The effects of biostimulation and bioaugmentation on crude oil biodegradation in two adjacent terrestrial oil spills of different age, in a hyper-arid region.

This study deals with two adjacent terrestrial oil spills, with similar properties, located in a hyper-arid region in Israel, one from 1975 and the other from 2014. It tests the effect of biostimulation on crude oil degradation in both spills and whether biostimulated sediments from the 1975 spill can bioaugment crude oil degradation in the 2014 spill. Soil hydrophobicity, expressed as Water Drop Penetration Time (WDPT), and Gasoline Range Organics (GRO) and Diesel Range Organics (DRO) content in sediments were measured in one-month ex-situ experiments. No significant reduction in hydrophobicity and GRO + DRO content was observed in non-biostimulated controls. A combined treatment of mineral fertilization at t0 and maintaining 50% water saturation, significantly accelerated the decrease in hydrophobicity and GRO + DRO content in sediments of both spills. The addition of biostimulated sediments from the 1975 spill failed to accelerate the reduction of GRO + DRO content and hydrophobicity in the 2014 spill. Surprisingly, the GRO + DRO degradation rate in biostimulated sediments from the 2014 spill was 36% higher than in biostimulated sediments from the 1975 spill. Crude oil composition in both spills changes during its degradation and is characterized by an increase in the GRO fraction. To a certain range, WDPT was found to serve as a reliable indicator for oil content in the soil. We conclude that even in a hyper-arid region, oil bio-degradation capabilities develop in a relatively short time. Moreover, while biostimulation was effective in accelerating biodegradation, bioaugmentation with biostimulated sediments from a nearby older spill was found ineffective.

Experimental tongue cancer in desalivated rats.

A group of 39 rats underwent excision of the submandibular and sublingual glands and ligation of the parotid ducts through the midventral incision of the neck, while the control group (41 rats) underwent a sham operation. All rats were administered 4NQO in a final concentration of 0.001% in drinking water. At 7, 14, 22 and 28 weeks after administering 4NQO, both groups of rats were killed and their tongues dissected, inspected and then fixed in 10% buffered formalin for histopathological examination. Clinical examination during the first 14 weeks revealed that rats in both groups looked healthy and no differences in body weight were noticed. Afterwards, the average weight gain of the desalivated rats was lower than in the control group (P < 0.01). The number of macroscopic oral lesions increased with time in both groups. However, in the desalivated rats, the first identifiable lesions were seen as early as week 7, whereas in the control group macroscopic lesions were seen only after 22 weeks. Histological examination revealed more affected rats in the desalivated group in the first 14 weeks after administering the carcinogen; lesions showed more severe pathological changes including two cases with evidence of squamous cell carcinoma. The differences between the desalivated groups and control decreased after 22 weeks with almost no differences at the end of the experiment.

Induction of urokinase-type plasminogen activator by UV light in human fetal fibroblasts is mediated through a UV-induced secreted protein.

Plasminogen activator was previously shown to be induced by UV light in human cells with low capacity to repair UV-induced DNA lesions. We now show that in human fetal fibroblasts UV light enhanced the two mRNA species coding for the urokinase-type plasminogen activator (uPA) and the tissue-type plasminogen activator, but immunological analysis revealed exclusively uPA activity. Several independent and complementary experiments indicated that induction of uPA was mediated, apparently entirely, through a UV-induced, secreted protein (UVIS) in the growth medium of irradiated cells. First, elevation of uPA mRNA after irradiation was severely blocked by cycloheximide. Second, replacement of conditioned medium in irradiated cells while the rate of plasminogen activator induction was maximal rapidly and completely stopped any further increase in uPA activity. Third, addition of the same removed conditioned medium to nonirradiated cells mimicked UV light in enhancing the level of uPA activity as well as that of uPA mRNA. Fourth, UVIS activity was completely lost by treating the conditioned medium with trypsin but not with nucleases. Kinetic measurements indicated that the accumulation of UVIS rather than the induction of uPA by UVIS conferred the rate-limiting step in the overall process of uPA induction. Both UV light and UVIS acted synergistically with inhibitors of DNA repair for uPA induction. Based on these results, a model is proposed implicating relaxation of DNA torsional stress of an as yet undefined DNA sequence(s) in the induction of UVIS, which is then responsible for activation of the uPA gene.