Regioselective Arylboration of 1,3-Butadiene.
Ontology highlight
ABSTRACT:
SUBMITTER: Bergmann AM
PROVIDER: S-EPMC8046179 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:A method for the regioselective arylboration of isoprene and its derivatives is presented. These reactions allow for the synthesis of useful building blocks from simple components. Through these studies, an unusual additive effect with DMAP has been uncovered that allows for altered reactivity and the formation of quaternary carbon centers. The utility of this method is demonstrated toward the formal synthesis of mesembrine.
| S-EPMC5606143 | biostudies-literature
Project description:The crystal structure of the title compound, [Fe(C(4)H(6))(CO)(3)], was previously reported by Mills & Robinson [Acta Cryst. (1963) ?, 16, 758-761]. The compound crystallizes in the centrosymmetric space goup Pnma with the complex located on a mirror plane. The redetermination of this structure at 100?K yielded almost equilibrated C-C bond lengths within the butadiene ligand according to a metal-to-ligand bonding-back-bonding mechanism. The C-C bond lengths presented herein are significantly shorter than those reported earlier. The H-atom positions that have not been reported so far were located by difference Fourier maps. The positional parameters of all H atoms and individual U(iso) values were refined freely.
| S-EPMC3009352 | biostudies-literature
Project description:In the title complex, [Cr(C(4)H(6))(CO)(4)], the Cr(0) atom shows a distorted octa-hedral environment from four C atoms of the carbonyl ligands and the two π-bonds of the s-cis-1,3-butadiene ligand. The complex has an approximate non-crystallographic mirror symmetry m passing through the chromium atom, two carbonyl ligands and the mid-point of the central C-C bond of the s-cis-1,3-butadiene ligand. The C-C bond lengths in the s-cis-1,3-butadiene ligand alternate, the terminal distances being shorter than the central distance.
| S-EPMC3052012 | biostudies-literature
Project description:The 1,4-functionalization of dienes is a synthetically useful strategy for incorporating molecular complexity into a class of simple substrates. We report the aminoarylation of acyclic and cyclic 1,3-dienes via the sequential [4+2] cycloaddition with a sulfurdiimide reagent and copper-catalyzed allylic substitution with Grignard reagents. The regioselective and diastereoselective aminoarylation of unsymmetrical dienes is also presented, which highlights the utility of this method for generating products with multiple functional groups and stereocenters.
| S-EPMC4242432 | biostudies-literature
Project description:The important industrial and environmental carcinogen 1,3-butadiene (BD) forms a range of adenine adducts in DNA, including N6-(2-hydroxy-3-buten-1-yl)-2'-deoxyadenosine (N6-HB-dA), 1,N6-(2-hydroxy-3-hydroxymethylpropan-1,3-diyl)-2'-deoxyadenosine (1,N6-HMHP-dA), and N6,N6-(2,3-dihydroxybutan-1,4-diyl)-2'-deoxyadenosine (N6,N6-DHB-dA). If not removed prior to DNA replication, these lesions can contribute to A ? T and A ? G mutations commonly observed following exposure to BD and its metabolites. In this study, base excision repair of BD-induced 2'-deoxyadenosine (BD-dA) lesions was investigated. Synthetic DNA duplexes containing site-specific and stereospecific (S)-N6-HB-dA, (R,S)-1,N6-HMHP-dA, and (R,R)-N6,N6-DHB-dA adducts were prepared by a postoligomerization strategy. Incision assays with nuclear extracts from human fibrosarcoma (HT1080) cells have revealed that BD-dA adducts were recognized and cleaved by a BER mechanism, with the relative excision efficiency decreasing in the following order: (S)-N6-HB-dA > (R,R)-N6,N6-DHB-dA > (R,S)-1,N6-HMHP-dA. The extent of strand cleavage at the adduct site was decreased in the presence of BER inhibitor methoxyamine and by competitor duplexes containing known BER substrates. Similar strand cleavage assays conducted using several eukaryotic DNA glycosylases/lyases (AAG, Mutyh, hNEIL1, and hOGG1) have failed to observe correct incision products at the BD-dA lesion sites, suggesting that a different BER enzyme may be involved in the removal of BD-dA adducts in human cells.
