Several pathways of hydrogen peroxide action that damage the E. coli genome

Abstract

Hydrogen peroxide is an important reactive oxygen species (ROS) that arises either during the aerobic respiration process or as a by-product of water radiolysis after exposure to ionizing radiation. The reaction of hydrogen peroxide with transition metals imposes on cells an oxidative stress condition that can result in damage to cell components such as proteins, lipids and principally to DNA, leading to mutagenesis and cell death. Escherichia coli cells are able to deal with these adverse events via DNA repair mechanisms, which enable them to recover their genome integrity. These include base excision repair (BER), nucleotide excision repair (NER) and recombinational repair. Other important defense mechanisms present in Escherichia coli are OxyR and SosRS anti-oxidant inducible pathways, which are elicited by cells to avoid the introduction of oxidative lesions by hydrogen peroxide. This review summarizes the phenomena of lethal synergism between UV irradiation (254 nm) and H 2 O 2 , the cross-adaptive response between different classes of genotoxic agents and hydrogen peroxide, and the role of copper ions in the lethal response to H 2 O 2 under low-iron conditions. Key words: hydrogen peroxide, cross-adaptive response, lethal synergism, copper and iron. General AspectsThe appearance of aerobic forms of life was an important step in the evolutionary process, since oxygen consumption leads to the production of ten-fold more energy from glucose than does anaerobic metabolism (Meneghini, 1987). However, this process imposes constraints on cell viability, because of the generation of reactive oxygen species during respiration.The consecutive univalent reduction of molecular oxygen to water produces three active intermediates: superoxide anion (O 2 -• ), hydrogen peroxide (H 2 O 2 ) and hydroxyl radical (OH • ). These intermediates, collectively referred to as reactive oxygen species (ROS) are potent oxidants of lipids, proteins, and nucleic acids (Halliwell and Gutteridge, 1984;Mello-Filho and Meneghini, 1985;Meneghini, 1988). Among the oxidative DNA lesions, one of the major classes of DNA damage leads to modification in purine and pyrimidine bases, together with oligonucleotide strand breaks, DNA-protein cross-links and abasic sites. Increasing evidence suggests that the cumulative damage caused by ROS contributes to numerous degenerative diseases associated with aging, such as atherosclerosis, rheumatoid arthritis and cancer (Ames et al., 1993;Halliwell and Gutteridge, 1999).Living organisms have developed specific mechanisms to prevent the production and effects of ROS. The reduction of O 2 by cytochrome oxidase without yielding ROS, the superoxide dismutase catalysis of O 2 -• into H 2 O 2 through a dismutation reaction, the decomposition of H 2 O 2 by catalase and peroxidases, and the scavenging of ROS by some vitamins comprise part of the set of cellular antioxidant defenses (Halliwell and Gutteridge, 1999). Synthesis of the enzymes that catalyze these reactions is a part of the adaptive response tr...

Under Increased Hydrogen Peroxide conditions, the Antioxidant Effects of Pequi Oil (Caryocar brasiliense Camb.) to Decrease DNA Damage in Runners are Influenced by Sex, Age and oxidative Stress-related Genetic Polymorphisms

“…[1,2] Before pequioil supplementation, results suggested that the tolerance for an increased oxidative stress and consequent DNA damage happened only with H 2 O 2 at up to 0.25 mM; the treatment with H 2 O 2 at 1 mM increased oxidative stress above the capacity of the organism to adapt. However, this tolerance did not occur for age group above 41 years, distances above 10 Km and the genotypes MnSOD Ala/Ala, CAT TT and ACE ID.…”

“…[1] If not controlled, the reaction of H 2 O 2 with transition metals can provoke oxidative stress in the under Increased Hydrogen Peroxide conditions, the Antioxidant Effects of Pequi oil (Caryocar brasiliense camb.) to decrease dnA damage in runners are Influenced by Sex, Age and oxidative Stress-related Genetic Polymorphisms www.antiox.org of ROS, deficient antioxidant defenses, or a combination of both.…”

Current Importance and Potential Use of Low Doses of Gamma Radiation in Forest Species

“…Thus, radioadaptive response induction expresses the ability of low dose radiation to induce cellular changes that alter the level of subsequent radiation-induced or spontaneous damage (Amundson et al, 1999). The exposure to minimal stress inducing a very low level of damage can trigger an AR resulting in increased resistance to higher levels of the same or of other types of stress (Patra et al, 2003;Asad et al, 2004;Girigoswami & Ghosh, 2005;Yan et al, 2006). The AR could be considered a nonspecific phenomenon and have been confirmed but not explained by many studies.…”

Adaptive response: some underlying mechanisms and open questions

“…Thus, radioadaptive response induction expresses the ability of low dose radiation to induce cellular changes that alter the level of subsequent radiation-induced or spontaneous damage. The AR could be considered a nonspecific phenomenon -the exposure to minimal stress inducing a very low level of damage can trigger an AR resulting in increased resistance to higher levels of the same or of other types of stress (Joiner et al, 1996;Wolff, 1998;Joiner et al, 1999;Patra et al, 2003;Asad et al, 2004;Girigoswami and Ghosh, 2005;Yan et al, 2006). The AR has been observed in many different organisms: bacteria, yeast, the algae Oedogonium cardiacam, Chlamydomonas reinhardtii, Closterium monoliferum and Chlorella pyrenoidosa, in higher plants, insect cells, mammalian cells, human cells in vitro, and in animal models in vivo during a protracted (low dose-rate) exposure prior to an acute dose treatment Laszlo, 1971, 1973;Bryant, 1974Bryant, , 1975Bryant, , 1976Bryant, , 1979Cowie, 1976, 1978;Olivieri et al, 1984;Santier et al, 1985;Wolff et al, 1988;Boreham and Mitchel, 1991;Rieger et al, 1993;Mahmood et al, 1996;Salone et al, 1996;Panda et al, 1997;Asad et al, 1997Asad et al, , 1998Wolff, 1998;Nikolova et al,showing gene expression changes, DNA single-and double-strand breaks, biochemical analyses of enzymatic and/or non-enzymatic antioxidant defence system (Hillova and Drasil 1967;Bryant, 1975Bryant, , 1976Bryant, , 1979Rieger et al, 1993;Ikushima et al, 1996;Rigaud and Moustacchi, 1996;Panda et al, 1997;…”