High air humidity is sufficient for successful egg incubation and early post‐embryonic development in the marbled crayfish (Procambarus virginalis)

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Effects of diets enriched in linoleic acid and its peroxidation products on brain fatty acids,oxylipins, and aldehydes in mice

Background

Linoleic acid (LA) is abundant in modern industrialized diets. Oxidized LA metabolites (OXLAMs) and reactive aldehydes, such as 4-hydroxy-2-nonenal (4-HNE), are present in heated vegetable oils and can be endogenously synthesized following consumption of dietary LA. OXLAMs have been implicated in cerebellar degeneration in chicks; 4-HNE is linked to neurodegenerative conditions in mammals. It unknown whether increasing dietary LA or OXLAMs alters the levels of oxidized fatty acids (oxylipins), precursor fatty acids, or 4-HNE in mammalian brain.

Molecular drift of the bride of sevenless (boss) gene in Drosophila

DNA sequences were determined for three to five alleles of the bride-of- sevenless (boss) gene in each of four species of Drosophila. The product of boss is a transmembrane receptor for a ligand coded by the sevenless gene that triggers differentiation of the R7 photoreceptor cell in the compound eye. Population parameters affecting the rate and pattern of molecular evolution of boss were estimated from the multinomial configurations of nucleotide polymorphisms of synonymous codons. The time of divergence between D. melanogaster and D. simulans was estimated as approximately 1 Myr, that between D. teissieri and D. yakuba as approximately 0.75 Myr, and that between the two pairs of sibling species as approximately 2 Myr. (The boss genes themselves have estimated divergence times approximately 50% greater than the species divergence times.) The effective size of the species was estimated as approximately 5 x 10(6), and the average mutation rate was estimated as 1-2 x 10(-9)/nucleotide/generation. The ratio of amino acid polymorphisms within species to fixed differences between species suggests that approximately 25% of all possible single-step amino acid replacements in the boss gene product may be selectively neutral or nearly neutral. The data also imply that random genetic drift has been responsible for virtually all of the observed differences in the portion of the boss gene analyzed among the four species.      

Interleukin-1-induced granulocytopenia and pulmonary leukostasis in rabbits

Pulmonary leukostasis is a postulated prerequisite lesion for acute lung injury. Interleukin-1 (IL-1) mediates components of the acute-phase response, stimulates granulocyte metabolism and secretion, and augments endothelial adhesiveness. We studied the effects of murine IL-1 infusion on circulating granulocytes, their sequestration within the pulmonary microvasculature, lung water, and bronchoalveolar lavage fluid (BALF) protein concentration in rabbits at 3 and 24 h after infusion. IL-1 administration induced significant (P less than 0.01) granulocytopenia compared with saline-injected controls and at 3 h induced significant increases in both mean alveolar septal wall granulocytes per high power field (HPF) (P less than 0.001) and mean myeloperoxidase (MPO) activity per gram lung tissue (P less than 0.001). At 24 h, IL-1 induced a marked granulocytosis and again significantly increased both mean alveolar septal wall granulocytes per HPF (P less than 0.001) and lung MPO (P less than 0.01). Increased lung water or BALF protein concentration could not be demonstrated in animals killed at either 3 or 24 h after IL-1 administration. Therefore, IL-1 can induce an early profound granulocytopenia followed by later granulocytosis, as well as sustained pulmonary leukostasis in the absence of detectable pulmonary edema formation or an alveolar-capillary leak.     

