Sustainable polymers for the next generation technologies

Many polymers synthesized today suffer from two major faults: non-degradability and lack of sustainability. While some of these polymers are recyclable, the consumer application may not align easily with recycling processes. For example, food contamination makes recycling very difficult, reducing sustainability for many polymer products. Creating degradable polymers is another strategy to improve sustainability. Degradability can be invoked in the material via an introduction of degradable functionalities. One way to accomplish this can be through copolymerization; however, copolymerization is typically limited to structurally similar monomers. In these studies, copolymerization of structurally distinct lactones and epoxides utilizing the classical Vandenberg catalyst was explored. Similarly, copolymerization of carbonates and lactones, epoxides and anhydrides were also explored utilizing the bis(μ-alkoxo)bis(alkylaluminum) catalysts. Sustainability can also be improved by obtaining monomers from sources other than petroleum, such as biological systems. Cells can be engineered to produce various products or to increase production of existing products that are relevant as polymer feedstocks. Another angle to achieve sustainability is through the use of the polymer. For example, utilizing polymers as barrier materials to extend produce shelf-life would be a great benefit. Lastly, sustainability can be achieved through the education of young scholars to be aware of the issues and opportunities in polymer engineering. This dissertation explores the aforementioned topics and provides support for the development of more sustainable polymers with collected data. Through the studies described herein, new polymerization methodologies were established for both sustainable and degradable polymers, and newly designed polymers were applied to the field of polymer electrolytes and plastic packagingChemical Engineerin

Interactions of the Gasotransmitters Contribute to Microvascular Tone (Dys)regulation in the Preterm Neonate

Background & Aims Hydrogen sulphide (H2S), nitric oxide (NO), and carbon monoxide (CO) are involved in transitional microvascular tone dysregulation in the preterm infant; however there is conflicting evidence on the interaction of these gasotransmitters, and their overall contribution to the microcirculation in newborns is not known. The aim of this study was to measure the levels of all 3 gasotransmitters, characterise their interrelationships and elucidate their combined effects on microvascular blood flow. Methods 90 preterm neonates were studied at 24h postnatal age. Microvascular studies were performed by laser Doppler. Arterial COHb levels (a measure of CO) were determined through co-oximetry. NO was measured as nitrate and nitrite in urine. H2S was measured as thiosulphate by liquid chromatography. Relationships between levels of the gasotransmitters and microvascular blood flow were assessed through partial correlation controlling for the influence of gestational age. Structural equation modelling was used to examine the combination of these effects on microvascular blood flow and derive a theoretical model of their interactions. Results No relationship was observed between NO and CO (p = 0.18, r = 0.18). A positive relationship between NO and H2S (p = 0.008, r = 0.28) and an inverse relationship between CO and H2S (p = 0.01, r = -0.33) exists. Structural equation modelling was used to examine the combination of these effects on microvascular blood flow. The model with the best fit is presented. Conclusions The relationships between NO and H2S, and CO and H2S may be of importance in the preterm newborn, particularly as NO levels in males are associated with higher H2S levels and higher microvascular blood flow and CO in females appears to convey protection against vascular dysregulation. Here we present a theoretical model of these interactions and their overall effects on microvascular flow in the preterm newborn, upon which future mechanistic studies may be based.The authors would like to acknowledge the parents of the neonates enrolled in the 2CANS study for their participation, the staff of the Kaleidoscope Neonatal Intensive Care Unit at the John Hunter Children’s Hospital, and Kimberly-Clark Australia for providing the diapers used in this stud

Treatment of chronic hemodialysis patients with low-dose fenofibrate effectively reduces plasma lipids and affects plasma redox status

Dyslipidemia is common in chronic hemodialysis patients and its underlying mechanism is complex. Hemodialysis causes an imbalance between antioxidants and production of reactive oxygen species, which induces the oxidative stress and thereby may lead to accelerated atherosclerosis. Statins have been found to be little effective in end-stage kidney disease and other lipid-lowering therapies have been only scarcely studied. The study aimed to assess the effect of low-dose fenofibrate therapy on plasma lipids and redox status in long-term hemodialysis patients with mild hypertriglyceridemia

Plasma levels of total, free and protein bound thiols as well as sulfane sulfur in different age groups of rats

