title: Nitric oxide contributes to copper tolerance by influencing ROS metabolism in Arabidopsis.
abstract: Nitric oxide improves copper tolerance via modulation of superoxide and hydrogen peroxide levels. This reflects the necessity of a well-coordinated interplay between NO and ROS during stress tolerance. Copper (Cu) excess causes toxicity and one probable consequence of this is the disturbance of cell redox state maintenance, inter alia, by reactive oxygen- (ROS) and nitrogen species (RNS). The objective of this paper was to examine the role of nitric oxide (NO) in Cu stress tolerance and its relationship with ROS in Arabidopsis. In agar-grown seedlings, concentration-dependent Cu accumulation was observed. The 5 μM Cu resulted in reduced cell viability in the NO overproducing nox1 and gsnor1-3 root tips compared to the wild-type (WT). In contrast, 25 and 50 μM Cu caused higher viability in these mutants, while in the NO-lacking nia1nia2 lower viability was detected than in the WT. The exogenous NO donor enhanced cell viability and scavenging endogenous NO decreased it in Cu-exposed WT seedlings. Besides, SNP in nia1nia2 roots led to the improvement of viability. The ascorbic acid-deficient mutants (vtc2-1, vtc2-3) possessing slightly elevated ROS levels proved to be Cu sensitive, while miox4 showing decreased ROS production was more tolerant to Cu than the WT. In nox1 and gsnor1-3, Cu did not induce superoxide formation, and H₂O₂ accumulation occurred only in the case of NO deficiency. Based on these, under mild stress NO intensifies cell injury, while in the case of severe Cu excess it contributes to better viability. ROS were found to be responsible for aggravation of Cu-induced damage. NO alleviates acute Cu stress via modulation of O₂(·-) and H₂O₂ levels reflecting the necessity of a well-coordinated interplay between NO and ROS during stress tolerance.
authors.affiliation: Department of Plant Biology, Faculty of Science and Informatics, University of Szeged, Szeged, Hungary.
authors.forename: Andrea
authors.initials: A
authors.lastname: Pető
authors.forename: Nóra
authors.initials: N
authors.lastname: Lehotai
authors.forename: Gábor
authors.initials: G
authors.lastname: Feigl
authors.forename: Nóra
authors.initials: N
authors.lastname: Tugyi
authors.forename: Attila
authors.initials: A
authors.lastname: Ördög
authors.forename: Katalin
authors.initials: K
authors.lastname: Gémes
authors.forename: Irma
authors.initials: I
authors.lastname: Tari
authors.forename: László
authors.initials: L
authors.lastname: Erdei
authors.forename: Zsuzsanna
authors.initials: Z
authors.lastname: Kolbert
mesh_terms: D000222:Adaptation, Physiological / Q000187:drug effects; D017360:Arabidopsis / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism* / Q000502:physiology*; D001205:Ascorbic Acid / Q000378:metabolism; D001692:Biological Transport / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D003300:Copper / Q000633:toxicity*; D006706:Homeostasis / Q000187:drug effects; D006861:Hydrogen Peroxide / Q000378:metabolism; D009154:Mutation / Q000235:genetics; D009569:Nitric Oxide / Q000494:pharmacology*; D018517:Plant Roots / Q000187:drug effects / Q000378:metabolism; D018520:Plant Shoots / Q000187:drug effects / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013312:Stress, Physiological / Q000187:drug effects; D013481:Superoxides / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species; D013481:Superoxides; D009569:Nitric Oxide; D003300:Copper; D006861:Hydrogen Peroxide; D001205:Ascorbic Acid