Solution processable poly(2,5-dialkyl-2,5-dihydro-3,6-di-2-thienyl- pyrrolo[3,4-c]pyrrole-1,4-dione) for ambipolar organic thin film transistors

Solution processable diketopyrrolopyrrole (DPP)-bithiophene polymers (PDBT) with long branched alkyl side chains on the DPP unit are synthesized. These polymers have favourable highest occupied molecular orbital (HOMO) and lowest unoccupied molecular orbital (LUMO) energy levels for the injection and transport of both holes and electrons. Organic thin film transistors (OTFTs) using these polymers as semiconductors and gold as source/drain electrodes show typical ambipolar characteristics with very well balanced high hole and electron mobilities (μ h = 0.024 cm 2 V -1 s -1 and μ e = 0.056 cm 2 V -1 s -1). These simple and high-performing polymers are promising materials for ambipolar organic thin film transistors for low-cost CMOS-like logic circuits.

A study of the effects metal residues in poly(9,9-dioctylfluorene) have on field-effect transistor device characteristics

The amount of metal residues from organometallic reagents used in preparation of poly(9,9-dioctylfluorene) by palladium catalysed Suzuki and nickel-induced Yamamoto polycondensations have been determined, and their effect upon the behaviour of the polymer in field-effect transistors (FETs) has been measured. The metal levels from material polymerised by Suzuki method were found to be much higher than from that made by the Yamamoto procedure. Simple treatment of the polymers with suitable metal trapping reagents lowered the metal levels significantly, with EDTA giving best results for nickel and triphenylphosphine for palladium. Comparison of the behaviour of FETs using polyfluorenes with varying levels of metal contamination, showed that the metal residues have little effect upon the mobility values, but often affect the degree of hysteresis, possibly acting as charge traps. Satisfactory device performances were obtained from polymer with palladium levels of 2000 μg/g suggesting that complete removal of metal residues may not be necessary for satisfactory device performance.

Comparative behavior of CdS and CdSe quantum dots in poly(3-hexylthiophene) based nanocomposites

CdS and CdSe nanoparticles have been prepared using conducting poly(3-hexylthiophene) (P3HT) matrix with an objective to understand the effect of nanoparticles on the polymer matrix using electrochemical and spectroscopic techniques. The spectroscopic results reveal that the electronic structure of polymer is strongly influenced by the characteristics of embedded semiconducting nanoparticles. SEM and TEM images show the ordered morphology of the CdS and CdSe nanoparticles in presence of the polymer matrix. Cyclic voltammetry performed both in the presence and absence of light enables us to understand the redox changes in P3HT due to CdS and CdSe quantum dots such as the generation of free radical in the excited state and their electrochemical band gaps.

Influence of polymorphisms of the human glutathione transferases and cytochrome P450 2E1 enzyme on the metabolism and toxicity of ethylene oxide and acrylonitrile

A cohort of 59 persons with industrial handling of low levels of acrylonitrile is being studied as part of a medical surveillance programme. Previously, an extended haemoglobin adduct monitoring (N-(cyanoethyl)valine and N-(hydroxyethyl)-valine) was performed regarding the glutathione transferases hGSTM1 and hGSTT1 polymorphisms but no influence of hGSTM1 or hGSTT1 polymorphisms on specific adduct levels was found. A compilation of case reports of human accidental poisonings had pointed to significant individual differences in human acrylonitrile metabolism and toxicity. Therefore, a re-evaluation of the industrial cohort included known polymorphisms of the glutathione transferases hGSTM3 and hGSTP1 as well as of the cytochrome P450 CYP2E1. A detailed statistical analysis revealed that exposed carriers of the allelic variants of hGSTP1, hGSTP1*B/hGSTP1*C, characterized by a single nucleotide polymorphism at nucleotide 313 which results in a change from Ile to Val at codon 104, had higher levels of the acrylonitrile-specific haemoglobin adduct N-(cyanoethyl)valine compared to the carriers of the codon 113 alleles hGSTP1*A and hGSTP1*D. The single nucleotide polymorphism at codon 113 of hGSTP1 (hGSTP1*A/hGSTP1*B versus hGSTP1*C/hGSTP1*D) did not show an effect, and also no influence was seen on specific haemoglobin adduct levels of the polymorphisms of hGSTM3 or CYP2E1. The data, therefore, point to a possible influence of a human enzyme polymorphism of the GSTP1 gene at codon 104 on the detoxication of acrylonitrile which calls for experimental toxicological investigation. The study also confirmed the impact of GSTT1 polymorphism on background N-(hydroxyethyl)-valine adduct levels in haemoglobin which are caused by endogenous ethylene oxide.

