Sharp intense line in the bioluminescence emission of the firefly

Numerous investigations have been carried out on the spectral distribution of the light of different species of fireflies. Here we record the emission spectrum of the Indian species of the firefly Luciola praeusta Kiesenwetter 1874 (Coleoptera : Lampyridae : Luciolinae) on a color film. Green and red color-sectors, with an intense yellow one in between, appear in this spectrum. Intensity profile of this spectrum reveals a hitherto undetected strong narrow yellow line, which lies within the full-width-at-half maximum (FWHM) of the intensity profile. The spectrum recorded in a high-resolution spectrometer confirms the presence of this sharp intense line. This finding lends support to an earlier drawn analogy between the in vivo emission of the firefly and laser light.     

Effects of retinoid beta-glucuronides and N-retinoyl amines on the differentiation of HL-60 cells in vitro

Retinoyl beta-glucuronide and retinyl beta-glucuronide, which are naturally occurring water-soluble metabolites of vitamin A, induce the granulocytic differentiation of HL-60 cells in vitro, as evidenced by an increased reduction of nitroblue tetrazolium. The relative effectiveness of various retinoids in differentiation is retinoic acid greater than retinoyl beta-glucuronide greater than retinyl beta-glucuronide. Under the selected assay conditions, retinol, hydroxyphenyl-retinamide, retinamide, and N-retinoyl-phenylalanine are essentially inactive in differentiation. At concentrations of retinoids from 10(-9) to 10(-5) M, cell viability was best with the retinoid beta-glucuronides and retinamide, less with retinoic acid and retinol, and poorest with the N-retinoyl aromatic amines. Cellular growth was depressed only slightly by retinyl beta-glucuronide and retinamide, but to a greater degree by the other derivatives. Retinoyl beta-glucuronide was hydrolyzed in part to retinoic acid, whereas retinyl beta-glucuronide was cleaved to retinol, if at all, at a very slow rate. Under the selected assay conditions, retinoic acid and the retinoid beta-glucuronides primarily induce the differentiation of HL-60 cells, whereas the N-retinoyl aromatic amines show cytotoxicity.     

Chemical synthesis of all-trans-[11-3H]retinoyl beta-glucuronide and its metabolism in rats in vivo.

All-trans-[11-3H]retinoyl beta-glucuronide (RAG) was synthesized in a single step from all-trans-[11-3H]retinoyl fluoride, with a 24% yield. After its intraperitoneal injection into rats, RAG was detected in the blood, liver, intestine and kidney during the following 24 h period. Although the concentration of radiolabelled metabolites decreased with time, RAG predominated at nearly all times in nearly all tissues. Small amounts of retinoic acid (RA) were also universally present, together with unidentified polar metabolites and small amounts of non-polar esters of RA. The major excretion products of RAG in faeces and urine were RA and polar metabolites. Thus RAG, although converted in part to RA in vivo, persists as a major component in blood and tissues for at least 24 h. These observations support the concept that the retinoid beta-glucuronides might serve a physiologically significant role in the function of vitamin A.     

Cloning and sequencing of the peroxisomal amine oxidase gene from Hansenula polymorpha

We have cloned the AMO gene, encoding the microbody matrix enzyme amine oxidase (EC 1.4.3.6) from the yeast Hansenula polymorpha. The gene was isolated by differential screening of a cDNA library, immunoselection, and subsequent screening of a H. polymorpha genomic library. The nucleotide sequence of a 3.6 kilobase stretch of DNA containing the amine oxidase (AMO) gene was determined. The AMO gene contains an open reading frame of 692 amino acids, with a relative molecular mass of 77,435. The 5' and 3' ends of the gene were mapped and show that the transcribed region measures 2134 nucleotides. The derived amino-acid sequence was confirmed by sequencing an internal proteolytic fragment of the purified protein. Amine oxidase contains the tripeptide sequence Ser-Arg-Leu, located 9 residues from the carboxy terminus, which may represent the topogenic signal for protein import into microbodies.     

Preparation of retinamides by use of retinoyl fluoride

Retinoyl fluoride (2) prepared from retinoic acid (1) by reaction with diethylaminosulfurtrifluoride is a stable crystalline compound not easily hydrolyzed by water. By reacting retinoyl fluoride with water-soluble amines in the presence of sodium bicarbonate, retinamide (4), N-retinoyl glycine (6), N-retinoyl DL-phenylalanine (7), alpha-N-retinoyl-L-lysine (11), N-retinoyl 4-aminophenol (4-hydroxyphenylretinamide) (8), and N-retinoyl-2-amino-2-deoxy-D-glucose (2-deoxy-D-glucose-2-retinamide) (9) have been prepared in good yields and characterized by UV absorption, 1H NMR, IR spectra, mass spectrometry, and elemental analysis.     

