PubMed · 5087886
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H Halvorson, M Ishaque, J Solomon, O W Grussendorf. 1971. A biodegradability test for insecticides.. https://doi.org/10.1139/m71-096
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We have studied hypoxia-induced inactivation of cells from three established human cell lines with different p53 status. Hypoxia was found to induce apoptosis in cells expressing wild-type p53 (MCF-7 cells), but not in cells where p53 is either mutated (T-47D cells), or abrogated by expression of the HPV18 E6 oncoprotein (NHIK 3025 cells). Apoptosis was demonstrated by DNA fragmentation, using agarose gel electrophoresis of DNA and DNA nick end labeling (TUNEL). We demonstrate that extremely hypoxic conditions (< 4 ppm O2) do not cause any change of expression in the p53 protein level in these three cell lines. In addition, the localization of p53 in MCF-7 cells was found exclusively in the nucleus in only some of the cells both under aerobic and hypoxic conditions. Furthermore, no correlation was found between the p53-expression level and whether or not a cell underwent apoptosis. Flow cytometric TUNEL analysis of MCF-7 cells revealed that initiation of apoptosis occurred in all phases of the cell cycle, although predominantly for cells in S phase. Apoptosis was observed only during a limited time window (i.e., approximately 10 to approximately 24 h) after the onset of extreme hypoxia. While 66% of the MCF-7 cells lost their ability to form visible colonies following 15 h exposure to extreme hypoxia, only approximately 28% were induced to apoptosis, suggesting that approximately 38% were inactivated by other death processes. Commitment to apoptotic cell death was observed in MCF-7 cells even for oxygen concentrations as high as 5000 ppm. Our present results indicate that the p53 status in these three tumor cell lines does not have any major influence on cell's survival following exposure to extremely hypoxic conditions, whereas following moderate hypoxia, cells expressing functional p53 enhanced their susceptibility to cell death. Taken together, although these results suggest that functional p53 might play a role in the induction of apoptosis during hypoxia, other factors seem to be equally important.
Organisms that perform oxygenic photosynthesis are subjected to inhibition of their photosynthetic functions when they are exposed to excessive illumination. Photoinhibition occurs mainly at the level of photosystem II, where a cyclic electron transport has often been proposed to be involved in photoprotection. However, a demonstration of direct protection by cyclic photosystem II against photoinhibitory damage has been lacking. In this report, we used the newly characterized compound 4-[methoxybis(trifluoromethyl)methyl]-2,6-dinitrophenylhydrazine methyl ketone (K-15), known to stimulate cyclic electron transport between the acceptor and donor sides of the photosystem [Klimov, V. V., Zharmukhamedov, S. K., Allakhverdiev, S. I., Kolobanova, L. P., & Baskakov, Y. A. (1993) Biol. Membr. 6, 715-732], to verify if photosystem II is significantly protected by cyclic electron transport against aerobic and anaerobic photoinhibitory damage. The photoinhibitory quenching of the maximal level of fluorescence and the decrease of the absorbance change at 685 nm related to pheophytin photoreduction observed during photoinhibitory illumination of untreated or Mn-depleted photosystem II submembrane fractions are significantly attenuated in the presence of K-15. The photodegradation of cytochrome b559 and the photobleaching of beta-carotene and chlorophyll-670 measured in Mn-depleted photosystem II preparations are also strongly retarded when K-15 is present. The detection, by photoacoustic spectroscopy, of the energy stored during the cyclic electron transport is also reported in Mn-depleted photosystem II submembrane fractions and in photosystem II reaction center complexes. This reaction is also gradually photoinhibited due to the progressive photodegradation of the required electron transport intermediates but is significantly more stable in the presence of K-15. It is deduced that cyclic electron transport around photosystem II constitutes an effective protective mechanism against photoinhibitory damage.
Flasks of tryptic soy broth (TSB), unacidified (pH 7.2) or acidified with HCl or lactic acid to pH 6.3 or 5.5, and samples of sterile pork fat or muscle tissue, were inoculated with logarithmic phase cultures of a strain of Aeromonas hydrophila or a strain of Listeria monocytogenes. The broth cultures were incubated at temperatures between 0 and 25 degrees C, and growth rates were determined from optical density increases. The tissue samples were incubated at temperatures between -2.4 and 25.2 degrees C, and growth rates were determined from viable count increases. Both organisms grew without lag in all broths at temperatures greater than 10 degrees C. A hydrophila did not grow at 5 degrees C in TSB acidified with lactic acid to pH 5.5, and grew in other broths at that temperature after a lag of about 10 h. The organism did not grow in either broth of pH 5.5 at 2 degrees C, but grew in other broths at that temperature after a lag of about 40 h. A hydrophila did not grow in any broth at 0 degrees C. L. monocytogenes grew in all broths at 5 degrees C only after a lag of about 60 h, and did not grow in any broth at 2 degrees C. For both organisms, the rates of growth, at any temperature, were lower in broths of pH 6.3, and lower again in broths of pH 5.5, than in the unacidified broth. Growth rates in the broths of pH 6.3 were similar, but growth rates were lower in lactic acid acidified broth of pH 5.5 than in HCl acidified broth of that pH. The data for the growth of each organism in each medium were well described by the regression line of the plot of the square roots of growth rates against temperature. A hydrophila grew on fat tissue of pH 6.3 +/- 0.3, without lag, at 1.8 degrees C and higher temperatures at rates greater than the rates of growth in unacidified TSB. Numbers of the organism declined on muscle tissue of pH 5.6 +/0 0.2 at any temperature. L. monocytogenes grew on fat tissue without lag at -0.3 degrees C and higher temperatures, at rates which at lower temperatures were greater than the rates of growth in unacidified TSB. The organism grew on muscle tissue only at temperatures greater than or equal to 15.4 degrees C, at rates which were less than the rates of growth in lactic acid acidified broth of pH 5.5. Models derived from the cultivation of A. hydrophila and L. monocytogenes in commercial broths appear to be highly unreliable guides to the behaviours of those organisms on pork.