Sustainable Epoxidized Guayule Natural Rubber,Blends and Composites with Improved Oil Resistance and Greater Stiffness

Production of petroleum-based synthetic rubbers (SRs) causes an enormous carbon footprint for the rubber industry. Carbon footprint would be reduced if natural rubber (NR) could take a larger market share and replace significant quantities of SR. However, some SRs have higher oil resistance than NRs, and, in applications where these properties are needed, chemically modified NR will be required. Epoxidation is a chemical modification of NR which partially converts unsaturated bonds on the backbone of NR to epoxy groups. In this research, epoxidized guayule natural rubber (EGNR)/guayule natural rubber (GNR) blends and GNR were used to make carbon black (CB) filled composites. The processability, mechanical properties, swelling behaviors and dynamic mechanical properties were characterized at various epoxide fractions. Composites made with EGNR/GNR had higher oil resistance, wet traction and stiffness than GNR composites, although tensile strength and elongation at break were reduced by epoxidation. EGNR is expected to lead to the development of new NR products with similar properties to SR, eroding SR markets and increasing the sustainability of the rubber industry.     

Cyclopenta[cd]fluoranthene and its precursors in combustion exhausts: a survey of their bacterial mutagenic activity

Cyclopenta[cd]fluoranthene (1) and 3-ethynylfluoranthene (2) have both recently been identified in combustion exhausts. In this study, their mutagenic activities were compared to that of fluoranthene (3), one of the most abundant polycyclic aromatic hydrocarbons (PAHs) in combustion exhausts, in the Salmonella/microsome reversion assay (Ames assay) using S. typhimurium strain TA98. The mutagenicity of 1 was modest in comparison to other active cyclopenta PAHs. Unexpectedly, 2 was mutagenic both with and without exogenous metabolic activation (rat liver S9). Furthermore, cyclopenta[cd]fluoranthene-3,4-epoxide (6) was synthesized in order to evaluate its role as the ultimate mutagenic active form of 1. The epoxide 6 was a direct-acting mutagen. In addition, a pyrolysate containing a mixture of 1 (85%), 2 (2%), and 3 (13%) obtained by flash vacuum thermolysis of 3-(1-chloroethenyl)fluoranthene (2a) at 1,050 degrees C was also mutagenic, but a significant mutagenic response was detected only in the presence of S9 activation. The results of this study indicate that 1 and 2 can contribute to the mutagenic activity of combustion exhausts.     

In vitro kinetics of coumarin 3,4-epoxidation: application to species differences in toxicity and carcinogenicity.

Coumarin, a natural product and fragrance ingredient, is a well recognized rat liver toxicant, and dietary administration at toxic dosages increased the incidence of rat cholangiocarcinomas and parenchymal liver-cell tumors in a chronic bioassay. Hepatotoxicity in rats is site- and species-specific, and is thought to result from the formation of coumarin 3,4-epoxide and its rearrangement product, o-hydroxyphenylacetaldehyde (o-HPA). The goals of the current study were to describe the in vitro kinetics of the metabolic activation of coumarin, and determine whether species differences in susceptibility to liver injury correlate with coumarin bioactivation determined in vitro. Coumarin 3,4-epoxidation was quantified via the formation of o-HPA in pooled hepatic microsomes from female B6C3F1 mice, male F344 rats, and individual humans (n = 12 subjects), and the apparent kinetic constants for o-HPA production were calculated using nonlinear regression and fitting to either a one-enzyme or two-enzyme model. Eadie-Hofstee analyses indicated that o-HPA formation was biphasic in both rat and mouse liver. Although the apparent high affinity K:(m) in rat and mouse liver microsomes was 38.9 and 47.2 microM, respectively, the overall rate of o-HPA formation was far greater in mouse than in rat liver microsomes. Furthermore, the total clearance (CL(int)) of coumarin via o-HPA formation in mouse liver microsomes was 4-fold greater than in rat liver microsomes. Since mice are relatively resistant to hepatotoxicity, the data indicated that rates of o-HPA formation in rat and mouse liver microsomes were not directly predictive of liver toxicity in vivo, and further suggested that o-HPA detoxification played a role in modulating coumarin-mediated toxicity. The current studies also indicated that coumarin 3,4-epoxidation in human hepatic microsomes was minimal. In human liver microsomes (n = 12), the kinetics of o-HPA formation were best described by a single enzyme model, with the K(m) for o-HPA formation ranging from 1320-7420 microM. In the most active human sample, the intrinsic clearance of coumarin via the 3,4-epoxidation pathway was 1/9 and 1/38 that of the rat and mouse, respectively. The in vitro kinetics of o-HPA formation, and in particular, the large quantities of coumarin required for o-HPA production in human liver microsomes, strongly suggest that humans are unlikely to produce toxicologically relevant concentrations of this metabolite following low level coumarin exposures.     

A Proposed Mechanism For Vitamin K-Dependent γ-Carboxylation Of Glutamic Acid

The vitamin K-dependent carboxylation of peptide-bound glutamate requires vitamin K hydroquinone, oxygen, carbon dioxide and Glu-peptide. It is proposed that the oxidation of KH₂ to vitamin K 2,3-epoxide and water is coupled to γ-carboxyglutamate (Gla) synthesis.     

