This research studies the effects that Sb toxicity (0.0, 0.5, and 1.0 mM) has on the growth, reactive oxygen and nitrogen species, and antioxidant systems in tomato plants. Sb is accumulated preferentially in the roots, with little capacity for its translocation to the leaves where the concentration is much lower. The growth of the seedlings is reduced, with alteration in the content in other nutrients. There is a decrease in the content of Fe, Mg, and Mn, while Cu and Zn increase. The contents in chlorophyll a and b decrease, as does the photosynthetic efficiency. On the contrary the carotenoids increase, indicating a possible action as antioxidants and protectors against Sb. The phenolic compounds do not change, and seem not to be involved in the defense response of the tomato against the stress by Sb. The water content of the leaves decreases while that of proline increases in response to the Sb toxicity. Fluorescence microscopy images and spectrofluorometric detection showed increases in the production of O 2 . − , H 2 O 2 , NO, and ONOO − , but not of nitrosothiols. The Sb toxicity induces changes in the SOD, POX, APX, and GR antioxidant activities, which show a clear activation in the roots. In leaves, only the SOD and APX increase. The DHAR activity is inhibited in roots but undergoes no changes in the leaves, as is also the case for the POX and GR activities. Ascorbate increases while GSH decreases in the roots. The total AsA + DHA content increases in the roots, but the total GSH + GSSG content decreases, while neither is altered in the leaves. Under Sb toxicity increases the expression of the SOD, APX, and GR genes, while the expression of GST decreases dramatically in roots but increases in leaves. In addition, an alteration is observed in the pattern of the growth of the cells in the elongation zone, with smaller and disorganized cells. All these effects appear to be related to the ability of the Sb to form complexes with thiol groups, including GSH, altering both redox homeostasis and the levels of auxin in the roots and the quiescent center.

Dittrichia viscosa plants were grown hydroponically with different concentrations of Sb. There was preferential accumulation of Sb in roots. Fe and Cu decreased, while Mn decreased in roots but not in leaves. Chlorophyll content declined, but the carotenoid content increased, and photosynthetic efficiency was unaltered. O2●− generation increased slightly, while lipid peroxidation increased only in roots. H2O2, NO, ONOO−, S-nitrosothiols, and H2S showed significant increases, and the enzymatic antioxidant system was altered. In roots, superoxide dismutase (SOD) and monodehydroascorbate reductase (MDAR) activities declined, dehydroscorbate reductase (DHAR) rose, and ascorbate peroxidase (APX), peroxidase (POX), and glutathione reductase (GR) were unaffected. In leaves, SOD and POX increased, MDAR decreased, and APX was unaltered, while GR increased. S-nitrosoglutathione reductase (GSNOR) and l-cysteine desulfhydrilase (l-DES) increased in activity, while glutathione S-transferase (GST) decreased in leaves but was enhanced in roots. Components of the AsA/GSH cycle decreased. The great capacity of Dittrichia roots to accumulate Sb is the reason for the differing behaviour observed in the enzymatic antioxidant systems of the two organs. Sb appears to act by binding to thiol groups, which can alter free GSH content and SOD and GST activities. The coniferyl alcohol peroxidase activity increased, possibly to lignify the roots’ cell walls. Sb altered the ROS balance, especially with respect to H2O2. This led to an increase in NO and H2S acting on the antioxidant system to limit that Sb-induced redox imbalance. The interaction NO, H2S and H2O2 appears key to the response to stress induced by Sb. The interaction between ROS, NO, and H2S appears to be involved in the response to Sb.

Dittrichia plants were exposed to thallium (Tl) stress (10, 50, and 100 µM) for 7 days. The Tl toxicity altered the absorption and accumulation of other nutrients. In both the roots and the leaves, there was a decline in K, Mg, and Fe content, but an increase in Ca, Mn, and Zn. Chlorophylls decreased, as did the photosynthetic efficiency, while carotenoids increased. Oxidative stress in the roots was reflected in increased lipid peroxidation. There was more production of superoxide (O2.−), hydrogen peroxide (H2O2), and nitric oxide (NO) in the roots than in the leaves, with increases in both organs in response to Tl toxicity, except for O2.− production in the roots, which fluctuated. There was increased hydrogen sulfide (H2S) production, especially in the leaves. Superoxide dismutase (SOD), ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR), monodehydroascorbate reductase (MDHAR), and glutathione reductase (GR) showed increased activities, except for APX and MDHAR in the roots and GR in the leaves. The components of the ascorbate–glutathione cycle were affected. Thus, ascorbate (AsA) increased, while dehydroascorbate (DHA), reduced glutathione (GSH), and oxidized glutathione (GSSG) decreased, except for in the roots at 100 µM Tl, which showed increased GSH. These Tl toxicity-induced alterations modify the AsA/DHA and GSH/GSSG redox status. The NO and H2S interaction may act by activating the antioxidant system. The effects of Tl could be related to its strong affinity for binding with -SH groups, thus altering the functionality of proteins and the cellular redox state.