Release Of Dimers Research Articles

Growth Hormone Dimer Release In Untrained Men And Women After Acute Resistance Exercise

Growth Hormone Dimer Release In Untrained Men And Women After Acute Resistance Exercise

A Molecular Tool for Carbon Transfer in Mechanosynthesis

Proposed advanced mechanosynthetic systems [1] require molecular tools able to bind and transfer reactive moieties with high reliability at 300 K (failure rates << 10–10 per transfer operation). Screening of a large number of candidate tools at the AM1 level enabled the identification of a structure, DC10c, that is calculated (at the B3LYP/6- 31G(d,p) level) to meet these stringent requirements when used to transfer carbon dimers to any of a target class of graphene-, nanotube-, and diamond-like structures [2]. The favorable energy of transfer (exoergic by a mean energy ≥ 0.261 aJ per dimer) results from avoidance of the generation of high-energy radical sites during dimer release by means of π-delocalization to form a strained aromatic ring on the binding face of the empty structure. These energies are compatible with transfer-failure rates ~ 10–24 per operation at 300 K, and overall failure rates << 10–10.

Carbon monoxide-releasing molecules: characterization of biochemical and vascular activities.

Carbon monoxide (CO) is generated in living organisms during the degradation of heme by the enzyme heme oxygenase, which exists in constitutive (HO-2 and HO-3) and inducible (HO-1) isoforms. Carbon monoxide gas is known to dilate blood vessels in a manner similar to nitric oxide and has been recently shown to possess antiinflammatory and antiapoptotic properties. We report that a series of transition metal carbonyls, termed here carbon monoxide-releasing molecules (CO-RMs), liberate CO to elicit direct biological activities. Specifically, spectrophotometric and NMR analysis revealed that dimanganese decacarbonyl and tricarbonyldichlororuthenium (II) dimer release CO in a concentration-dependent manner. Moreover, CO-RMs caused sustained vasodilation in precontracted rat aortic rings, attenuated coronary vasoconstriction in hearts ex vivo, and significantly reduced acute hypertension in vivo. These vascular effects were mimicked by induction of HO-1 after treatment of animals with hemin, which increases endogenously generated CO. Thus, we have identified a novel class of compounds that are useful as prototypes for studying the bioactivity of CO. In the long term, transition metal carbonyls could be utilized for the therapeutic delivery of CO to alleviate vascular- and immuno-related dysfunctions. The full text of this article is available at http://www.circresaha.org.

Cyclodimers of p‐coumaric and ferulic acids in the cell walls of tropical grasses

AbstractCell walls from leaves and stems of three tropical grasses (Setaria anceps cv Nandi (Schumach) Moss), pangola grass Digitara decumbens Stent and spear grass Heteropogon contortus (L) Beauv ex Roemer & Schultes were extracted with alkali, and ether‐soluble fractions were prepared from the acidified solutions. Cyclobutane dimers derived from p‐coumaric acid (CA: 3‐(4‐hydroxypheny) propenoic acid) and ferulic acid (FA: 3‐(4‐hydroxy‐3‐methoxyphenyl) propenoic acid) were found in all plant residues. Structural information on the dimers was obtained by gas chromatography‐mass spectrometry. Stem cell walls differed from those of leaf in having major dimer components which contained residues tentatively identified as coniferyl alcohol (3‐(4‐hydroxy‐3‐methoxyphenyl)‐2‐propen‐l‐ol). Species differences in leaf cell wall cyclodimers were evident. Pangola and setaria grasses had dimers mainly derived from FA, whereas spear grass had over 70% of dimers derived from CA. Di‐esterification of some dimers in the cell walls was confirmed by the release of dimers containing the reduced forms of CA and FA (coumaryl and coniferyl alcohols respectively) when leaf cell walls were extracted with borohydride. Head to tail dimerisation giving derivatives of truxillic acid (t‐2, c‐4‐diphenyl‐r‐l, t‐3‐cyclobutanedicarboxylic acid) predominated, although evidence was obtained for the presence of head‐to‐head coumaric acid dimers (derivatives of truxinic acid, t‐3, t‐4‐diphenyl‐rl, c‐2‐cyclobutanedicarboxylic acid) in setaria stem and spear grass leaf. The results suggested that cyclodimers in grass cell walls occurred in cross‐linking structures of varying complexity between macromolecules, where they would possibly contribute to fibre strength and thus have an adverse efect on the nutritional value of forage.

Differential Secretion ofO-Glycosylated Gonadotropinα-Subunit and Luteinizing Hormone (LH) in the Presence of LH-Releasing Hormone

The pituitary hormones LH, FSH, and TSH are secreted as dimers of two subunits, alpha and beta. The alpha-subunit, identical in all three hormones, is produced by the pituitary in excess of beta and secreted as free subunit. Bovine free alpha does not combine with purified beta-subunit and contains an extra O-linked oligosaccharide not found on dimer alpha. We have developed an assay to quantitate this modified form of alpha in the medium of incubated steer pituitary slices. The assay, based on reverse phase HPLC analysis of radiolabeled alpha-subunit tryptic peptides, shows that under basal conditions, 75% of secreted free alpha is O-glycosylated. When the secretagogue LHRH is added to the slices, a 14-fold increase in LH dimer release is observed, but secretion of the modified alpha is increased by only 2-fold. Our results indicate that the majority of free alpha-subunit secreted by the pituitary contains O-linked oligosaccharide, and that secretion of this form of alpha differs from that of LH dimer.

