scholarly journals Biological links between nanoparticle biosynthesis and stress responses in bacteria

2018 ◽  
Vol 3 (4) ◽  
pp. 44-69
Author(s):  
Angela Chen ◽  
Benjamin K. Keitz ◽  
Lydia M. Contreras
Keyword(s):  
Oxidative Stress ◽  
Resistance Genes ◽  
Stress Responses ◽  
Molecular Mechanisms ◽  
Metal Resistance ◽  
Reduction Mechanisms ◽  
Nanoparticle Morphology ◽  
Nanoparticle Biosynthesis ◽  
Oxidative Stress Responses

There is rising interest in nanoparticle biosynthesis using bacteria due to the potential for applications in bioremediation, catalysis, or as antimicrobials. However, biosynthesis remains limited by the inability to control nanoparticle morphology and size due to the lack of knowledge regarding explicit molecular mechanisms. Due to their importance in nanoparticle biosynthesis and as antimicrobials, we focus our discussion on silver, gold, and copper nanoparticles. We discuss recent efforts to elucidate reduction mechanisms that have identified generic enzymes and metal resistance genes as strong candidates to facilitate nanoparticle biosynthesis. Although it is known that these enzymes and genes play significant roles in maintaining bacterial homeostasis, there are few reports discussing this topic. Thus, we discuss examples of how metal resistance genes are conserved across bacteria and have been shown to be important for both nanoparticle biosynthesis and processes such as virulence or oxidative stress responses. Overall, this review highlights biological connections between nanoparticle biosynthesis and stress responses by examining the role of reductases and metal resistance genes in both processes. This understanding provides a greater role for nanoparticle biosynthesis in bacteria and could enable a systems biology level of control over nanoparticle biosynthesis.

scholarly journals The Transcriptional Response to a Peroxisome Proliferator-activated Receptor α Agonist Includes Increased Expression of Proteome Maintenance Genes

2004 ◽  
Vol 279 (50) ◽  
pp. 52390-52398 ◽  
Author(s):  
Steven P. Anderson ◽  
Paul Howroyd ◽  
Jie Liu ◽  
Xun Qian ◽  
Rainer Bahnemann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Responses ◽  
Transcriptional Response ◽  
Lipid Homeostasis ◽  
Peroxisome Proliferator ◽  
Wild Type ◽  
Peroxisome Proliferator Activated Receptor ◽  
Proteasomal Genes ◽  
Oxidative Stress Responses

The nuclear receptor peroxisome proliferator-activated receptor α (PPARα), in addition to regulating lipid homeostasis, controls the level of tissue damage after chemical or physical stress. To determine the role of PPARα in oxidative stress responses, we examined damage after exposure to chemicals that increase oxidative stress in wild-type or PPARα-null mice. Primary hepatocytes from wild-type but not PPARα-null mice pretreated with the PPAR pan-agonist WY-14,643 (WY) were protected from damage to cadmium and paraquat. The livers from intact wild-type but not PPARα-null mice were more resistant to damage after carbon tetrachloride treatment. To determine the molecular basis of the protection by PPARα, we identified by transcript profiling genes whose expression was altered by a 7-day exposure to WY in wild-type and PPARα-null mice. Of the 815 genes regulated by WY in wild-type mice (p≤ 0.001; ≥1.5-fold or ≤-1.5-fold), only two genes were regulated similarly by WY in PPARα-null mice. WY increased expression of stress modifier genes that maintain the health of the proteome, including those that prevent protein aggregation (heat stress-inducible chaperones) and eliminate damaged proteins (proteasome components). Although the induction of proteasomal genes significantly overlapped with those regulated by 1,2-dithiole-3-thione, an activator of oxidant-inducible Nrf2, WY increased expression of proteasomal genes independently of Nrf2. Thus, PPARα controls the vast majority of gene expression changes after exposure to WY in the mouse liver and protects the liver from oxidant-induced damage, possibly through regulation of a distinct set of proteome maintenance genes.

The role of a Brugia malayi p38 MAP kinase ortholog (Bm-MPK1) in parasite anti-oxidative stress responses

2011 ◽  
Vol 176 (2) ◽  
pp. 90-97 ◽  
Author(s):  
Akruti Patel ◽  
Agnieszka Nawrocka Chojnowski ◽  
Katie Gaskill ◽  
William De Martini ◽  
Ronald L. Goldberg ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Map Kinase ◽  
Stress Responses ◽  
Brugia Malayi ◽  
P38 Map Kinase ◽  
Oxidative Stress Responses

scholarly journals Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy

2016 ◽  
Vol 2016 ◽  
pp. 1-17 ◽  
Author(s):  
Xiaochun Duan ◽  
Zunjia Wen ◽  
Haitao Shen ◽  
Meifen Shen ◽  
Gang Chen
Keyword(s):  
Oxidative Stress ◽  
Intracerebral Hemorrhage ◽  
Stress Responses ◽  
Secondary Brain Injury ◽  
Mortality And Morbidity ◽  
Systemic Oxidative Stress ◽  
Preclinical And Clinical Studies ◽  
Apoptosis And Necrosis ◽  
Oxidative Stress Responses

Hemorrhagic stroke is a common and severe neurological disorder and is associated with high rates of mortality and morbidity, especially for intracerebral hemorrhage (ICH). Increasing evidence demonstrates that oxidative stress responses participate in the pathophysiological processes of secondary brain injury (SBI) following ICH. The mechanisms involved in interoperable systems include endoplasmic reticulum (ER) stress, neuronal apoptosis and necrosis, inflammation, and autophagy. In this review, we summarized some promising advances in the field of oxidative stress and ICH, including contained animal and human investigations. We also discussed the role of oxidative stress, systemic oxidative stress responses, and some research of potential therapeutic options aimed at reducing oxidative stress to protect the neuronal function after ICH, focusing on the challenges of translation between preclinical and clinical studies, and potential post-ICH antioxidative therapeutic approaches.

scholarly journals Genome-Wide Screening of Oxidizing Agent Resistance Genes in Escherichia coli

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 861
Author(s):  
Hao Chen ◽  
Jessica Wilson ◽  
Carson Ercanbrack ◽  
Hannah Smith ◽  
Qinglei Gan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Resistance Genes ◽  
Stress Responses ◽  
Host Cells ◽  
E Coli ◽  
Oxidizing Agents ◽  
Genome Wide ◽  
A Genome ◽  
Basic Studies ◽  
Oxidative Stress Responses

The use of oxidizing agents is one of the most favorable approaches to kill bacteria in daily life. However, bacteria have been evolving to survive in the presence of different oxidizing agents. In this study, we aimed to obtain a comprehensive list of genes whose expression can make Escherichiacoli cells resistant to different oxidizing agents. For this purpose, we utilized the ASKA library and performed a genome-wide screening of ~4200 E. coli genes. Hydrogen peroxide (H2O2) and hypochlorite (HOCl) were tested as representative oxidizing agents in this study. To further validate our screening results, we used different E. coli strains as host cells to express or inactivate selected resistance genes individually. More than 100 genes obtained in this screening were not known to associate with oxidative stress responses before. Thus, this study is expected to facilitate both basic studies on oxidative stress and the development of antibacterial agents.

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