RESUMO
The microbiologically influenced corrosion (MIC) behavior of carbon steel is investigated in the presence of Vibrio and Pseudomonas. Sterilized natural seawater inoculated with Pseudomonas, Vibrio, and the mixture of Pseudomonas and Vibrio, separately, and they are utilized as the media for corrosion characterizations, which are closer to the natural environment in seawater. Weight loss measurements, electrochemical techniques (the open-circuit potential, electrochemical impedance spectroscopy (EIS), and potentiodynamic polarization curves), and surface analysis (scanning electron microscopy (SEM)) are performed to explore the synergistic effect of Pseudomonas and Vibrio on the corrosion behavior of carbon steel. As seen from the growth curves of bacteria, the growth and propagation of Pseudomonas and Vibrio are affected by their metabolic activities. Besides, the results obtained by SEM show that more severe pitting corrosion is observed on the coupons exposed to the sterilized natural seawater inoculated with the mixture of Pseudomonas and Vibrio. Further, the results from electrochemical measurements and weight loss measurements suggest that under the synergistic effect of Pseudomonas and Vibrio, the initial corrosion rate of carbon steel is inhibited, while the latter corrosion is enhanced.
RESUMO
Cells exposed to oxygen deprivation in vitro have been shown to reduce proliferation and/or engage in programmed cell death. There is considerable controversy in the literature as to the role of hypoxia-inducible factor-1 (HIF-1) and HIF-1 target genes in initiating these responses. We therefore examined the oxygen dependence and the role of the hypoxia-responsive transcription factor HIF-1 in making the cellular death decision. Oxygen concentrations as low as 0.5% did not alter the growth of HIF-1-proficient or HIF-1-deficient murine fibroblasts, or human tumor cells, despite the appropriate induction of HIF-1 target genes. Severe hypoxia (<0.01% oxygen) did induced apoptosis, resulting in decreased colony formation, chromatin condensation, DNA fragmentation, and caspase activation but also independent of HIF1alpha status. Transcriptional induction of HIF-1-dependent genes putatively involved in cell death like BNip3 and BNip3L was therefore disassociated from hypoxia-dependent toxicity. Likewise, forced overexpression of a nondegradable form of HIF-1alpha in several human tumor cell lines was not sufficient to induce apoptosis under normoxic conditions. Taken together, these findings indicate that additional molecular events are triggered by anoxia in a HIF-1-independent manner, and these changes are necessary for cell death observed in low-oxygen environments.
