Please use this identifier to cite or link to this item: http://hdl.handle.net/10773/26615
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dc.contributor.authorSantos, Ana L.pt_PT
dc.contributor.authorGomes, Newton C. M.pt_PT
dc.contributor.authorHenriques, Isabelpt_PT
dc.contributor.authorAlmeida, Adelaidept_PT
dc.contributor.authorCorreia, Antóniopt_PT
dc.contributor.authorCunha, Ângelapt_PT
dc.date.accessioned2019-09-25T14:30:49Z-
dc.date.available2019-09-25T14:30:49Z-
dc.date.issued2012-
dc.identifier.issn1011-1344pt_PT
dc.identifier.urihttp://hdl.handle.net/10773/26615-
dc.description.abstractThe present work aimed to identify the reactive oxygen species (ROS) produced during UV-B exposure and their biochemical targets, in a set of bacterial isolates displaying different UV susceptibilities. For that, specific exogenous ROS scavengers (catalase/CAT, superoxide dismutase/SOD, sodium azide and mannitol) were used. Biological effects were assessed from total bacterial number, colony counts and heterotrophic activity (glucose uptake and respiration). DNA strand breakage, ROS generation, oxidative damage to proteins and lipids were used as markers of oxidative stress. Sodium azide conferred a statistically significant protection in terms of lipid oxidation and cell survival, suggesting that singlet oxygen might play an important role in UV-B induced cell inactivation. Mannitol exerted a significant protection against DNA strand breakage and protein carbonylation, assigning hydroxyl radicals to DNA and protein damage. The addition of exogenous CAT and SOD significantly protected the capacity for glucose uptake and respiration, suggesting that superoxide and H(2)O(2) are involved in the impairment of activity during UV-B exposure. The observation that amendment with ROS scavengers can sometimes also exert a pro-oxidant effect suggests that the intracellular oxidant status of the cell ultimately determines the efficiency of antioxidant defenses.pt_PT
dc.description.sponsorshipAcknowledgments are due to the two anonymous reviewers whose insightful comments and suggestions contributed to improve the original manuscript. We also acknowledge Attila Köfalvi and Caroline Veloso at the Center for Neurosciences and Cell Biology of the University of Coimbra for providing access to the scintillation counter. Financial support for this work was provided by CESAM (Centre for Environmental and Marine Studies, University of Aveiro) and the Portuguese Foundation for Science and Technology (FCT) in the form of a PhD grant to A.L. Santos (SFRH/BD/40160/2007) and a post-doctoral grant to I. Henriques (SFRH/BPD/63487/2009).pt_PT
dc.language.isoengpt_PT
dc.publisherElsevierpt_PT
dc.relationinfo:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBD%2F40160%2F2007/PTpt_PT
dc.relationinfo:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBPD%2F63487%2F2009/PTpt_PT
dc.rightsrestrictedAccesspt_PT
dc.subjectBacteriapt_PT
dc.subjectUV radiationpt_PT
dc.subjectReactive oxygen speciespt_PT
dc.subjectOxidative damagept_PT
dc.titleContribution of reactive oxygen species to UV-B-induced damage in bacteriapt_PT
dc.typearticlept_PT
dc.description.versionpublishedpt_PT
dc.peerreviewedyespt_PT
degois.publication.firstPage40pt_PT
degois.publication.lastPage46pt_PT
degois.publication.titleJournal of photochemistry and photobiology. B, Biologypt_PT
degois.publication.volume117pt_PT
dc.identifier.doi10.1016/j.jphotobiol.2012.08.016pt_PT
dc.identifier.essn1873-2682pt_PT
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