Generation of electron spin polarization in disordered organic semiconductors

The generation mechanisms of electron spin polarization (ESP) of charge carriers (electrons and holes, called "doublets") in doublet-doublet recombination and triplet-doublet quenching in disordered organic semiconductors are analyzed in detail. The ESP is assumed to result from quantum transitions between the states of the spin Hamiltonian of the pair of interacting particles. The value of the ESP is essentially determined by the mechanism of relative motion of particles. In our work we have considered the cage and free diffusion models. The effect of possible attractive spin-independent interactions between particles is also analyzed. Estimation with obtained formulas shows that the proposed mechanisms can lead to a fairly strong ESP much larger than the thermal one (at room temperatures)Comment: 10 pages, 3 figure

Magnetic field effects on electron-hole recombination in disordered organic semiconductors

Characteristic properties of magnetic field effects on spin selective geminate and bulk electron-hole polaron pair (PP) recombination are analyzed in detail within the approach based on the stochastic Liouville equation. Simple expressions for the magnetic field (B) dependence of recombination yield and rate are derived within two models of relative PP motion: free diffusion and diffusion in the presence of well (cage). The spin evolution of PPs is described taking in account the relaxation induced by hyperfine interaction, anisotropic part of the Zeeman interaction induced, as well as $\Delta g$-mechanism. A large variety of the $B$-dependences of the recombination yield $Y(B)$ and rate $K(B)$ is obtained depending on the relative weights of above-mentioned mechanisms. The proposed general method and derived particular formulas are shown to be quite useful for the analysis of recent experimental results.Comment: 12 pages, 3 figure

n-CdSe/p-ZnTe based wide band-gap light emitters: Numerical simulation and design

The only II‐VI/II‐VI wide band‐gap heterojunction to provide both good lattice match and p‐ and n‐type dopability is CdSe/ZnTe. We have carried out numerical simulations of several light emitter designs incorporating CdSe, ZnTe, and Mg alloys. In the simulations, Poisson’s equation is solved in conjunction with the hole and electron current and continuity equations. Radiative and nonradiative recombination in bulk material and at interfaces are included in the model. Simulation results show that an n‐CdSe/p‐ZnTe heterostructure is unfavorable for efficient wide band‐gap light emission due to recombination in the CdSe and at the CdSe/ZnTe interface. An n‐CdSe/Mg_(x)Cd_(1−x)Se/p‐ZnTe heterostructure significantly reduces interfacial recombination and facilitates electron injection into the p‐ZnTe layer. The addition of a Mg_(y)Zn_(1−y)Te electron confining layer further improves the efficiency of light emission. Finally, an n‐CdSe/Mg_(x)Cd_(1−x)Se/Mg_(y)Zn_(1−y)Te/p‐ZnTe design allows tunability of the wavelength of light emission from green into the blue wavelength regime

X-ray photoelectron spectroscopy measurement of valence-band offsets for Mg-based semiconductor compounds

We have used x-ray photoelectron spectroscopy to measure the valence-band offsets for the lattice matched MgSe/Cd0.54Zn0.46Se and MgTe/Cd0.88Zn0.12Te heterojunctions grown by molecular beam epitaxy. By measuring core level to valence-band maxima and core level to core level binding energy separations, we obtain values of 0.56+/-0.07 eV and 0.43+/-0.11 eV for the valence-band offsets of MgSe/Cd0.54Zn0.46Se and MgTe/Cd0.88Zn0.12Te, respectively. Both of these values deviate from the common anion rule, as may be expected given the unoccupied cation d orbitals in Mg. Application of our results to the design of current II-VI wide band-gap light emitters is discussed

Molecular dosimetry of DNA and hemoglobin adducts in mice and rats exposed to ethylene oxide.

Experiments involving ethylene oxide (ETO) have been used to support the concept of using adducts in hemoglobin as a surrogate for DNA adducts in target tissues. The relationship between repeated exposures to ETO and the formation of N-(2-hydroxyethyl)valine (HEtVal) in hemoglobin and 7-(2-hydroxyethyl)guanine (7-HEG) in DNA was investigated in male rats and mice exposed by inhalation to 0, 3, 10, 33, or 100 ppm ETO for 6 hr/day for 4 weeks, or exposed to 100 ppm (mice) or 300 ppm (rats) for 1, 3, 5, 10, or 20 days (5 days/week). HEtVal was determined by Edman degradation, and 7-HEG was quantitated by HPLC separation and fluorescence detection. HEtVal formation was linear between 3 and 33 ppm ETO and increased in slope above 33 ppm. The dose-response curves for 7-HEG in rat tissues were linear between 10 and 100 ppm ETO and increased in slope above 100 ppm. In contrast, only exposures to 100 ppm ETO resulted in significant accumulation of 7-HEG in mice. Hemoglobin adducts were lost at a greater rate than predicted by normal erythrocyte life span. The loss of 7-HEG from DNA was both species and tissue dependent, with the adduct half-lives ranging from 2.9 to 5.8 days in rat tissues (brain, kidney, liver, lung, spleen, testis) and 1.0 to 2.3 days in all mouse tissues except kidney (t1/2 = 6.9 days). The concentrations of HEtVal were similar in concurrently exposed rats and mice, whereas DNA from rats had at least 2-fold greater concentrations of 7-HEG than DNA from mice.(ABSTRACT TRUNCATED AT 250 WORDS