Augmented mitogenesis and impaired metabolic signaling mediated by a truncated insulin receptor

Recently, we have described a COOH-terminal deletion mutation of the human insulin receptor (HIR delta CT) that exhibits normal insulin-mediated kinase activity and endocytosis, but is inefficient in stimulating glucose transport and glycogen synthase (McClain, D. A., Maegawa, H., Levy, J., Huecksteadt, T., Dull, T. J., Lee, J., Ullrich, A., and Olefsky, J.M. (1988) J. Biol. Chem. 263, 8904-8911; Maegawa, H., McClain, D. A., Freidenberg, G., Olefsky, J. M., Napier, M., Lipari, T., Dull, T. J., Lee, J., and Ullrich, A. (1988) J. Biol. Chem. 263, 8912-8917). In this paper, we report that despite this defect in metabolic signaling, the truncated receptor exhibits augmented mitogenic activity compared to normal receptors. These results were verified in three independently isolated clones of Rat 1 fibroblasts transfected with the HIR delta CT cDNA. The increase in insulin sensitivity of mitogenic stimulation was proportional to the number of HIR delta CT receptors expressed on the cells. By contrast, only the cells with normal receptors and none of the HIR delta CT clones exhibit increased sensitivity for a metabolic action of insulin, the stimulation of glucose uptake. Stimulation of cells by other mitogens and autoradiographic analysis confirm that the enhanced mitogenic effects seen in HIR delta CT cells are attributable only to the presence of the truncated insulin receptors. These receptors mediate the tyrosine phosphorylation of a number of cellular proteins, and the pattern of these phosphorylations differs quantitatively from that seen in cells with normal receptors. We conclude: 1) The COOH terminus plays a role in signaling metabolic actions of insulin, perhaps through its recognition of substrates for the receptor kinase. 2) By contrast, the COOH terminus is an inhibitory regulator of mitogenesis, and removal of the terminal 43 amino acids converts the receptor from a moderately active growth signaler to a very active one. 3) The changes seen in biologic activities of the HIR delta CT receptor are associated with quantitative changes in substrate phosphorylation by the receptor kinase.     

The psu1+ amber suppressor gene of bacteriophage T4: identification of its amino acid and transfer RNA

Previous work identified the psu⁺₁ amber suppressor gene of bacteriophage T4. Analysis of protein arising from suppression now shows that psu⁺₁ specifies the insertion of serine in response to the amber triplet. The efficiency of suppression is 70%.The psu₁⁺ gene affects a serine transfer RNA coded by bacteriophage T4. Comparative ribonuclease T₁ fingerprint analysis of the serine transfer RNAs made by wild type T4 and psu⁺₁ strains shows a specific alteration in the patterns, presumably reflecting a mutational alteration in the anticodon of the transfer RNA. Mutations which result in the loss of suppressor activity define two genes: one is apparently the structural gene for the serine transfer RNA; the function of the second gene, M1, is less clear. Mutational inactivation of either gene prevents the appearance of the serine transfer RNA and a second transfer RNA, which has not yet been associated with its cognate amino acid. M1 mutants are also deficient in the production of several additional transfer RNA species, as well as several larger RNAs. The significance of these results in relation to transfer RNA biosynthesis is discussed.     

Ethanol exposure modulates hepatic S-adenosylmethionine and S-adenosylhomocysteine levels in the isolated perfused rat liver through changes in the redox state of the NADH/NAD system

Methionine metabolism is disrupted in patients with alcoholic liver disease, resulting in altered hepatic concentrations of S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), and other metabolites. The present study tested the hypothesis that reductive stress mediates the effects of ethanol on liver methionine metabolism. Isolated rat livers were perfused with ethanol or propanol to induce a reductive stress by increasing the NADH/NAD⁺ ratio, and the concentrations of SAM and SAH in the liver tissue were determined by high-performance liquid chromatography. The increase in the NADH/NAD⁺ ratio induced by ethanol or propanol was associated with a marked decrease in SAM and an increase in SAH liver content. 4-Methylpyrazole, an inhibitor the NAD⁺-dependent enzyme alcohol dehydrogenase, blocked the increase in the NADH/NAD⁺ ratio and prevented the alterations in SAM and SAH. Similarly, co-infusion of pyruvate, which is metabolized by the NADH-dependent enzyme lactate dehydrogenase, restored the NADH/NAD⁺ ratio and normalized SAM and SAH levels. The data establish an initial link between the effects of ethanol on the NADH/NAD⁺ redox couple and the effects of ethanol on methionine metabolism in the liver.