PHOTOREACTIVATION OF LETHAL DAMAGE AND DAMAGE LEADING TO CHROMATID DELETIONS INDUCED IN G1 PHASE HAMSTER x Xenopus HYBRID CELLS BY UV

A86 Xenopus cells, cloned from a Xenopus line that exhibited a high level of photoreactivation of UV-induced lethal damage, and V79M1 hamster cells, cloned from a hamster line that did not exhibit efficient photoreactivation of such damage, were fused to produce the V79M1 x A86 cell line--a hybrid line in which approximately 84% of the cells contained the entire V79M1 and A86 genomes. Ultraviolet and UV plus photoreactivation fluence-survival relations were then determined and compared for hybrid and parental G1 phase cells in a first attempt to elucidate interactions of the parental genetic potentials for photoreactivation in the hybrid. Specifically, it was anticipated that the combined V79M1 and A86 genomes in the hybrid would produce photoreactivating enzymes sufficient to efficiently photoreactivate UV-induced lethal damage in both A86 and V79M1 DNA and little difference would be observed in the levels of photoreactivation exhibited by V79M1 x A86 and A86 G1 phase cells. To the contrary, the level of photoreactivation observed for the hybrid did not closely approach that observed for the A86 line. To assist in the interpretation of this somewhat unexpected observation, three additional studies were performed: (1) comparison of 'optimal' schemes for photoreactivation of UV-induced lethal damage in the hybrid and parental G1 phase cells, (2) comparison of the effects of some different types of growth medium on photoreactivation of UV-induced lethal damage in hybrid and parental G1 phase cells, and (3) comparison of the levels of photoreactivation of UV-induced chromatid deletions in the V79M1 and A86 chromosomes of G1 phase hybrid cells.(ABSTRACT TRUNCATED AT 250 WORDS)     

TIME COURSE OF PHOTOREACTIVATION OF UV-INDUCED CHROMOSOMAL ABERRATIONS AND LETHAL DAMAGE IN INTERPHASE XENOPUS CELLS

Abstract— Sets of G1, S, and G2 phase Xenopus cells were exposed to 15.0 Jm⁻² UV and their ability to photoreactivate the induced cell killing (loss of colony forming ability) and chromosomal aberrations was determined as a function of time following the UV exposure. Most of the lesions induced in G1 cells that lead to cell death were converted to a non-photoreactivable state before the cells entered the S phase, while lesions leading to chromosomal aberrations were converted to a non-photoreactivable state as the cells entered the S phase. In S phase cells the UV-induced lesions leading to aberrations appeared to be converted to a non-photoreactivable state at a much faster rate than those leading to cell death. A significant fraction of the lesions induced in G2 cells, that lead to cell death, were converted to a non-photoreactivable state before the progeny of the exposed cells reached the next succeeding S phase. Few, if any, lesions were induced in G2 cells that were expressed as aberrations at the first mitosis following exposure. Some of the lesions induced in the G2 cells led to aberrations that were observable in the progeny that progressed to the second mitosis following exposure. These lesions were converted to a non-photoreactivable state as the progeny of the exposed G2 cells progressed through the first S phase following exposure. These results suggest that the intracellular mechanism which expresses photoreactivable UV-induced lesions as cell death is not identical to the mechanism which expresses such lesions as chromosomal aberrations, and the two mechanisms operate with different efficiencies in different phases of the cell cycle.     

Electronic Absorption and Emission Spectra of 1, 3-Diaryltriazenes

The Pariser-Parr-Pople (PPP) type LCI-SCF-MO calculations were used to study the models of 1, 3-diphenyltriazene (1) , 1, 3-bis(3-pyridyl)triazene (2) , 1, 3-bis (2, 4-dichlorophenyl)triazene (3) , and 1, 3-bis (4-ethoxycarbonyl)triazene (4) . The results of the calculations were compared with the experimental electronic absorption and emission (fluorescence, phosphorescence) spectra of these compounds.     

Hindered rotation in an "exploded" biphenyl

The first cases of hindered rotation around the triple bond in simple diphenylacetylenes were observed, including that in chiral 2,2'-bis(trimethylsilyl)-6,6'-bis(dimethylthexylsilyl)diphenylacetylene.     