Carcinogenicity and genotoxicity of ethylene oxide : new aspects and recent advances

Long-term inhalation studies in rodents have presented unequivocal evidence of experimental carcinogenicity of ethylene oxide, based on the formation of malignant tumors at multiple sites. However, despite a considerable body of epidemiological data only limited evidence has been obtained of its carcinogenicity in humans. Ethylene oxide is not only an important exogenous toxicant, but it is also formed from ethylene as a biological precursor. Ethylene is a normal body constituent; its endogenous formation is evidenced by exhalation in rats and in humans. Consequently, ethylene oxide must also be regarded as a physiological compound. The most abundant DNA adduct of ethylene oxide is 7-(2-hydroxyethyl)guanine (HOEtG). Open questions are the nature and role of tissue-specific factors in ethylene oxide carcinogenesis and the physiological and quantitative role of DNA repair mechanisms. The detection of remarkable individual differences in the susceptibility of humans has promoted research into genetic factors that influence the metabolism of ethylene oxide. With this background it appears that current PBPK models for trans-species extrapolation of ethylene oxide toxicity need to be refined further. For a cancer risk assessment at low levels of DNA damage, exposure-related adducts must be discussed in relation to background DNA damage as well as to inter- and intraindividual variability. In rats, subacute ethylene oxide exposures on the order of 1 ppm (1.83 mg/m3) cause DNA adduct levels (HOEtG) of the same magnitude as produced by endogenous ethylene oxide. Based on very recent studies the endogenous background levels of HOEtG in DNA of humans are comparable to those that are produced in rodents by repetitive exogenous ethylene oxide exposures of about 10 ppm (18.3 mg/m3). Experimentally, ethylene oxide has revealed only weak mutagenic effects in vivo, which are confined to higher doses. It has been concluded that long-term human occupational exposure to low airborne concentrations to ethylene oxide, at or below current occupational exposure limits of 1 ppm (1.83 mg/m3), would not produce unacceptable increased genotoxic risks. However, critical questions remain that need further discussions relating to the coherence of animal and human data of experimental data in vitro vs. in vivo and to species-specific dynamics of DNA lesions.

Haemoglobin adducts of acrylonitrile and ethylene oxide in acrylonitrile workers, dependent on polymorphisms of the glutathione transferases GSTT1 and GSTM1

Fifty-nine persons with industrial handling of low levels of acrylonitrile (AN) were studied. As part of a medical surveillance programme an extended haemoglobin adduct monitoring [N-(cyanoethyl)valine, CEV; N- (methyl)valine, MV; N-(hydroxyethyl)valine, HEV] was performed. Moreover, the genetic states of the polymorphic glutathione transferases GSTM1 and GSTT1 were assayed by polymerase chain reaction (PCR). Repetitive analyses of CEV and MV in subsequent years resulted in comparable values (means, 59.8 and 70.3 μg CEV/1 blood; 6.7 and 6.7 μg MV/1 blood). Hence, the industrial AN exposures were well below current official standards. Monitoring the haemoglobin adduct CEV appears as a suitable means of biomonitoring and medical surveillance under such exposure conditions. There was also no apparent correlation between the CEV and HEV or CEV and MV adduct levels. The MV and HEV values observed represented background levels, which apparently are not related to any occupational chemical exposure. There was no consistent effect of the genetic GSTM1 or GSTT1 state on CEV adduct levels induced by acrylonitrile exposure. Therefore, neither GSTM1 nor GSTT1 appears as a major AN metabolizing isoenzyme in humans. The low and physiological background levels of MV were also not influenced by the genetic GSTM1 state, but the MV adduct levels tended to be higher in GSTT1- individuals compared to GSTT1 + persons. With respect to the background levels of HEV adducts observed, there was no major influence of the GSTM1 state, but GST- individuals displayed adduct levels that were about 1/3 higher than those of GSTT1+ individuals. The coincidence with known differences in rates of background sister chromatid exchange between GSTT1- and GSTT1 + persons suggests that the lower ethylene oxide (EO) detoxification rate in GSTT1- persons, indicated by elevated blood protein hydroxyethyl adduct levels, leads to an increased genotoxic effect of the physiological EO background.