VO(Ⅱ)席夫碱配合物催化活性的研究

目的研究4种N,N-二(取代亚水杨基)-2,6-吡啶二氨合钒氧(Ⅱ)席夫碱配合物催化苯乙烯环氧化反应的催化活性.方法N2保护下,H2O2为氧源,VO(Ⅱ)席夫碱配合物为催化剂,25℃下苯乙烯发生环氧化反应;气相色谱法分离环氧化反应产物,标准样品定性、内标法定量测定.结果产物中有环氧化产物苯基环氧乙烷,催化剂苯环上有取代基的环氧化物产量高,取代基在5-位上的比在3-位上的环氧化物产量高.结论VO(Ⅱ)席夫碱配合物具有催化苯乙烯环氧化反应的催化活性;催化剂苯环上有取代基,对反应的活性和选择性有明显的影响、配体的空间构型对反应也有重要影响.     

低压固定床反应器中丙烯直接环氧化连续反应

在固定床反应器中,以自制挤条成型的ZSM-5型含钛(TS-1)分子筛为催化剂,采用丙烯气相进料,并预先与双氧水的甲醇溶液混合,系统考察了液体空速、丙烯与过氧化氢摩尔比、反应温度、双氧水甲醇混合溶液中双氧水浓度以及水含量等工艺条件对丙烯直接环氧化连续反应的影响。结果表明:当反应压力为0.7MPa,反应温度为50℃,进料中wH2O2=0.015,进料液体的质量空速为48h-1时,双氧水的转化率和环氧丙烷的选择性分别在90%和85%以上。     

脱氢枞胺键合交联聚苯乙烯树脂的制备

运用高分子反应法,制备脱氢枞胺键合交联聚苯乙烯树脂,反应分三步进行：醚化反应,双键环氧化和脱氢枞胺与环氧基开环反应,探讨了每一步合成的最佳工艺条件,通过红外光谱对该功能高分子进行了结构表征,并对该合成产物进行对映体分离的初步应用。     

Measurement and diagnostic use of hepatic cytochrome P450 metabolism of oleic acid in liver disease

Background: Oleic acid is a major systemically circulating fatty acid in humans with atheroprotective and immunomodulatory properties. As of today, the contribution of individual cytochrome P450 (CYP) mono‐oxygenases to the epoxidation of this fatty acid is unknown. Furthermore, the extent of the oleic acid oxidation product cis‐9,10‐epoxyoctadecanoic acid (cis‐EODA) in humans and its plasma levels in patients with impaired liver function are not known. Patients and methods: We studied cis‐EODA in plasma of patients suffering from chronic liver diseases, a condition that often displays impaired liver CYP enzyme activities. Fifteen CYP mono‐oxygenases were investigated in vitro as a potential source of cis‐EODA. Results: Strikingly, plasma levels of cis‐EODA were significantly repressed (P<0.0005) when patients with liver impairment (n=16) were compared with healthy subjects (n=14). Production of cis‐EODA was catalysed by CYP in the following order: 2C8, 2C9, 2C19, 3A4, 1A2 and CYP3A7. Conclusion: cis‐EODA plasma concentrations are decreased in hepatic disease with impaired liver function. Oleic acid is primarily oxidized to oleic acid oxide (cis‐EODA) by CYP2C and CYP3A mono‐oxygenases. The liver is the major organ responsible for the oxidation of oleic acid to cis‐EODA, and thus, cis‐EODA may be a suitable biomarker to assess liver function.     

Altered mechanisms underlying hypoxic dilation of skeletal muscle resistance arteries of hypertensive versus normotensive Dahl rats

OBJECTIVE: To determine mechanisms underlying hypoxic dilation of skeletal muscle resistance arteries from normotensive (NT) and hypertensive (HT) Dahl salt-sensitive (SS) rats. METHODS: Isolated gracilis arteries (GA) from both rat groups were viewed via television microscopy and vascular responses to a reduction in PO2 from 145 mm Hg to 40 mm Hg were measured with a video micrometer. Responses were determined following endothelium removal and following inhibition of specific biochemical pathways regulating vascular tone. RESULTS: Hypoxic dilation was impaired in HT rats versus NT controls. Endothelium removal abolished hypoxic dilation in NT rats, although a significant dilation to hypoxia remained in vessels from HT animals. Inhibition of cytochrome P450 (CP450) 4A enzymes blunted hypoxic dilation in both groups, while inhibition of epoxyeicosatrienoic acid (EET) production impaired responses in NT rats only. Inhibition of 20-hydroxyeicosatetraenoic acid (20-HETE) production or blockade of membrane receptors for 20-HETE reduced hypoxic dilation in HT rats, with minimal effects in NT animals. Nitric oxide synthase inhibition had no effect on hypoxic dilation in either group, while cyclooxygenase inhibition significantly reduced this response in both groups. CONCLUSIONS: These results suggest that the mechanisms of hypoxic dilation in GA from NT Dahl-SS rats are altered with HT, impairing the response to reduced PO2. While hypoxia induces substantial prostanoid release in both groups, the role of CP450 4A enzymes is shifted from EET production in NT rats toward inhibition of 20-HETE production in HT rats.     

N,N''-双(1-羟基甲基-2,3-二羟基丙基)-2,3,5,6-四碘对苯二甲酰胺的合成

目的设计并合成标题化合物。方法以1,4-丁烯二醇为原料,经过酯化、环氧化、氨解开环,再与四碘对苯二甲酰氯反应合成目标产物。结果产物经红外、核磁共振氢谱、元素分析得到确认。结论成功的合成了所设计的标题化合物,有助于新一代四碘苯类非离子型X线造影剂的研制。