implicate gene order as a reliable phylogenetic character. Shifts in gene order define major lineages without evidence of parallelism or reversal. The loss of the origin of light-strand replication from its typical vertebrate position evolves in parallel and, therefore, is a less reliable phylogenetic character. Gene junctions also evolve in parallel. Sequencing across multigenic regions, in particular transfer RNA genes, should be a major focus of future systematic studies to locate novel gene orders and to provide a better understanding of the evolution of the vertebrate mitochondrial genome.      

Structural characterization of a follicle-stimulating hormone action inhibitor in porcine ovarian follicular fluid. Its identification as the insulin-like growth factor-binding protein.

Recently, an inhibitory polypeptide that could block the follicle-stimulating hormone-induced estradiol and progesterone production in rat ovary granulosa cells has been isolated from porcine ovarian follicular fluid. Amino-terminal sequence analysis of the purified inhibitor suggests that it could be the porcine congener of the 53-kDa subunit of the growth hormone-dependent insulin-like growth factor binding protein (IGF-BP3). Using amino acid sequence information derived from the purified inhibitor to construct oligonucleotide probes, we have now identified the complementary deoxyribonucleic acids (cDNAs) encoding the inhibitory polypeptide from a porcine liver and a porcine ovary library. The nucleotide and predicted amino acid sequences revealed that the cDNAs indeed encode the porcine homolog of the recently characterized human IGF-BP3. The mature polypeptide consists of 266 amino acids, which is 2 amino acids longer than the human sequence. Between the two species, there are 42 amino acid substitutions, but the 18 cysteines and the three Asn-linked glycosylation sites are totally conserved. A single mRNA species of 2.6 kilobases encoding the IGF-BP3 was detected in porcine gonadal, brain, and liver tissues by Northern analysis.     

Accumulation of oleate-rich cholesteryl esters by acetyl-LDL in macrophages in the presence of an acyl-CoA: cholesterol acyltransferase inhibitor (Sandoz 58-035)

The mechanism through which cholesteryl esters rich in oleic acid accumulate in the cytoplasm was studied. The fatty acid composition of the cholesteryl esters in acetyl-LDL was high in linoleic acid, while that of cholesteryl ester inclusion bodies accumulated in the cytoplasm was high in oleic acid. This compositional change of fatty acids in cholesteryl esters occurred even in the presence of an acyl-CoA: cholesterol acyltransferase (ACAT) inhibitor, Sandoz 58-035. These results suggest that oleate-rich cholesteryl esters accumulated in the cytoplasm, even though the reesterification in microsome was inhibited by an ACAT inhibitor.     

Energetic aspects of CO oxidation in desulfovibrio desulfuricans

In cell suspension of Desulfovibrio desulfuricans B-1388, oxidation of CO as the only energy source is associated with reduction of SO42-. After a 2-h incubation of cells in 8% CO, 81% of the gas is converted. Oxidation of 1 mole CO results in formation of 0.23 mole H2S. Intracellular ATP content increases from 2.5 (control) to 8.3 nmoles/mg (during CO conversion). Dinitrophenol inhibits sulfate reduction and CO oxidation. CO dehydrogenase was detected in cytoplasmic and membrane cell fractions (59 and 34%, respectively).     

Role of ERK1/2 in the differential synthesis of progesterone and estradiol by granulosa cells.

A major concept in mammalian ovarian physiology is that follicle-stimulating hormone (FSH) activates the granulosa cells (GCs) in the Graafian follicle to selectively produce estradiol, but not progesterone, during the follicular phase of the menstrual or estrous cycle. However, given the fact that FSH can induce production of both estradiol and progesterone by GCs cultured in vitro, it has been postulated for a long time that there is a factor present in the ovary that selectively prevents FSH-induced progesterone production. Here, we provide evidence that two members of the mitogen-activated protein kinase family, extracellular signal-regulated kinase-1 and -2 (ERK1/2) can differentially regulate FSH-stimulated estradiol and progesterone production. Using primary rat GCs from early antral follicles cultured in serum-free medium for 48 h, we found that the addition of a specific inhibitor of ERK1/2 activation, U0126, caused the attenuation or enhancement of FSH-induced progesterone or estradiol production, respectively, in a dose-dependent manner. Throughout the 48-h culture period in this culture system ERK1/2 molecules in their activated state (phospho-ERK1/2) were clearly detectable in GCs exposed to FSH. The addition of U0126 caused a decrease in the levels of phosphorylated but not unphosphorylated ERK1/2 which was maintained throughout the 48-h culture, suggesting that U0126 was continuously active to inhibit the phosphorylation of ERK1/2. The divergent regulation of FSH-induced progesterone and estradiol synthesis by U0126 was further supported by demonstrating that U0126 inhibits and stimulates FSH-induced mRNA levels of steroidogenic acute regulatory protein and P450 aromatase, respectively. Collectively, this study clearly identified ERK1/2 as the first intracellular signaling molecules that differentially regulate FSH-induced progesterone and estradiol synthesis in GCs.     

Structures and inclusion properties of racemic and enantiopure dimethyl and diphenyl 9,9'-bianthryl-2,2'-dicarboxylates

The authors prepared the dimethyl and diphenyl esters of 9,9'-bianthryl-2,2'-dicarboxylic acid in racemic and enantiopure (M) forms. The enantiopure dimethyl ester forms inclusion compounds with various organic compounds such as benzene, methanol, phenol, and aniline whereas the racemic form does this only with benzene. No guest molecules are included by the racemic and enantiopure diphenyl esters. These effects of substituents and homochirality on the inclusion properties are discussed on the basis of X-ray structures of some inclusion and guest-free compounds.     

Proton-Induced X-ray Emission (PIXE) Analysis and DNA-chain Break study in rat hepatocarcinogenesis: A possible chemopreventive role by combined supplementation of vanadium and beta-carotene

Combined effect of vanadium and beta-carotene on rat liver DNA-chain break and Proton induced X-ray emission (PIXE) analysis was studied during a necrogenic dose (200 mg/kg of body weight) of Diethyl Nitrosamine (DENA) induced rat liver carcinogenesis. Morphological and histopathological changes were observed as an end point biomarker. Supplementation of vanadium (0.5 ppm ad libitum) in drinking water and beta-carotene in the basal diet (120 mg/Kg of body weight) were performed four weeks before DENA treatment and continued till the end of the experiment (16 weeks). PIXE analysis revealed the restoration of near normal value of zinc, copper, and iron, which were substantially altered when compared to carcinogen treated groups. Supplementation of both vanadium and beta-carotene four weeks before DENA injection was found to offer significant (64.73%, P < 0.001) protection against generation of single-strand breaks when compared with the carcinogen control counter parts. A significant stabilization of hepatic architecture of the cells was observed as compared to carcinogen control in vanadium plus beta-carotene treated group. This study thus suggests that vanadium, a prooxidant but potential therapeutic agent yield safe and effective pharmacological formulation with beta-carotene, an antioxidant, in the inhibition of experimental rat hepatocarcinogenesis.