Remediation efforts for the oil spill from the Exxon Valdez tanker in Alaska have focused on the use of pressurized water at high temperature to remove oil from the beaches. We have tested a biological surfactant from Pseudomonas aeruginosa for its ability to remove oil from contaminated Alaskan gravel samples under various conditions, including concentration of the surfactant, time of contact, temperature of the wash, and presence or absence of xanthan gum. The results demonstrate the ability of the microbial surfactant to release oil to a significantly greater extent (2 to 3 times) than water alone, particularly at temperatures of 30 degrees C and above.

Rapid growth of BHK cells in methioninedeficient medium required supplementation with homocysteine, B12, and over 40-fold greater levels of folic acid than growth in methionine-supplemented medium. The activity of the B12-dependent 5-methyltetrahydrofolate:homocysteine methyltransferase was studied in extracts of BHK cells grown in media containing various concentrations of the components of the enzyme reaction. The methyltransferase activity increased over 4-fold when B12-deficient medium was supplemented with optimal levels of B12; this increase was not prevented by puromycin. Addition of homocysteine to growth medium containing methionine, B12, and folic acid was without effect. However, methyltransferase activity increased 2.5-to 4.0-fold further beyond the highest levels obtained in the presence of methionine, B12, and folic acid when homocysteine was substituted for methionine in the growth medium. This increase was blocked by puromycin and was not due to removal of feedback inhibition of activity by the product methionine. These results suggest that methyltransferase activity may be regulated in part by derepression of the enzyme's synthesis on substitution of the substrate homocysteine for the product methionine.

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Cultured mouse and human cells were arrested in their growth by artificially depriving them of phosphate. The quiescent cells could be stimulated to synthesize DNA and to divide by addition to the growth medium of insulin, dialyzed serum and/or the full concentration of phosphate. In order to gain insight into mechanisms by which insulin and serum stimulate growth, the inhibitory effects of antimitotic agents were examined. Of the inhibitors tested, vinblastine and cytocalasin B abolished the growth promoting activity of insulin, while colchicine inhibited the activity of both serum and insulin. The present results suggest that insulin-stimulated growth is meciated by a different path way than serum-stimulated growth and is sensitive to mechanisms that occur at various times prior to insulin addition.

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