Figure 1 Scheme MLN2238 purchase illustrating the effects of reactive oxygen species (ROS) into the cell (a) and antioxidant defense mechanisms (b) evaluated in this work. (a) Growth in the presence of reactive oxygen species (ROS): superoxide radical [O2 .-], hydrogen peroxide [H2O2], hydroxyl radical [OH-] and hydroperoxyl radical [HOO-]. These ROS can damage nucleic acids

(RNA and DNA) as well as proteins and lipids, leading to cell death. (b) The superoxide dismutases (SOD), which are cytosolic (Mn-SOD and Fe-SOD) and periplasmic (Cu-SOD) allow O2 .- detoxification. The catalase activity responsible for the reduction of H2O2 to H2O is effected by two hydroperoxydases [hydroperoxydase I (HPI) and hydroperoxydase II (HPII)], and the alkyl hydroperoxydase (AhpC). The glutathione is synthetised from glutamate, cysteine and glycine, by 2 unrelated ligases: the γ-glutamylcysteine synthetase (GshA) and the glutathione synthetase (GshB). The glutathione oxidoreductase (Gor) reduces glutathione disulfide (GSSG), which is formed upon oxidation. The glucose 6-phosphate dehydrogenase (G6PDH) Fer-1 molecular weight allows indirectly the reduction of NADP to NADPH. The Fenton reaction is the result of electron transfer from donor to H2O2 catalyzed by iron Fe3+. The stars show dosages effected

in this study. It has been demonstrated that growth under starvation conditions generates oxidative stress and significant changes in glutathione homeostasis [15–17]. The increased level of ROS comes from the imbalance between production and antioxidant mechanisms. Human urine is a high-osmolarity, Meloxicam moderately oxygenated, iron and nutrient-limited environment [18–21]. Therefore, growth in urine could be perceived as a stressful environment. In order to evaluate the importance of endogenous oxidative stress of growing cells in urine, oxidative damages to lipids were assayed in a range of E. coli strains

representative of various pathovars and phylogenetic groups. Antioxidant defense mechanisms in four representatives of these E. coli strains were also analysed. Methods Strains The twenty-one E. coli strains used in this study are described in Table 1; nine were pathogenic, three were commensal and nine ABU. The archetypal UPEC strain CFT073 was originally isolated from the blood and urine of a woman admitted to the University of Maryland Medical System [22]. Seven other UPEC prototypes, E. coli UTI 89, J96, UMN026, IAI39, IAI74, IH11128 and 536, were also studied [23–25]. E. coli ABU 83972, the archetypal ABU strain, is a clinical isolate capable of long-term bladder colonization [26]. Eight other ABU strains were also included [27]. E. coli K-12 MG 1655, a commensal, laboratory derived strain, was originally isolated from the faeces of a convalescent diphtheria patient in Palo Alto in 1922 [28]. E.