Formaldehyde Carcinogenicity Research: 30 Years and Counting for Mode of Action, Epidemiology, and Cancer Risk Assessment

Formaldehyde is a widely used high production chemical that is also released as a byproduct of combustion, off-gassing of various building products, and as a fixative for pathologists and embalmers. What is not often realized is that formaldehyde is also produced as a normal physiologic chemical in all living cells. In 1980, chronic inhalation of high concentrations of formaldehyde was shown to be carcinogenic, inducing a high incidence of nasal squamous cell carcinomas in rats. Some epidemiologic studies have also found increased numbers of nasopharyngeal carcinoma and leukemia in humans exposed to formaldehyde that resulted in formaldehyde being considered a Known Human Carcinogen. This article reviews the data for rodent and human carcinogenicity, early Mode of Action studies, more recent molecular studies of both endogenous and exogenous DNA adducts, and epigenetic studies. It goes on to demonstrate the power of these research studies to provide critical data to improve our ability to develop science-based cancer risk assessments, instead of default approaches. The complexity of constant physiologic exposure to a known carcinogen requires that new ways of thinking be incorporated into determinations of cancer risk assessment for formaldehyde, other endogenous carcinogens, and the role of background endogenous DNA damage and mutagenesis

Formaldehyde and Epigenetic Alterations: MicroRNA Changes in the Nasal Epithelium of Nonhuman Primates

Background: Formaldehyde is an air pollutant present in both indoor and outdoor atmospheres. Because of its ubiquitous nature, it is imperative to understand the mechanisms underlying formaldehyde-induced toxicity and carcinogenicity. MicroRNAs (miRNAs) can influence disease caused by environmental exposures, yet miRNAs are understudied in relation to formaldehyde. Our previous investigation demonstrated that formaldehyde exposure in human lung cells caused disruptions in miRNA expression profiles in vitro

Formaldehyde-Associated Changes in microRNAs: Tissue and Temporal Specificity in the Rat Nose, White Blood Cells, and Bone Marrow

MicroRNAs (miRNAs) are critical regulators of gene expression, yet much remains unknown regarding their changes resulting from environmental exposures as they influence cellular signaling across various tissues. We set out to investigate miRNA responses to formaldehyde, a critical air pollutant and known carcinogen that disrupts miRNA expression profiles. Rats were exposed by inhalation to either 0 or 2 ppm formaldehyde for 7, 28, or 28 days followed by a 7-day recovery. Genome-wide miRNA expression profiles were assessed within the nasal respiratory epithelium, circulating white blood cells (WBC), and bone marrow (BM). miRNAs showed altered expression in the nose and WBC but not in the BM. Notably in the nose, miR-10b and members of the let-7 family, known nasopharyngeal carcinoma players, showed decreased expression. To integrate miRNA responses with transcriptional changes, genome-wide messenger RNA profiles were assessed in the nose and WBC. Although formaldehyde-induced changes in miRNA and transcript expression were largely tissue specific, pathway analyses revealed an enrichment of immune system/inflammation signaling in the nose and WBC. Specific to the nose was enrichment for apoptosis/proliferation signaling, involving let-7a, let-7c, and let-7f. Across all tissues and time points assessed, miRNAs were predicted to regulate between 7% and 35% of the transcriptional responses and were suggested to play a role in signaling processes including immune/inflammation-related pathways. These data inform our current hypothesis that formaldehyde-induced inflammatory signals originating in the nose may drive WBC effects

Debio 0507 primarily forms diaminocyclohexane-Pt-d(GpG) and -d(ApG) DNA adducts in HCT116 cells

To characterize the cellular action mechanism of Debio 0507, we compared the major DNA adducts formed by Debio 0507- and oxaliplatin-treated HCT116 human colon carcinoma cells by a combination of inductively coupled plasma mass spectrometry (ICP-MS) and ultra-performance liquid chromatography mass spectrometry (UPLC-MS/MS)