Factors contributing to the outcome of oxidative damage to nucleic acids

Evans, Mark D.; Cooke, Marcus S.

doi:10.1002/bies.20027

Cited by 234 publications

(170 citation statements)

References 62 publications

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“…17-20 Oxidative stress can also damage lipids and impair cell structure and function 21 and can damage DNA, resulting in strand breaks, DNA-DNA and DNA-protein crosslinks, and other oxidation and fragmentation products. 22 The present study is limited in that oxidative damage to lipids and DNA were not measured. In addition to damaging biomolecules directly, reactive oxygen species can trigger redox sensitive transcription factors such as NF-kappa B and AP-1 that are involved in the upregulation of inflammatory cytokines such as interleukin-6.…”

Section: Discussionmentioning

confidence: 91%

Oxidative Stress and Severe Walking Disability among Older Women

Semba

Ferrucci

Sun

et al. 2007

The American Journal of Medicine

115

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Section: Discussionmentioning

confidence: 91%

Oxidative Stress and Severe Walking Disability among Older Women

Semba

Ferrucci

Sun

et al. 2007

The American Journal of Medicine

115

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“…This latent accumulation of oxidized DNA could possibly come from two sources. The latent increase in A␤ could promote the formation of reactive oxygen species, thus damaging the DNA; and/or epigenetic modulation in the methylation pattern of cytosines could interfere with the repair of oxidized guanines or render them more susceptible to oxidative damage (Evans and Cooke, 2004).…”

Section: Discussionmentioning

confidence: 99%

Alzheimer's Disease (AD)-Like Pathology in Aged Monkeys after Infantile Exposure to Environmental Metal Lead (Pb): Evidence for a Developmental Origin and Environmental Link for AD

Wu¹,

Basha²,

Brock³

et al. 2008

J. Neurosci.

443

271

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The sporadic nature of Alzheimer's disease (AD) argues for an environmental link that may drive AD pathogenesis; however, the triggering factors and the period of their action are unknown. Recent studies in rodents have shown that exposure to lead (Pb) during brain development predetermined the expression and regulation of the amyloid precursor protein (APP) and its amyloidogenic ␤-amyloid (A␤) product in old age. Here, we report that the expression of AD-related genes [APP, BACE1 (␤-site APP cleaving enzyme 1)] as well as their transcriptional regulator (Sp1) were elevated in aged (23-year-old) monkeys exposed to Pb as infants. Furthermore, developmental exposure to Pb altered the levels, characteristics, and intracellular distribution of A␤ staining and amyloid plaques in the frontal association cortex. These latent effects were accompanied by a decrease in DNA methyltransferase activity and higher levels of oxidative damage to DNA, indicating that epigenetic imprinting in early life influenced the expression of AD-related genes and promoted DNA damage and pathogenesis. These data suggest that AD pathogenesis is influenced by early life exposures and argue for both an environmental trigger and a developmental origin of AD.

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“…While mechanisms exist to repair these DNA lesions, the level of DNA damage may exceed the capacity of the cellular repair mechanisms. Furthermore, mtDNA is believed to be particularly susceptible to sustained damage, since mitochondria may lack appropriate DNA repair mechanisms (Evans and Cooke 2004).…”

Section: Dna Damagementioning

confidence: 99%

An overview of chagasic cardiomyopathy: pathogenic importance of oxidative stress

Zacks

Wen

Vyatkina

et al. 2005

An. Acad. Bras. Ciênc.

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There is growing evidence to suggest that chagasic myocardia are exposed to sustained oxidative stressinduced injuries that may contribute to disease progression. Pathogen invasion-and replication-mediated cellular injuries and immune-mediated cytotoxic reactions are the common source of reactive oxygen species (ROS) in infectious etiologies. However, our understanding of the source and role of oxidative stress in chagasic cardiomyopathy (CCM) remains incomplete. In this review, we discuss the evidence for increased oxidative stress in chagasic disease, with emphasis on mitochondrial abnormalities, electron transport chain dysfunction and its role in sustaining oxidative stress in myocardium. We discuss the literature reporting the consequences of sustained oxidative stress in CCM pathogenesis.Key words: chagasic cardiomyopathy, reactive oxygen species, inflammation, mitochondria, oxidant/antioxidant status, oxidative damage. PARASITE, VECTOR AND TRANSMISSIONTrypanosoma cruzi, a parasitic protozoan of the ancient branch of eukaryotes (Kingdom Eukaryota, Order Kinetoplastida), is the etiological agent of Chagas disease in humans (Miles 2003). Currently, the World Health Organization estimates that 11-18 million individuals are infected worldwide (WHO 2002). Transmission of T. cruzi occurs predominantly via insect vectors of the subfamily Triatoma, family Reduviidae, referred to as " kissing bugs". Residing in the peridomestic habitat of mud-thatch Correspondence to: Nisha Garg Ph.D. E-mail: nigarg@utmb.edu houses in rural areas (Mott et al. 1978), Triatoma infestans in South America, Rhodnius prolixus in Venezuela, Colombia and Central America (Schofi eld and Dias 1999), and Triatoma barberi in Mexico (Guzman 2001), are the most common species responsible for transmission. Improvements in housing conditions and vector control measures instituted by the Southern Cone Initiative in 1991 have contributed to a decline in transmission in endemic countries (Schofi eld and Dias 1999). However, concern remains that reinfestation of homes by secondary sylvatic vectors, e.g. Triatoma sordida, will compromise the long-term effi cacy of vector control measures in Brazil and other Southern American countries (Monteiro et al. 2001, WHO 2002. Blood transfusion and organ transplantation represent further routes of T. cruzi transmission. Although many countries in Latin America screen blood donations for T. cruzi, infection rates ranging from 0.1% to 24.4% are estimated to occur through transfusion (WHO 2002).In the U.S., vector-transmitted human infections have been reported in the southern States (Ochs et al. 1996, Herwaldt et al. 2000. Several studies have shown the presence of the insect vector as well as infection of domestic dogs and wild animals in the US (Meurs et al. 1998, Bradley et al. 2000, Beard et al. 2003, Yabsley and Noblet 2002. Further, due to signifi cant increases in immigration to the USA and Canada from endemic countries and perinatal transmission, it is estimated that ∼ 100, 000 people residing...

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Factors contributing to the outcome of oxidative damage to nucleic acids

Cited by 234 publications

References 62 publications

Oxidative Stress and Severe Walking Disability among Older Women

Oxidative Stress and Severe Walking Disability among Older Women

Alzheimer's Disease (AD)-Like Pathology in Aged Monkeys after Infantile Exposure to Environmental Metal Lead (Pb): Evidence for a Developmental Origin and Environmental Link for AD

An overview of chagasic cardiomyopathy: pathogenic importance of oxidative stress

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