Selenium excess can cause toxicity symptoms, e.g. root growth inhibition in non-hyperaccumulator plants such as Arabidopsis. Selenite-induced hormonal and signalling mechanisms in the course of development are poorly understood; therefore this study set out to investigate the possible hormonal and signalling processes using transgenic and mutant Arabidopsis plants. Significant alterations were observed in the root architecture of the selenite-treated plants, due to the loss of cell viability in the root apex. During mild selenite excess, the plants showed symptoms of the morphogenic response: primary root (PR) shortening and increased initiation of laterals, ensuring better nutrient and water uptake and stress acclimation. As well as lower meristem cell activity, the second reason for the Se-induced growth hindrance is the hormonal imbalance, since the in situ expression of the auxin-responsive DR5::GUS, and consequently the auxin levels, significantly decreased, while that of the cytokinin-inducible ARR5::GUS and the ethylene biosynthetic ACS8::GUS increased. It is assumed that auxin and ethylene might positively regulate selenium tolerance, since reduced levels of them resulted in sensitivity. Moreover, high cytokinin levels caused notable selenite tolerance. During early seedling development, nitric oxide (NO) contents decreased but hydrogen peroxide levels increased reflecting the antagonism between the two signal molecules during Se excess. High levels of NO in gsnor1-3, lead to selenite tolerance, while low NO production in nia1nia2 resulted in selenite sensitivity. Consequently, NO derived from the root nitrate reductase activity is responsible for the large-scale selenite tolerance in Arabidopsis.

Copper (Cu) is an essential microelement for growth and development, but in excess it can cause toxicity in plants. In this comparative study, the uptake and accumulation of Cu as well as the morphological and physiological responses of Indian mustard (Brassica juncea L. Czern.) and rapeseed (Brassica napus L.) roots to Cu treatment were investigated. The possible involvement of redox active molecules (reactive oxygen species and nitric oxide) and modification in cell wall structure associated with Cu-induced morphological responses were also studied. In short- and long-term treatments, B. juncea suffered more pronounced growth inhibition as compared with B. napus. In addition to the shortening of primary and lateral roots, the number and the density of the laterals were also decreased by Cu. Exposure to copper induced nitric oxide generation in the root tips and this event proved to be dependent on the duration of the exposure and on the plant species. In short- and long-term treatments, Indian mustard showed more significant activation of superoxide dismutase (SOD), inhibition of ascorbate peroxidase (APX) and oxidation of ascorbate (AsA) than B. napus. Moreover, H2O2-dependent lignification was also observed in the Cu-exposed plants. In longer term, significant AsA accumulation and callose deposition were observed, reflecting serious oxidative stress in B. juncea. Based on the morphological and physiological results, we conclude that rapeseed tolerates Cu excess better than Indian mustard.

The results indicate a clear relationship between ROS and RNS metabolism as a mechanism of response against stress caused by an excess of Zn. The oxidative stress components seem to be more dominant than the elements of the nitrosative stress in the root system of these two Brassica species.

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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.