ABSTRACT
The Fe-on-Ti and Ti-on-Fe interfaces were studied experimentally by Mössbauer spectroscopy (MS), transmission electron microscopy (TEM) and x-ray reflectometry (XRR) on Ti/Fe/Ti trilayers grown on Si(1 1 1) substrates by vacuum evaporation. The nanoscale structure and composition were explored in cross sections using TEM, the layer structure and the interface widths by specular x-ray reflectometry. MS was applied to identify the interface alloy phases and to determine the pure and alloyed Fe layer fractions. The experimental results were compared with molecular dynamics (MD) simulations of layer growth on Fe or Ti underlayers of different orientations. The concentration distributions provided by MD simulations show an asymmetry at the interfaces in the layer growth direction. The transition is atomically sharp at the Ti-on-Fe interface for the (0 0 1) and (1 1 0) crystallographic orientations of the Fe underlayer, while it spreads over a few atomic layers for Fe(1 1 1) underlayer and for all studied Ti underlayer orientations at the Fe-on-Ti interface. MS and XRR data on Ti/Fe/Ti trilayers confirm the asymmetry between the bottom and top Fe interface, but the inferred interface widths considerable exceed those deduced from the MD simulations.
ABSTRACT
The aim of the study was to investigate the early effect of Transplatin (the stereo-isomer of Cisplatin) on oncogenes in inbred CBA/Ca mice. Cisplatin is commonly used for the treatment of squamous cell carcinomas of the head and neck. Cisplatin has a strong oncogene activation effect compared to the structural analogue Transplatin. Body weight equivalent amounts of a human dose of Transplatin were administered intra-peritoneally to 6- to 8-week-old, inbred, female CBA/Ca mice. Twenty-four, 48 and 72 hours after the treatment, RNA was isolated from the target organs and the expressions of c-myc, Ha-ras and p53 genes were examined. Investigation of early changes showed no significant overexpression compared to Cisplatin, which had a significant effect on oncogene expression in the "short-term" in vivo test system.
Subject(s)
Cisplatin/pharmacology , Genes, myc/drug effects , Genes, p53/drug effects , Genes, ras/drug effects , Animals , Female , Gene Expression Regulation/drug effects , Genes, myc/genetics , Genes, p53/genetics , Genes, ras/genetics , Kidney/drug effects , Kidney/physiology , Liver/drug effects , Liver/physiology , Lung/drug effects , Lung/physiology , Mice , Mice, Inbred CBA , Spleen/drug effects , Spleen/physiologyABSTRACT
In vivo investigations on oncogenes and onco-suppressor genes may provide new findings on the potential carcinogenic effects of various cytostatic protocols inducing secondary tumours of the head and neck. Further surgeries are often necessary due to regional recurrence after the Cisplatin-supplemented BVM (Bleomycin, Vincristine, Methotrexate) protocol in the treatment of human head and neck tumours. Our earlier studies have illustrated the carcinogenic and mutagenic potential of Cisplatin. The effect of Cisplatin on the alteration of different onco- and suppressor genes has also been proven. Our present study aimed at investigating the early effects of the BVM and the CFu (Cisplatin, 5-Fluorouracil) protocols on early oncogene and tumour suppressor gene expressions in mice. Body weight equivalent amounts of cytostatics were administered intraperitoneally to 6- to 8-week-old, inbred, female CBA/Ca mice. Twenty-four, 48 and 72 hours after the treatment, RNA was isolated from the target organs and the quantitative expression of c-myc, Ha-ras and p53 genes were examined. The protocols caused detectable changes. A "short-term" in vivo test, the 24-hour examination of gene expression, is suitable for detecting early effects of carcinogen exposure. The alterations of gene expression, caused by the Cisplatin-containing protocol, draw attention to the probable role of Cisplatin in the development of regional recurrence and to the possibility of prevention.