Naturally occurring anhydrovitamin A2: Transformation into retinene2

1. ;Naturally occurring anhydrovitamin A(2)' obtained from the liver oil of freshwater fish Bagarius bagarius yielded, after six-stage chromatography, a pure product showing characteristic bands at 350, 368 (E(1%) (1cm.) 1006) and 390mmu in ethanol, and producing a green colour with antimony trichloride (E(1%) (1cm.) 1884 at 693mmu). 2. On distribution of the material between light petroleum and 95% methanol, 70% of it is found in methanol, which points to its hydroxylic character. 3. It gives an acetyl derivative, from which the original hydroxy compound can be regenerated on hydrolysis. 4. The infrared spectrum shows, besides other bands, one at 3460cm.(-1) attributable to a hydroxy group. 5. On passing a light-petroleum solution of naturally occurring anhydrovitamin A(2) through manganese dioxide a 6% conversion into retinene(2) is observed. 6. A 3-hydroxyanhydroretinol structure is proposed for naturally occurring anhydrovitamin A(2) and a mechanism of its transformation into retinene(2) on this basis is suggested.     

Oxidation of zeaxanthin: Isolation and properties of 3-hydroxyretinene

1. Anthers of Delonix regia flowers are a rich source of zeaxanthin. 2. Oxidation of zeaxanthin with hydrogen peroxide in the presence of osmium tetroxide results in the formation of 3-hydroxyretinene as one of the products. 3. 3-Hydroxyretinene gives 3-acetoxyretinene with acetic anhydride, and an oxime with hydroxylamine hydrochloride. 4. Reduction of 3-hydroxyretinene with sodium borohydride yields 3-hydroxyvitamin A. 5. Treatment of 3-hydroxyvitamin A with dry ethanolic hydrogen chloride results in the formation of 3-ethoxyanhydrovitamin A (anhydrovitamin A₂) and a compound that resembles naturally occurring anhydrovitamin A₂.     

Formation of vitamin A in a freshwater fish. Isolation of retinoic acid.

The intestines of freshly caught Saccobranchus fossilis (a freshwater fish that contains dehydroretinol) became free from carotenoids and from vitamin A when the fish were starved for about 20 days. When beta-carotene was administered to such fish, retinoic acid could be isolated from the intestines after approx. 4h. When lutein was administered to such fish, dehydroretinol and 3-hydroxyretinol could be isolated from the intestines after approx. 5h.     

Dissociation of intracellular lysosomal rupture from the cell death caused by silica

The relationship between intracellular lysosomal rupture and cell death caused by silica was studied in P388d(1) macrophages. After 3 h of exposure to 150 μg silica in medium containing 1.8 mM Ca(2+), 60 percent of the cells were unable to exclude trypan blue. In the absence of extracellular Ca(2+), however, all of the cells remained viable. Phagocytosis of silica particles occurred to the same extent in the presence or absence of Ca(2+). The percentage of P388D(1) cells killed by silica depended on the dose and the concentration of Ca(2+) in the medium. Intracellular lyosomal rupture after exposure to silica was measured by acridine orange fluorescence or histochemical assay of horseradish peroxidase. With either assay, 60 percent of the cells exposed to 150 μg silica for 3 h in the presence of Ca(2+) showed intracellular lysosomal rupture, was not associated with measureable degradation of total DNA, RNA, protein, or phospholipids or accelerated turnover of exogenous horseradish peroxidase. Pretreatment with promethazine (20 μg/ml) protected 80 percent of P388D(1) macrophages against silica toxicity although lysosomal rupture occurred in 60-70 percent of the cells. Intracellular lysosomal rupture was prevented in 80 percent of the cells by pretreatment with indomethacin (5 x 10(-5)M), yet 40-50 percent of the cells died after 3 h of exposure to 150 μg silica in 1.8 mM extracellular Ca(2+). The calcium ionophore A23187 also caused intracellular lysosomal rupture in 90-98 percent of the cells treated for 1 h in either the presence or absence of extracellular Ca(2+). With the addition of 1.8 mM Ca(2+), 80 percent of the cells was killed after 3 h, whereas all of the cells remained viable in the absence of Ca(2+). These experiments suggest that intracellular lysosomal rupture is not causally related to the cell death cause by silica or {"type":"entrez-nucleotide","attrs":{"text":"A23187","term_id":"833253","term_text":"A23187"}}A23187. Cell death is dependent on extracellular Ca(2+) and may be mediated by an influx of these ions across the plasma membrane permeability barrier damaged directly by exposure to these toxins.