Preparation of Protein Extracts from Schizosaccharomyces pombe Using Trichloroacetic Acid Precipitation.

Schizosaccharomyces pombe is an attractive model organism with which to study core principles of conserved molecular cell biology processes. The ability to monitor protein behavior following separation by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) underpins much of this activity. Here we describe a robust protocol for the preparation of protein samples for analysis by SDS-PAGE.

Potentials of biological oxidation processes for the treatment of spent sulfidic caustics containing thiols.

This research focused on the biological treatment of sulfidic spent caustics from refineries, which contain mainly hydrogen sulfide, methanethiol (MT) and ethanethiol (ET). Also various organic compounds can be present such as BTEX. Biological oxidation of 2.5 mM MT in batch experiments occurred after MT was first auto-oxidized into dimethyldisulfide (DMDS) whereafter oxidation into sulfate was completed in 350 h. DMDS as sole substrate was completely oxidized within 40 h. Therefore, DMDS formation seems to play an important role in detoxification of MT. Biological oxidation of ET and buthanethiol was not successful in batch experiments. Complete oxidation of MT and ET was observed in flow-through reactor experiments. Simultaneous oxidation of sulfide and MT was achieved when treating a synthetic spent caustic, containing 10 mM sulfide and 2.5 mM MT, in a bubble column reactor with carrier material at a hydraulic retention time of 6 h. Addition of 7.5 mM phenol, a common pollutant of spent caustics, did not adversely affect the biological oxidation process and phenol was completely removed from the effluent. Finally, three different spent caustics solutions from refineries were successfully treated.

Lesiones digestivas producidas por cáusticos / Digestive injuries produced by caustic

La ingestión de sustancias cáusticas, ácidas o alcalinas, constituyen una situación relativamente frecuente en nuestro medio, capaz de lesionar con menor o mayor severidad, sobre todo el esófago y el estómago, a consecuencia de una reacción química relacionada con la naturaleza del cáustico, el móvil de la ingesta (accidental o suicida), la cantidad y concentración del agente ingerido.

Trichloroacetic acid in the environment.

Suppositions that the trichloroacetic acid (TCA, CCl3C(O)OH) found in nature was a consequence solely of the use of chlorinated hydrocarbon solvents prompted this critical review of the literature on its environmental fluxes and occurrences. TCA is widely distributed in forest soils (where it was rarely used as an herbicide) and measurements suggest a soil flux of 160 000 tonnes yr(-1) in European forests alone. TCA is also produced during oxidative water treatment and the global flux could amount to 55 000 tonnes yr(-1) (from pulp and paper manufacture, potable water and cooling water treatments). By contrast, the yields of TCA from chlorinated hydrocarbon solvents are small: from tetrachloroethene 13 600 tonnes yr(-1) and from 1,1,1-trichloroethane 4300 tonnes yr(-1) on a global basis, at the atmospheric burdens and removal rates typical of the late 1990s. TCA is ubiquitous in rainwater and snow. Its concentrations are highly variable and the variations cannot be connected with location or date. However, there is no significant difference between the concentrations found in Chile and in eastern Canada (by the same analysts), or between Malawi and western Canada, or between Antarctica and Switzerland, nor any significant difference globally between the concentrations in cloud, rain and snow (although local enhancement in fog water has been shown). TCA is present in old ice and firn. At the deepest levels, the firn was deposited early in the 19th century, well before the possibility of contamination by industrial production of reactive chlorine, implying a non-industrial background. This proposition is supported by plume measurements from pulp mills in Finland. TCA is ubiquitous in soils; concentrations are very variable but there are some indications that soils under coniferous trees contain higher amounts. The concentrations of TCA found in plant tissue are region-specific and may also be plant-specific, to the extent that conifers seem to contain more than other species. TCA is removed from the environment naturally. There is abundant evidence that soil microorganisms dehalogenate TCA and it is lost from within spruce needles with a half-life of 10 days. There is also recent evidence of an abiotic aqueous decarboxylation mechanism with a half-life of 22 days. The supposedly widespread effects of TCA in conifer needles are not shown in controlled experiments. At concentrations in the needles of Scots pine similar to those observed in needles in forest trees, changes consequent on TCA treatment of field laboratory specimens were almost all insignificant.

Protective effect of deferoxamine on chromium (VI)-induced DNA single-strand breaks, cytotoxicity, and lipid peroxidation in primary cultures of rat hepatocytes.

Incubation of primary cultures of rat hepatocytes with K2CR2O7 and deferoxamine (DFO), an iron chelator, resulted in a marked decrease in cellular levels of DNA single-strand breaks caused by K2Cr2O7. Cellular treatment with DFO also suppressed both dichromate-induced cytotoxicity--evaluated by the leakage of lactate dehydrogenase, and lipid peroxidation--as monitored by malondialdehyde formation. In addition, treatment with DFO attenuated the suppression of the levels of vitamin E and C as well as the inhibition of alkaline phosphatase and glutathione peroxidase activity attributed to K2Cr2O7. However, DFO had no influence on the cellular level of glutathione or the activity of glutathione reductase and superoxide dismutase suppressed by dichromate. Under the same experimental conditions, cellular uptake and distribution of chromium were not affected by DFO. These results indicate that DFO protects cells from chromium (VI)-induced DNA strand breaks, cytotoxicity, lipid peroxidation, vitamin E and C depression, and glutathione peroxidase inhibition The role of antioxidants in chromium (VI)-induced cytotoxicity, DNA breaks, and lipid peroxidation is discussed.