Potential of the homeopathic remedy, Arnica Montana 30C, to reduce DNA damage in Escherichia coli exposed to ultraviolet irradiation through up-regulation of nucleotide excision repair genes

2012 ◽  
Vol 10 (3) ◽  
pp. 337-346 ◽  
Author(s):  
S Das
Keyword(s):  
Escherichia Coli ◽  
Dna Damage ◽  
Nucleotide Excision Repair ◽  
Ultraviolet Irradiation ◽  
Excision Repair ◽  
Homeopathic Remedy ◽  
Arnica Montana ◽  
Nucleotide Excision ◽  
Repair Genes

Overexpression of Escherichia coli nucleotide excision repair genes after cisplatin-induced damage

DNA Repair ◽  
2013 ◽  
Vol 12 (1) ◽  
pp. 63-72 ◽  
Author(s):  
Deise Fonseca Felício ◽  
Leonardo da Silva Vidal ◽  
Roberto Silva Irineu ◽  
Alvaro Costa Leitão ◽  
Wanda Almeida von Kruger ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Nucleotide Excision ◽  
Repair Genes

The role of nucleotide excision repair of Escherichia coli in repair of spontaneous and gamma-radiation-induced DNA damage in the lacZα gene

2000 ◽  
Vol 460 (2) ◽  
pp. 117-125 ◽  
Author(s):  
Gitta K Kuipers ◽  
Ben J Slotman ◽  
Hester A Poldervaart ◽  
Ingrid M.J van Vilsteren ◽  
Carola A Reitsma-Wijker ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Dna Damage ◽  
Gamma Radiation ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Nucleotide Excision ◽  
Radiation Induced

scholarly journals Nucleotide Excision Repair Is a Predominant Mechanism for Processing Nitrofurazone-Induced DNA Damage in Escherichia coli

2009 ◽  
Vol 191 (15) ◽  
pp. 4959-4965 ◽  
Author(s):  
Katherine R. Ona ◽  
Charmain T. Courcelle ◽  
Justin Courcelle
Keyword(s):  
Escherichia Coli ◽  
Dna Damage ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Short Exposure ◽  
Direct Inhibition ◽  
Pol Iv ◽  
Primary Mechanism ◽  
Nucleotide Excision ◽  
High Concentrations

ABSTRACT Nitrofurazone is reduced by cellular nitroreductases to form N 2-deoxyguanine (N 2-dG) adducts that are associated with mutagenesis and lethality. Much attention recently has been given to the role that the highly conserved polymerase IV (Pol IV) family of polymerases plays in tolerating adducts induced by nitrofurazone and other N 2-dG-generating agents, yet little is known about how nitrofurazone-induced DNA damage is processed by the cell. In this study, we characterized the genetic repair pathways that contribute to survival and mutagenesis in Escherichia coli cultures grown in the presence of nitrofurazone. We find that nucleotide excision repair is a primary mechanism for processing damage induced by nitrofurazone. The contribution of translesion synthesis to survival was minor compared to that of nucleotide excision repair and depended upon Pol IV. In addition, survival also depended on both the RecF and RecBCD pathways. We also found that nitrofurazone acts as a direct inhibitor of DNA replication at higher concentrations. We show that the direct inhibition of replication by nitrofurazone occurs independently of DNA damage and is reversible once the nitrofurazone is removed. Previous studies that reported nucleotide excision repair mutants that were fully resistant to nitrofurazone used high concentrations of the drug (200 μM) and short exposure times. We demonstrate here that these conditions inhibit replication but are insufficient in duration to induce significant levels of DNA damage.

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