High quality epitaxial layers of GaAs, InP, AlAs, InGaAs, InGaP, InGaAlP have been grown by low-pressure metalorganic chemical vapor deposition using TMIn, TMGa, TMAl and the less hazardous group V precursors, ΤΒA, TBP. Excellent morphology was obtained for GaAs and InP in the temperature ranges of 570-650°C and 520-650°C, respectively. The V/III ratio as low as 1.5 was used to grow epilayers of InP. The 77 K mobility of InGaAs lattice matched to InP (grown with ΤΒA) was 72360 cm^{2}/(V s) for n = 1.5 × 10^{15}/cm^{-3} and a thickness of 2 μm. Comparable photoluminescence parameters of InGaP between layers grown with TBP and PH_{3} were achieved, but for InGaAlP (TBP) photoluminescence intensity was significantly lower than for InGaAlP (PH_{3}). The promising results allow one to apply of ΤΒA and TBP for developing of device structures.
The effects of mutagens on DNA replication and DNA repair were studied in peripheral blood lymphocytes (BPL) obtained 21 healthy subjects, 2 samples from healthy heterozygote of Xeroderma pigmentosum (XP) and 2 samples from patient with clinically recognized XP.Inter-individual variations were found in DNA replication and in the level of spontanous DNA repair measured under standard culture condition.Exposure of human PBL proliferating in vitro to B(a)P was followed by a partial inhibition of replicative DNA synthesis in all subjects and by induction of DNA repair in healthy subjects.In XP patients DNA repair sythesis remained at the level attributed to spontaneous DNA repair.The response to mutagen varied individually.Results were analysed statistically.It was established that the studied indices of DNA synthesis correlete well with each other.The highest correlation was found between the levels of spontaneous and B(a)P-induced DNA repair.It is concluded that the level of spontaneous DNA repair is predictive for an estimation of cells ability to repair DNA damage.Inter-individual variations in the inhibition of DNA replication and in DNA repair sythesis are also dependet on the type of mutagen as shown by effect of other mutagens.Different effects of mutagen exposure on the inhibition of DNA replicative sythesis and induction of DNA repair can be explained by genetically controlled differences in the activity of enzymes responsible for mutagen processing and lesion removal.
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