Collaborative effects of Photobacterium CuZn superoxide dismutase (SODs and human AP endonuclease in DNA repair and sod-deficient Escherichia coli under oxidative stress

2004 ◽  
Vol 36 (2) ◽  
pp. 173-179 ◽  
Author(s):  
Y Kim
Keyword(s):  
Oxidative Stress ◽  
Escherichia Coli ◽  
Dna Repair ◽  
Superoxide Dismutase ◽  
Ap Endonuclease ◽  
Cuzn Superoxide Dismutase

Aging and oxidative stress alter DNA repair mechanisms in male germ cells of superoxide dismutase-1 null mice

2021 ◽  
Author(s):  
Paulina Nguyen-Powanda ◽  
Bernard Robaire
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Repair ◽  
Superoxide Dismutase ◽  
Germ Cells ◽  
Superoxide Dismutase 1 ◽  
Male Germ Cells ◽  
Dna Repair Mechanisms ◽  
Repair Mechanisms ◽  
And Oxidative Stress

Abstract The efficiency of antioxidant defense system decreases with aging, thus resulting in high levels of reactive oxygen species (ROS) and DNA damage in spermatozoa. This damage can lead to genetic disorders in the offspring. There are limited studies investigating the effects of the total loss of antioxidants, such as superoxide dismutase-1 (SOD1), in male germ cells as they progress through spermatogenesis. In this study, we evaluated the effects of aging and removing SOD1 (in male germ cells of SOD1-null (Sod1−/−) mice) in order to determine the potential mechanism(s) of DNA damage in these cells. Immunohistochemical analysis showed an increase in lipid peroxidation and DNA damage in the germ cells of aged wild-type (WT) and Sod1−/− mice of all age. Immunostaining of OGG1, a marker of base excision repair (BER), increased in aged WT and young Sod1−/− mice. In contrast, immunostaining intensity of LIGIV and RAD51, markers of non-homologous end-joining (NHEJ) and homologous recombination (HR), respectively, decreased in aged and Sod1−/− mice. Gene expression analysis showed similar results with altered mRNA expression of these key DNA repair transcripts in pachytene spermatocytes and round spermatids of aged and Sod1−/− mice. Our study indicates that DNA repair pathway markers of BER, NHEJ, and HR are differentially regulated as a function of aging and oxidative stress in spermatocytes and spermatids, and aging enhances the repair response to increased oxidative DNA damage, whereas impairments in other DNA repair mechanisms may contribute to the increase in DNA damage caused by aging and the loss of SOD1.

scholarly journals Skeletal muscle weakness due to deficiency of CuZn-superoxide dismutase is associated with loss of functional innervation

2011 ◽  
Vol 301 (5) ◽  
pp. R1400-R1407 ◽  
Author(s):  
Lisa M. Larkin ◽  
Carol S. Davis ◽  
Catrina Sims-Robinson ◽  
Tatiana Y. Kostrominova ◽  
Holly Van Remmen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Muscle Weakness ◽  
Muscle Atrophy ◽  
Muscle Stimulation ◽  
Wild Type ◽  
Functional Changes ◽  
Fiber Number ◽  
Cuzn Superoxide Dismutase

An association between oxidative stress and muscle atrophy and weakness in vivo is supported by elevated oxidative damage and accelerated loss of muscle mass and force with aging in CuZn-superoxide dismutase-deficient ( Sod1−/−) mice. The purpose was to determine the basis for low specific force (N/cm2) of gastrocnemius muscles in Sod1−/− mice and establish the extent to which structural and functional changes in muscles of Sod1−/− mice resemble those associated with normal aging. We tested the hypothesis that muscle weakness in Sod1−/− mice is due to functionally denervated fibers by comparing forces during nerve and direct muscle stimulation. No differences were observed for wild-type mice at any age in the forces generated in response to nerve and muscle stimulation. Nerve- and muscle-stimulated forces were also not different for 4-wk-old Sod1−/− mice, whereas, for 8- and 20-mo-old mice, forces during muscle stimulation were 16 and 30% greater, respectively, than those obtained using nerve stimulation. In addition to functional evidence of denervation with aging, fiber number was not different for Sod1−/− and wild-type mice at 4 wk, but 50% lower for Sod1−/− mice by 20 mo, and denervated motor end plates were prevalent in Sod1−/− mice at both 8 and 20 mo and in WT mice by 28 mo. The data suggest ongoing denervation in muscles of Sod1−/− mice that results in fiber loss and muscle atrophy. Moreover, the findings support using Sod1−/− mice to explore mechanistic links between oxidative stress and the progression of deficits in muscle structure and function.