The redox status of plasma thiols can be a diagnostic indicator of different pathological states. The aim of this study was to identify the age dependent changes in the plasma levels of total, free and protein bound glutathione, cysteine and homocysteine. The determination was conducted in plasma of three groups of rats: 1) young (3-month-old), 2) middle aged (19-month-old), and 3) old (31-month-old). Total levels of glutathione, cysteine and homocysteine and their respective free and protein-bound fractions decreased with age. The only exception was a rise in free homocysteine concentration in the middle group, which indicates a different pattern of transformations of this thiol in plasma. The drop in the level of protein-bound thiols suggests that the antioxidant capacity of plasma diminishes with age, which, consequently, leads to impaired protection of -SH groups through irreversible oxidation. The plasma sulfane sulfur level also declines with age, which means that aging is accompanied by inhibition of anaerobic sulfur metabolism

Determination of lipoic acid in human plasma by high-performance liquid chromatography with ultraviolet detection

This paper describes the development and validation of an HPLC method for the determination of protein bound and total lipoic acid in human plasma. The essential steps in the total lipoic acid assay include reduction of disulfide bridge with tris(2-carboxyethyl)phosphine, derivatization via thiol group with 1-benzyl-2-chloropyridinium bromide and HPLC analysis of S-pyridinium derivative. Protein-bound lipoic acid is first separated from free lipoic acid with the use of liquid extraction, converted to its reduced counterpart then processed as total lipoic acid. The method is reproducible, precise and accurate. The inter- and intraday related standard deviation varied from 1.5% to 11.5% and from 1.8% to 19.6%, respectively, while recovery is in the range of 80.0–106.0% and 80.4–110.8%, respectively. The mean concentration of total lipoic acid in healthy donors after supplementation with 600 mg and 1200 mg was 0.67 ±0.40 lmol L -1 (137.6± 82.1 lg L -1) and 1.57 ± 0.34 lmol L -1 (323.34 ± 70.07 lg L -1), respectively

Determination of lipoic acid in human plasma by high-performance liquid chromatography with ultraviolet detection

AbstractThis paper describes the development and validation of an HPLC method for the determination of protein bound and total lipoic acid in human plasma. The essential steps in the total lipoic acid assay include reduction of disulfide bridge with tris(2-carboxyethyl)phosphine, derivatization via thiol group with 1-benzyl-2-chloropyridinium bromide and HPLC analysis of S-pyridinium derivative. Protein-bound lipoic acid is first separated from free lipoic acid with the use of liquid extraction, converted to its reduced counterpart then processed as total lipoic acid. The method is reproducible, precise and accurate. The inter- and intraday related standard deviation varied from 1.5% to 11.5% and from 1.8% to 19.6%, respectively, while recovery is in the range of 80.0–106.0% and 80.4–110.8%, respectively. The mean concentration of total lipoic acid in healthy donors after supplementation with 600mg and 1200mg was 0.67±0.40μmolL−1 (137.6±82.1μgL−1) and 1.57±0.34μmolL−1 (323.34±70.07μgL−1), respectively

Alterations in the antioxidant enzyme activities in the neurodevelopmental rat model of schizophrenia induced by glutathione deficiency during early postnatal life

The aim of the present study was to assess the e ects of l-buthionine-(S,R)-sulfoximine (BSO), a glutathione (GSH) synthesis inhibitor, and GBR 12909, a dopamine reuptake inhibitor, administered alone or in combination to Sprague-Dawley rats during early postnatal development (p5–p16), on the levels of reactive oxygen species (ROS), lipid peroxidation (LP) and the activities of antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione disulfide reductase (GR) in peripheral tissues (liver, kidney) and selected brain structures (prefrontal cortex, PFC; hippocampus, HIP; and striatum, STR) of 16-day-old rats. The studied parameters were analyzed with reference to the content of GSH and sulfur amino acids, methionine (Met) and cysteine (Cys) described in our previous study. This analysis showed that treatment with a BSO + GBR 12909 combination caused significant decreases in the lipid peroxidation levels in the PFC and HIP, in spite of there being no changes in ROS. The reduction of lipid peroxidation indicates a weakening of the oxidative power of the cells, and a shift in balance in favor of reducing processes. Such changes in cellular redox signaling in the PFC and HIP during early postnatal development may result in functional changes in adulthood

A Simplified Method for Simultaneous Determination of α-Lipoic Acid and Low-Molecular-Mass Thiols in Human Plasma