| S-EPMC5098428 | biostudies-literature
Project description:We describe a cobalt-catalyzed hydroacylation of 1,3-dienes with non-chelating aldehydes. Aromatic aldehydes provide 1,4-addition products as the major isomer, while aliphatic aldehydes favor 1,2-hydroacylation products. The kinetic profile supports an oxidative cyclization mechanism involving a cobaltacycle intermediate that undergoes transformation with high regio- and stereoselectivity.
| S-EPMC4117386 | biostudies-literature
Project description:Human exposure to 1,3-butadiene (BD) present in automobile exhaust, cigarette smoke, and forest fires is of great concern because of its potent carcinogenicity. The adverse health effects of BD are mediated by its epoxide metabolites such as 3,4-epoxy-1-butene (EB), which covalently modify genomic DNA to form promutagenic nucleobase adducts. Because of their direct role in cancer, BD-DNA adducts can be used as mechanism-based biomarkers of BD exposure. In the present work, a mass spectrometry-based methodology was developed for accurate, sensitive, and precise quantification of EB-induced N-7-(1-hydroxy-3-buten-2-yl) guanine (EB-GII) DNA adducts in vivo. In our approach, EB-GII adducts are selectively released from DNA backbone by neutral thermal hydrolysis, followed by ultrafiltration, offline HPLC purification, and isotope dilution nanoLC/ESI(+)-HRMS(3) analysis on an Orbitrap Velos mass spectrometer. Following method validation, EB-GII lesions were quantified in human fibrosarcoma (HT1080) cells treated with micromolar concentrations of EB and in liver tissues of rats exposed to sub-ppm concentrations of BD (0.5-1.5 ppm). EB-GII concentrations increased linearly from 1.15?±?0.23 to 10.11?±?0.45 adducts per 10(8) nucleotides in HT1080 cells treated with 0.5-10 ?M EB. EB-GII concentrations in DNA of laboratory rats exposed to 0.5, 1.0, and 1.5 ppm BD were 0.17?±?0.05, 0.33?±?0.08, and 0.50?±?0.04 adducts per 10(8) nucleotides, respectively [corrected]. We also used the new method to determine the in vivo half-life of EB-GII adducts in rat liver DNA (2.20?±?0.12 d) and to detect EB-GII in human blood DNA. To our knowledge, this is the first application of nanoLC/ESI(+)-HRMS(3) Orbitrap methodology to quantitative analysis of DNA adducts in vivo.
| S-EPMC5076477 | biostudies-literature
Project description:We hypothesize that the differences in lung cancer risk in Native Hawaiians, whites, and Japanese Americans may, in part, be due to variation in the metabolism of 1,3-butadiene, one of the most abundant carcinogens in cigarette smoke.We measured two biomarkers of 1,3-butadiene exposure, monohydroxybutyl mercapturic acid (MHBMA) and dihydroxybutyl mercapturic acid (DHBMA), in overnight urine samples among 584 Native Hawaiians, Japanese Americans, and white smokers in Hawaii. These values were normalized to creatinine levels. Ethnic-specific geometric means were compared adjusting for age at urine collection, sex, body mass index, and nicotine equivalents (a marker of total nicotine uptake).We found that mean urinary MHBMA differed by race/ethnicity (P = 0.0002). The values were highest in whites and lowest in Japanese Americans. This difference was only observed in individuals with the GSTT1-null genotype (P = 0.0001). No difference across race/ethnicity was found among those with at least one copy of the GSTT1 gene (P ? 0.72). Mean urinary DHBMA did not differ across racial/ethnic groups.The difference in urinary MHBMA excretion levels from cigarette smoking across three ethnic groups is, in part, explained by the GSTT1 genotype. Mean urinary MHBMA levels are higher in whites among GSTT1-null smokers.The overall higher excretion levels of MHBMA in whites and lower levels of MHBMA in Japanese Americans are consistent with the higher lung cancer risk in the former. However, the excretion levels of MHBMA in Native Hawaiians are not consistent with their disease risk and thus unlikely to explain their high risk of lung cancer.