Repair of ultraviolet-damaged DNA in Micrococcus lysodeikticus: II. In vivo investigation on endonuclease activity specific for ultraviolet-irradiated DNA

1. 1. An investigation was carried out to clarify the in vivo role of an endonuclease found in extracts of Micrococcus lysodeikticus, which induces single-strand breaks in ultraviolet-irradiated DNA but not in non-irradiated DNA (referred to as UV-endonuclease). For this purpose, the occurrence of single-strand break, pyrimidine dimer excision and DNA breakdown after ultraviolet irradiation were examined in mutants of this organism. 2. 2. An ultraviolet-sensitive mutant, G7, did not show single-strand breaks and pyrimidine dimer excision after ultraviolet irradiation. This mutant was also defective in UV-endonuclease activity in its extract. However, transformants to ultraviolet resistance of G7, which were obtained by treatment with wild-type DNA and subsequent selection on nutrient agar containing mitomycin C, did not display UV-endonuclease activity in their extracts, but they could nevertheless produce single-strand breaks in their DNA and rejoin them in vivo. Thus, a discrepancy was observed between in vivo and in vitro endonuclease activity. The same relation was also obtained with Strain 1312 which displayed little UV-endonuclease activity in extracts but was ultraviolet-resistant. It seems that the in vivo activity of endonuclease specific for ultraviolet-irradiated DNA is essential for dark repair. 3. 3. Slower rates of pyrimidine dimer excision and subsequent rejoining of the gaps were observed in the transformant and Strain 1312. UV-endonuclease might participate in the release of dimer from ultraviolet-irradiated DNA, but the mechanism is unknown. 4. 4. An ultraviolet-sensitive, hcr − mutant, UV s N1, showed DNA degradation. In alkaline sucrose gradient centrifugation, however, single-strand breaks and rejoining were observed in this type of mutant. 5. 5. The relationship between the in vivo activity and the in vitro activity (UV-endonuclease) inducing single-strand breaks in ultraviolet-irradiated DNA is considered and the natures of the mutants are discussed from this point of view.

Mechanism of repair of DNA in bacteriophage. I. Excision of pyrimidine dimers from ultraviolet-irradiated DNA by an extract of T4-infected cells.

Abstract When [14C]thymine-labeled T4 DNA, after exposure to ultraviolet light, was incubated with an extract of T4-infected Escherichia coli, pyrimidine dimers were selectively released into the acid-soluble fraction; the rate of release of dimers was about five times greater than that for thymine. The reaction requires Mg2+ and proceeds at pH 7 to 8 in the dark. The amount of thymine and thymine-containing dimers released from the ultraviolet-irradiated DNA into the acid-soluble fraction was determined by Dowex 1 column chromatography. Dimers lost from the DNA were almost quantitatively recovered, in the form of nuoleotides but not of free bases or nucleosides, in the acid-soluble fraction. As a result of the specific release of dimers, the content of dimers in the DNA decreases progressively during the incubation. Thus the excision in vitro is similar to the reaction observed in vivo in ultraviolet-resistant cells. An extract of normal cells does not exhibit the preferential release of dimers even when the homologous E. coli DNA is used as substrate. Only a small amount of dimers is released into the acid-soluble fraction during the incubation of irradiated E. coli or T4 DNA with the normal cell extract. Thus the level of dimer-excising activity of normal cells, if any, must be very low compared with that of T4-infected cells. It is likely that enzyme(s) responsible for excision of dimers is induced by infection with T4.

Mechanism of repair of DNA in bacteriophage. II. Inability of ultraviolet-sensitive strains of bacteriophage in inducing an enzyme activity to excise pyrimidine dimers.

Abstract T4 v 1 and T4 v 2 , mutants of bacteriophage T4 having increased sensitivity to ultraviolet radiation, are unable to induce an enzyme activity which excises pyrimidine dimers from ultraviolet-irradiated DNA. Bacteriophage T2, which is as sensitive to ultraviolet light as the T4 v mutants, also fails to induce the activity. These results suggest that the T4-induced dimer-excising activity may be concerned with dark repair of ultraviolet-damaged DNA in vivo . Extracts of T4-infected cells are capable of inducing single-stranded interruptions specifically in ultraviolet-irradiated DNA. The process appears to be associated with the excision of dimers, since extracts of T4 v 1 -, T4 v 2 - and T2-infected cells, which contain no dimer-excising activity, do not induce such strand interruptions. The formation of breaks in irradiated DNA by the T4-infected cell extract occurs in the presence of EDTA. The T4-induced enzyme activity acts on DNA's of varied origins. The selective release of dimers as well as the formation of breaks in irradiated DNA take place when irradiated T2 or Escherichia coli DNA is treated with the extract of T4-infected cells. This is compatible with the finding in vivo that the v + gene product enhances the survival of not only T4 but also T2 and E. coli exposed to ultraviolet radiation.