α-Lipoic acid, glutathione, cysteine, and cysteinylglycine can be applied as therapeutic agents in civilization diseases such as diabetes mellitus, cardiovascular diseases, and cancers. On the other hand, a higher concentration of homocysteine can result in health problems and has been indicated as an independent risk factor for cardiovascular disease and accelerated atherosclerosis. Here, the first simplified HPLC-UV assay that enables simultaneous determination of α-lipoic acid and low-molecular-mass thiols in plasma, reduces the number of steps, shortens the total time of sample preparation, and limits the amount of single-use polypropylene laboratory materials is described. The assay is based on reversed-phase high performance liquid chromatography with UV detection and simultaneous reduction of disulfide bound with tris(2-carboxyethyl)phosphine and the selective pre-column derivatization of the thiol group with 1-benzyl-2-chloropyridinium bromide. Linearity in the detector responses for plasma samples were observed in ranges: 0.12–5.0 nmol mL−1 for α-lipoic acid; 2.0–20.0 nmol mL−1 for glutathione, cysteinylglycine, and homocysteine; and 40.0–400.0 for cysteine. The LODs for α-lipoic acid and low-molecular-mass thiols were 0.08 and 0.12 nmol mL−1 , respectively, while LOQs were 0.12 and 0.16 nmol mL−1 , respectively. The usefulness of the proposed method has been proven by its application to real samples

Glutathione deficiency and alterations in the sulfur amino acid homeostasis during early postnatal development as potential triggering factors for schizophrenia-like behavior in adult rats

Impaired glutathione (GSH) synthesis and dopaminergic transmission are important factors in the pathophysiology of schizophrenia. Our research aimed to assess the effects of l-buthionine-(S,R)-sulfoximine (BSO), a GSH synthesis inhibitor, and GBR 12909, a dopamine reuptake inhibitor, administered alone or in combination, to Sprague-Dawley rats during early postnatal development (p5-p16), on the levels of GSH, sulfur amino acids, global DNA methylation, and schizophrenia-like behavior. GSH, methionine (Met), homocysteine (Hcy), and cysteine (Cys) contents were determined in the liver, kidney, and in the prefrontal cortex (PFC) and hippocampus (HIP) of 16-day-old rats. DNA methylation in the PFC and HIP and schizophrenia-like behavior were assessed in adulthood (p90-p93). BSO caused the tissue-dependent decreases in GSH content and alterations in Met, Hcy, and Cys levels in the peripheral tissues and in the PFC and HIP. The changes in these parameters were accompanied by alterations in the global DNA methylation in the studied brain structures. Parallel to changes in the global DNA methylation, deficits in the social behaviors and cognitive functions were observed in adulthood. Only BSO + GBR 12909-treated rats exhibited behavioral alterations resembling positive symptoms in schizophrenia patients. Our results suggest the usefulness of this neurodevelopmental model for research on the pathomechanism of schizophrenia

The Effects of Cocaine on Different Redox Forms of Cysteine and Homocysteine, and on Labile, Reduced Sulfur in the Rat Plasma Following Active versus Passive Drug Injections

Received: 28 November 2012 / Revised: 19 April 2013 / Accepted: 6 May 2013 / Published online: 16 May 2013 The Author(s) 2013. This article is published with open access at Springerlink.comThe aim of the present studies was to evaluate cocaine-induced changes in the concentrations of different redox forms of cysteine (Cys) and homocysteine (Hcy), and products of anaerobic Cys metabolism, i.e., labile, reduced sulfur (LS) in the rat plasma. The above-mentioned parameters were determined after i.p. acute and subchronic cocaine treatment as well as following i.v. cocaine self-administration using the yoked procedure. Additionally, Cys, Hcy, and LS levels were measured during the 10-day extinction training in rats that underwent i.v. cocaine administration. Acute i.p. cocaine treatment increased the total and protein-bound Hcy contents, decreased LS, and did not change the concentrations of Cys fractions in the rat plasma. In turn, subchronic i.p. cocaine administration significantly increased free Hcy and lowered the total and protein-bound Cys concentrations while LS level was unchanged. Cocaine self-administration enhanced the total and protein-bound Hcy levels, decreased LS content, and did not affect the Cys fractions. On the other hand, yoked cocaine infusions did not alter the concentration of Hcy fractions while decreased the total and protein-bound Cys and LS content. This extinction training resulted in the lack of changes in the examined parameters in rats with a history of cocaine self-administration while in the yoked cocaine group an increase in the plasma free Cys fraction and LS was seen. Our results demonstrate for the first time that cocaine does evoke significant changes in homeostasis of thiol amino acids Cys and Hcy, and in some products of anaerobic Cys metabolism, which are dependent on the way of cocaine administration