| S-EPMC4220266 | biostudies-literature
Project description:The anionic polymerization of styrene and 1,3-butadiene in the presence of phosphazene bases (t-BuP4, t-BuP2 and t-BuP1), in benzene at room temperature, was studied. When t-BuP1 was used, the polymerization proceeded in a controlled manner, whereas the obtained homopolymers exhibited the desired molecular weights and narrow polydispersity (Ð < 1.05). In the case of t-BuP2, homopolymers with higher than the theoretical molecular weights and relatively low polydispersity were obtained. On the other hand, in the presence of t-BuP4, the polymerization of styrene was uncontrolled due to the high reactivity of the formed carbanion. The kinetic studies from the polymerization of both monomers showed that the reaction rate follows the order of [t-BuP4]/[sec-BuLi] >>> [t-BuP2]/[sec-BuLi] >> [t-BuP1]/[sec-BuLi] > sec-BuLi. Furthermore, the addition of t-BuP2 and t-BuP1 prior the polymerization of 1,3-butadiene allowed the synthesis of polybutadiene with a high 1,2-microstructure (~45 wt %), due to the delocalization of the negative charge. Finally, the one pot synthesis of well-defined polyester-based copolymers [PS-b-PCL and PS-b-PLLA, PS: Polystyrene, PCL: Poly(ε-caprolactone) and PLLA: Poly(L-lactide)], with predictable molecular weights and a narrow molecular weight distribution (Ð < 1.2), was achieved by sequential copolymerization in the presence of t-BuP2 and t-BuP1.
| S-EPMC6418745 | biostudies-literature
Project description:N(6)-(2-Hydroxy-3-buten-1-yl)-2'-deoxyadenosine (N(6)-HB-dA I) and N(6),N(6)-(2,3-dihydroxybutan-1,4-diyl)-2'-deoxyadenosine (N(6),N(6)-DHB-dA) are exocyclic DNA adducts formed upon alkylation of the N(6) position of adenine in DNA by epoxide metabolites of 1,3-butadiene (BD), a common industrial and environmental chemical classified as a human and animal carcinogen. Since the N(6)-H atom of adenine is required for Watson-Crick hydrogen bonding with thymine, N(6)-alkylation can prevent adenine from normal pairing with thymine, potentially compromising the accuracy of DNA replication. To evaluate the ability of BD-derived N(6)-alkyladenine lesions to induce mutations, synthetic oligodeoxynucleotides containing site-specific (S)-N(6)-HB-dA I and (R,R)-N(6),N(6)-DHB-dA adducts were subjected to in vitro translesion synthesis in the presence of human DNA polymerases ?, ?, ?, and ?. While (S)-N(6)-HB-dA I was readily bypassed by all four enzymes, only polymerases ? and ? were able to carry out DNA synthesis past (R,R)-N(6),N(6)-DHB-dA. Steady-state kinetic analyses indicated that all four DNA polymerases preferentially incorporated the correct base (T) opposite (S)-N(6)-HB-dA I. In contrast, hPol ? was completely blocked by (R,R)-N(6),N(6)-DHB-dA, while hPol ? and ? inserted A, G, C, or T opposite the adduct with similar frequency. HPLC-ESI-MS/MS analysis of primer extension products confirmed that while translesion synthesis past (S)-N(6)-HB-dA I was mostly error-free, replication of DNA containing (R,R)-N(6),N(6)-DHB-dA induced significant numbers of A, C, and G insertions and small deletions. These results indicate that singly substituted (S)-N(6)-HB-dA I lesions are not miscoding, but that exocyclic (R,R)-N(6),N(6)-DHB-dA adducts are strongly mispairing, probably due to their inability to form stable Watson-Crick pairs with dT.
| S-EPMC4704788 | biostudies-literature