Photoreduction of the long wavelength bacteriopheophytin in reaction centers and chromatophores of the photosynthetic bacterium Chromatium vinosum.
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Bacterial Chromatophores↗
Biomedical subjects
J C Romijn
Publications and source records attributed to J C Romijn.
Photochemical activities of reaction centers from Rhodopseudomonas sphaeroides at low temperature and in the presence of chaotropic agents.
Light-induced absorbance changes were measured at low temperatures in reaction center preparations from Rhodopseudomonas sphaeroides. Absorbance difference spectra measured at 100 degrees K show that ubiquinone is photoreduced at this temperature, both by continuous light and by a short actinic flash. The reduction occurred with relatively high efficiency. These results give support to the idea that ubiquinone is involved in the primary photochemical reaction in Rhodopseudomonas sphaeroides. Reduction of ubiquinone was accompanied by a shift of the infrared absorption band of bacteriopheophytin. The rate of decay of the primary photoproducts (P+870 and ubisemiquinone) appeared to be approximately independent of temperature below 180 degrees K and above 270 degrees K; in the region between 180 and 270 degrees K it increased with decreasing temperature. The rate of decay was not affected by 0-phenanthroline. Secondary reactions were inhibited by lowering the temperature. The light-induced absorbance changes were inhibited by chaotropic agents, like thiocyanate and perchlorate. It was concluded that these agents lower the efficiency of the primary photoconversion. The kinetics indicated that the degree of inhibition was not the same for all reaction centers. The absorption spectrum of the photoconverted reaction centers appeared to be somewhat modified by thiocyanate.
Acetates↗
Some studies on the fatty acid composition of total lipids and phosphatidylglycerol from Acholeplasma laidlawii B and their relation to the premeability of intact cells of this organism.
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Acholeplasma laidlawii↗
Inhibition of apoptotic proteins causes multidrug resistance in renal carcinoma cells.
Renal Cell Carcinomas (RCCs) exhibit strong resistance to the most chemotherapeutic treatments probably due to the expression of various multidrug resistance (MDR) genes. Overexpression of P-glycoprotein (Pgp) is established as one such factor, but other mechanisms such as at-MDR, characterized by attenuated DNA-topoisomerase II (topoII) activity, may be functional as well. In addition, regulating proteins involved in apoptosis can exhibit multidrug resistant features. However, prevention of apoptosis as a mechanism of MDR has not yet been assessed in RCC, nor has the cytotoxicity of a variety of chemotherapeutic agents known to trigger apoptotic or necrotic cell death been tested in RCC in a systematic fashion. Using immunohistochemistry and Western blotting, Bcl-2 and Bax expression was determined in a panel of multidrug resistant RCC lines featuring Pgp and/or at-MDR. The results were related to apoptotic activity and kind of cell death in these cell lines, demonstrated by incubation with Hoechst 33342 and propidium iodide after treatment with various cytotoxic agents and quantitated by MTT. In the drug resistant sublines, some decreased Bax and strongly increased Bcl-2 expression was seen by immunohistochemistry indicating prevention of apoptosis as a distinct feature of MDR in RCC. This was confirmed by Western blotting. Sublines revealed significant resistance for all drugs, except for CC-313 and DiMIQ. However, these drugs induced necrotic cell death, in contrast to all other drugs tested, which induced apoptotic cell death. We conclude that, in chemoselected RCC sublines, multidrug resistance appears to be functional due to inhibition of apoptosis, apart from the MDR1 and at-MDR resistance mechanisms. CC-313 and DiMIQ are very potent cytotoxic agents in RCC, probably because they do not kill by induction of apoptosis.
Amsacrine↗
Negative control of epithelial cell proliferation by prostatic stroma.
The influence of prostatic fibroblasts on the growth of the prostatic carcinoma cell lines PC-3 and LNCaP was examined. In a double layer soft agar system, clonal growth of both cell lines was inhibited by all prostatic fibroblasts tested, irrespective of whether they were derived from malignant or non malignant prostate tissue. Irradiated fibroblasts and quiescent fibroblasts showed similar effects. The finding that growth was also inhibited in the presence of fibroblasts conditioned medium suggests that the observed effects were mediated by a diffusable growth inhibiting factor. Organ-specific production was suggested by the observation that skin fibroblasts stimulated rather than inhibited PC-3 cell growth. These findings indicate a negative control of epithelial cell proliferation by prostatic stroma.
Cell Division↗