Spectrophotometric study of the acid-base equilibria of an imidazobenzodiazepine,midazolam, and its determination in pharmaceutical formulations

The acid-base behaviour of midazolam, a psychotropic drug derived from imidazobenzodiazepine family, has been studied spectro-photometrically. This compound hydrolyzes at pH values lower than 4. Reversible cleavage of the azomethine bond takes place and the open-ring compound is in equilibrium with the closed-ring compound (protonated form of the parent drug). Absorbance-time data (measured at 225 nm and for different pH values) have been evaluated by a pseudo-first order logarithmic approach, leading to different apparent kinetic constants, depending on pH and temperature. A simple mechanism of hydrolysis, corresponding to fast protonation and slow hydrolysis with opening of the ring is in good agreement with the kinetic results. From data obtained at pH values greater than 4, the deprotonation constant of the nitrogen atom at position 2 of the imidazole ring has been calculated and a pK_a value of 5.50 ± 0.05 obtained. In addition, a Spectrophotometric method has been developed which allows the determination of midazolam at concentrations from 1.23 × 10^–6 M to 3.38 × 10^–5 M. This method has been applied to a pharmaceutical formulation midazolam; the Dormicum error, in terms of relative standard deviation, was lower than 1.5%.     

Rapid palladium-catalyzed aminations of aryl chlorides with aliphatic amines under temperature-controlled microwave heating

Rapid Buchwald-Hartwig amination of electron neutral and rich aryl chlorides and bromides have been achieved using temperature-controlled microwave heating. Primary and secondary aliphatic amines can be coupled with these substrates in good yields within a reaction time of only 10 min.     

Interaction of Boron Nitride Nanosheets with Model Cell Membranes

Boron nitride nanomaterials have attracted attention for biomedical applications, due to their improved biocompatibility when compared with carbon nanomaterials. Recently, graphene and graphene oxide nanosheets have been shown, both experimentally and computationally, to destructively extract phospholipids from Escherichia coli. Boron nitride nanosheets (BNNSs) have exciting potential biological and environmental applications, for example the ability to remove oil from water. These applications are likely to increase the exposure of prokaryotes and eukaryotes to BNNSs. Yet, despite their promise, the interaction between BNNSs and cell membranes has not yet been investigated. Here, all‐atom molecular dynamics simulations were used to demonstrate that BNNSs are spontaneously attracted to the polar headgroups of the lipid bilayer. The BNNSs do not passively cross the lipid bilayer, most likely due to the large forces experienced by the BNNSs. This study provides insight into the interaction of BNNSs with cell membranes and may aid our understanding of their improved biocompatibility.     

Chromium Speciation Using Ion Chromatography-Atomic Absorption System with On-Line Preconcentration

A method using ion chromatography-atomic absorption system (IC-AA) with on-line preconcentration unit is developed for the speciation of chromium in aqueous samples. Both Cr(III) and Cr(VI) species are pre-treated with sodium salt of ethylenediaminetetraacetic acid (EDTA) in consecutive steps. The treated samples can then be injected into an on-line preconcentration unit followed by ion chromatographic separation with UV or selective flame AA detection. Both chromium species can be separated within 10 minutes, and the method is applicable for aqueous samples with ppm levels of chromium.     

Cyclophosphazenes and Relatives as Anticancer Drugs

Abstract

Aziridinocyclophosphazenes N₃P₃Az₆ (code name MYKO 63), N₄P₄Az₈ (code name MYKO 83) and relatives constituted the first generation of anticancer drugs whose efficiency on several rodent neoplasms was made conspicuous in a quantitative manner from 1976 to 1978 both in our Laboratory and by EORTC Screening Pharmacology Groups¹. MYKO 63 appeared at that time as a promising drug for industrial development owing to its wide spectrum of activity and its very low mutagenicity². However, this hope failed as a consequence of a cumulative toxicity which occurs upon heavy polyinjections schedules. In other words, MYKO 63 exhibits an uncomfortable kinetics of action on the tumor - and, consequently, of excretion - presumably due (it was our assumption) to a too high chemical stability of the molecule.     

Global Spectral Gap for Dirichlet-Kac Random Motions

We prove that the global spectral gap, for any Dirichlet-Kac random motion, is equal to the convergence rate of the limit motion.