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Oxidative Stressors (oxidative + stressor)
Selected AbstractsMicrobial interactions and differential protein expression in Staphylococcus aureus ,Candida albicans dual-species biofilmsFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2010Brian M. Peters Abstract The fungal species Candida albicans and the bacterial species Staphylococcus aureus are responsible for a majority of hospital-acquired infections and often coinfect critically ill patients as complicating polymicrobial biofilms. To investigate biofilm structure during polymicrobial growth, dual-species biofilms were imaged with confocal scanning laser microscopy. Analyses revealed a unique biofilm architecture where S. aureus commonly associated with the hyphal elements of C. albicans. This physical interaction may provide staphylococci with an invasion strategy because candidal hyphae can penetrate through epithelial layers. To further understand the molecular mechanisms possibly responsible for previously demonstrated amplified virulence during coinfection, protein expression studies were undertaken. Differential in-gel electrophoresis identified a total of 27 proteins to be significantly differentially produced by these organisms during coculture biofilm growth. Among the upregulated staphylococcal proteins was l -lactate dehydrogenase 1, which confers resistance to host-derived oxidative stressors. Among the downregulated proteins was the global transcriptional repressor of virulence factors, CodY. These findings demonstrate that the hyphae-mediated enhanced pathogenesis of S. aureus may not only be due to physical interactions but can also be attributed to the differential regulation of specific virulence factors induced during polymicrobial growth. Further characterization of the intricate interaction between these pathogens at the molecular level is warranted, as it may aid in the design of novel therapeutic strategies aimed at combating fungal,bacterial polymicrobial infection. [source] Chromate tolerance caused by reduced hydroxyl radical production and decreased glutathione reductase activity in Schizosaccharomyces pombeJOURNAL OF BASIC MICROBIOLOGY, Issue 2 2003Zoltán Gazdag The stable Cr(VI)-tolerant chr1-66T mutant of Schizosaccharomyces pombe, which carries one simple gene mutation responsible for Cr(VI) tolerance, accumulated and reduced the chromate anion (CrO42,) significantly more slowly than did its parental strain 6chr+. The mutant chr1-66T proved to be sensitive to oxidative stressors such as H2O2, menadione, tert -butyl hydroperoxide and Cd2+. Both the Cr(VI) tolerance and the oxidative stress sensitivity were attributed to a decreased specific glutathione reductase activity. These effects were also enhanced with a decrease in the specific mitochondrial Mn-SOD activity. [source] Dopamine activates Nrf2-regulated neuroprotective pathways in astrocytes and meningeal cellsJOURNAL OF NEUROCHEMISTRY, Issue 1 2007Andy Y. Shih Abstract The transcription factor Nrf2 controls inducible expression of multiple antioxidant/detoxification genes. We previously found that Nrf2 -/- mice have increased sensitivity to in vivo mitochondrial stress and ischemia. Although Nrf2 regulated these forms of neuronal toxicity, it was unclear which injury-triggered signal(s) led to Nrf2 activation in vivo. In this study, we use primary cultures to test the hypothesis that excessive dopamine release can act as an endogenous Nrf2-inducing signal. We cultured two cell types that show increased Nrf2 activity during ischemia in vivo, astrocytes and meningeal cells. Cultures were infected with an adenovirus reporter of Nrf2 transcriptional activity. Dopamine-induced Nrf2 activity in both cell types by generating oxidative stressors, H2O2 and dopamine-quinones. Nrf2 activation in meningeal cells was significantly higher than astrocytes. The effect of dopamine was blocked by antioxidants, and by over-expression of either dominant-negative Nrf2 or Keap1. Nrf2 induction was specific to oxidative stress caused by catecholaminergic neurotransmitters as epinephrine also induced Nrf2, but the monoamine serotonin had no significant effect. These in vitro results suggest Nrf2 activity in astrocytes and meningeal cells link the neurotoxic actions of dopamine to neuroprotective pathways that may potentially modulate ischemic injury and neurodegeneration. [source] Peroxynitrite: just an oxidative/nitrosative stressor or a physiological regulator as well?BRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2006Péter Ferdinandy British Journal of Pharmacology (2006) 148, 1,3. doi:10.1038/sj.bjp.0706693 [source] | |||||||||||||