Synechocystis Fe superoxide dismutase gene confers oxidative stress tolerance to Escherichia coli

2004 ◽  
Vol 316 (2) ◽  
pp. 540-544 ◽  
Author(s):  
Jyotirmoy Bhattacharya ◽  
Krishnarup GhoshDastidar ◽  
Anirban Chatterjee ◽  
Manoj Majee ◽  
Arun Lahiri Majumder
Keyword(s):  
Oxidative Stress ◽  
Escherichia Coli ◽  
Superoxide Dismutase ◽  
Stress Tolerance ◽  
Oxidative Stress Tolerance ◽  
Superoxide Dismutase Gene

Further investigation of the mechanism of Vitreoscilla hemoglobin (VHb) protection from oxidative stress in Escherichia coli

Biologia ◽  
2011 ◽  
Vol 66 (5) ◽  
Author(s):  
Meltem Akbas ◽  
Tugrul Doruk ◽  
Serhat Ozdemir ◽  
Benjamin Stark
Keyword(s):  
Oxidative Stress ◽  
Escherichia Coli ◽  
Hydrogen Peroxide ◽  
Superoxide Dismutase ◽  
Stationary Phase ◽  
Exponential Phase ◽  
Vitreoscilla Hemoglobin ◽  
Sod Activity ◽  
E Coli ◽  
Hydrogen Peroxide Treatment

AbstractIn Escherichia coli, Vitreoscilla hemoglobin (VHb) protects against oxidative stress, perhaps, in part, by oxidizing OxyR. Here this protection, specifically VHb-associated effects on superoxide dismutase (SOD) and catalase levels, was examined. Exponential or stationary phase cultures of SOD+ or SOD− E. coli strains with or without VHb and oxyR antisense were treated with 2 mM hydrogen peroxide without sublethal peroxide induction, and compared to untreated control cultures. The hydrogen peroxide treatment was toxic to both SOD+ and SOD− cells, but much more to SOD− cells; expression of VHb in SOD+ strains enhanced this toxicity. In contrast, the presence of VHb was generally associated in the SOD+ background with a modest increase in SOD activity that was not greatly affected by oxyR antisense or peroxide treatment. In both SOD+ and SOD− backgrounds, VHb was associated with higher catalase activity both in the presence and absence of peroxide. Contrary to its stimulatory effects in stationary phase, in exponential phase oxyR antisense generally decreased VHb levels.

scholarly journals Susceptibility to Antibiotics and Reactive Oxygen Species in Escherichia coli: A Survey of Clinical and Environmental Isolates

2021 ◽  
pp. 64-71
Author(s):  
Carlos F. Amábile-Cuevas ◽  
Leticia Martínez ◽  
Irma Rosas
Keyword(s):  
Oxidative Stress ◽  
Escherichia Coli ◽  
Superoxide Dismutase ◽  
Antibiotic Resistance ◽  
Cross Resistance ◽  
Bacterial Cells ◽  
Urban Dust ◽  
Beta Lactam ◽  
Gastrointestinal Infections ◽  
Selection Of

Aims: Some bacterial responses to oxidative stress also diminish antibiotic susceptibility; also, some antibiotics do increase oxidative stress within bacterial cells. Linkage or cross-resistance to prooxidants and antibiotics could facilitate the selection of antibiotic resistance and/or virulence. We made this survey in order to detect this possible linkage in Escherichia coli isolates. Methodology: The susceptibility of 102 E. coli clinical (causative of urinary or gastrointestinal infections) and environmental (rural or urban dust) isolates towards paraquat, H2O2, and antibiotics was measured using disc assays. Catalase and superoxide-dismutase (SOD) activities were measured. Results: Susceptibility to prooxidants was similar across isolates of all four sources, but urinary and urban dust isolates were more resistant to antibiotics. H2O2 "resistant" organisms had more antibiotic resistance phenotypes, particularly towards sulfadiazine and tetracycline. Paraquat "resistance" seems associated to beta-lactam resistance; but paraquat "susceptibility" seems associated to resistance towards chloramphenicol, gentamicin, ciprofloxacin and nitrofurantoin. Prooxidant disc assays correlate to catalase and superoxide-dismutase activities. A weak relationship H2O2/antibiotic-resistance, but not superoxide/antibiotic-resistance, is suggested. Conclusion: Overall, antibiotics exerting their action through oxidative stress, do not seem to have resulted in the co-selection of oxidative stress resistance, or vice versa. However, a possible link between resistance to some antibiotics and to H2O2 might contribute to co-selection between these two chemical insults.

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