Abiotic stresses like heavy metals, drought, salt, low temperature, etc. are the major factors that limit crop productivity and yield. These stresses are associated with production of certain deleterious chemical entities called reactive oxygen species (ROS), which include hydrogen peroxide (H₂O₂), superoxide radical (O₂(-)), hydroxyl radical (OH(-)), etc. ROS are capable of inducing cellular damage by degradation of proteins, inactivation of enzymes, alterations in the gene and interfere in various pathways of metabolic importance. Our understanding on ROS in response to abiotic stress is revolutionized with the advancements in plant molecular biology, where the basic understanding on chemical behavior of ROS is better understood. Understanding the molecular mechanisms involved in ROS generation and its potential role during abiotic stress is important to identify means by which plant growth and metabolism can be regulated under acute stress conditions. ROS mediated oxidative stress, which is the key to understand stress related toxicity have been widely studied in many plants and the results in those studies clearly revealed that oxidative stress is the main symptom of toxicity. Plants have their own antioxidant defense mechanisms to encounter ROS that is of enzymic and non-enzymic nature . Coordinated activities of these antioxidants regulate ROS detoxification and reduces oxidative load in plants. Though ROS are always regarded to impart negative impact on plants, some reports consider them to be important in regulating key cellular functions; however, such reports in plant are limited. Molecular approaches to understand ROS metabolism and signaling have opened new avenues to comprehend its critical role in abiotic stress. ROS also acts as secondary messenger that signals key cellular functions like cell proliferation, apoptosis and necrosis. In higher eukaryotes, ROS signaling is not fully understood. In this review we summarize our understanding on ROS and its signaling behavior in plants under abiotic stress.

The article presents an overview of the mechanism of chromium stress in plants. Chromium is known to be a toxic metal that can cause severe damage to plants and animals. Chromium-induced oxidative stress involves induction of lipid peroxidation in plants that causes severe damage to cell membranes. Oxidative stress induced by chromium initiates the degradation of photosynthetic pigments causing decline in growth. High chromium concentration can disturb the chloroplast ultrastructure thereby disturbing the photosynthetic process. Like copper and iron, chromium is also a redox metal and its redox behaviour exceeds that of other metals like Co, Fe, Zn, Ni, etc. The redox behaviour can thus be attributed to the direct involvement of chromium in inducing oxidative stress in plants. Chromium can affect antioxidant metabolism in plants. Antioxidant enzymes like SOD, CAT, POX and GR are found to be susceptible to chromium resulting in a decline in their catalytic activities. This decline in antioxidant efficiency is an important factor in generating oxidative stress in plants under chromium stress. However, both metallothioneins and organic acids are important in plants as components of tolerance mechanisms and are also involved in detoxification of this toxic metal.

The effect of short-term Pb and Cr (0, 100 and 1000µM) stress in moss Taxithelium nepalense (Schwaegr.) Broth., the possible generation of oxidative stress, antioxidant metabolism and changes in the chloroplast and cell membrane ultrastructure were investigated. In moss cells, treatment of Pb and Cr for 12 and 24 h decreased the dry mass and total chlorophyll content with marked inhibition under Pb. Both Pb and Cr accumulated after 24 h of their treatment where highest accumulation of Pb was visible than that of Cr. The ultrastructural studies at 1000 µM of Pb and Cr showed distortion of the thylakoid, distortion of chloroplast membrane and changes in the chloroplast structure. Chloroplast distortion was highly visible under Pb than that of Cr. The distortion in the cell membrane was evident at high concentration of Pb, while under Cr, minor changes were visible as compared to controls. Both Pb and Cr significantly increased the production of ROS like H 2 O 2 and O − 2 radical with marked production after 24 h under Pb than that of Cr. The alteration in metabolism of activated oxygen in moss cells was evidenced by the increase in the lipid peroxidation in moss cells, with pronounced effect after 24 h than that of 12 h after Pb and Cr treatment. The SOD activity showed an increasing trend followed by decrease in CAT, POX and GR activity after 12 and 24 h. Both ascorbate and glutathione showed higher accumulation under Pb followed by Cr. The results showed that at high concentration of metals, oxidative stress could be induced in moss cells characterized by the generation of ROS and initiation lipid peroxidation that inhibited the major antioxidant metabolism. Both physiological and ultrastructural studies suggested the possible induction of oxidative stress in Taxithelium nepalense (Schwaegr.) Broth. under Pb and Cr toxicity.

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The main aim of this paper was to investigate the effect of chromium (Cr), copper (Cu) and zinc (Zn) on nitrate reductase (NR) activity and oxidative stress responses in the moss Polytrichum commune. Cr, Cu and Zn resulted in the inhibition of NR activity. A decline in total chlorophyll content was observed after 24 and 48 h of metal treatment. Accumulation of the metals showed a dose and time dependent increase. High accumulation of Cu, Cr and Zn were seen in moss shoots after 24 and 48 h of treatment. Treatment of Cr, Cu and Zn for 24 or 48 h resulted in the increase of malondialdehyde (MDA) content in moss shoots. The highest increase was observed in shoots under Cu treatment followed by Cr and Zn. The MDA content was significantly higher after 48h. Antioxidant enzymes viz., catalase (CAT), guaiacol peroxidase (GPx), glutathione reductase (GR) and superoxide dismutase (SOD) were affected by elevated concentrations of the three metals. Increase in the activity of CAT, GR and SOD was seen after 24 and 48 h of treatment. GPx activity declined under Cr treatment. However, under Cu and Zn, an increase in GPx was seen after 24 h and 48 h of treatment. For Zn, the antioxidant efficiency was less affected as compared to Cr and Cu. The response of Polytrichum commune to toxic concentrations of Cr, Cu and Zn appears to induce oxidative damage as observed by the increase in MDA content and antioxidant metabolism.

Elevation in the levels of reactive oxygen and nitrogen species (RONS), and downregulation of cellular antixoidants, have ubiquitously been reported from studies in animal models of neurodegenerative diseases, including Parkinson’s disease (PD) and Alzheimer’s disease (AD). Thus, plant-derived compounds are widely being investigated for their beneficial effects in these models. However, while studies have reported antioxidant potentials of several phytochemicals, a large number of studies have demonstrated different phytochemicals to be rather pro-oxidant and exaggerate oxidative stress (OS). One such study aimed to investigate possible ameliorative effect of Pomegranate juice (PJ) in rat model of toxin-induced parkinsonism revealed that PJ exacerbates OS, inflammation and promotes neurodegeneration. Thus, it remains to be investigated whether different constituents and metabolites of PJ are pro-oxidant or anti-oxidant. Using computational modeling, we investigated possible inhibitory potential of different constituents of PJ and their metabolites viz. delphinidin-3-glucoside, dimethylellagic acid-glucuronide, ellagic acid, ellagitannin, gallic acid, gallotannin 23, pelargonidin, punicalagin, urolithin A, urolithin A-glucuronide and urolithin B, on anti-oxidant defense system of the brain. The results indicate that the constituents of PJ have the potential to inhibit five key enzymes of the neuronal antioxidant defense system, viz. catalase, superoxide dismutase, glutathione peroxidase 4, glutathione reductase and glutathione-S-transferase. Thus, it is surmised that the constituents of PJ may contribute to OS and neurodegeneration by way of affecting antioxidant defense mechanism. This may particularly be more pronounced in neurodegenerative diseases, since neurons are known to be more vulnerable to OS. Thus, the present findings caution the use of PJ in patients prone to OS, especially those suffering from neurodegenerative diseases, and warrant further experimental studies to unveil the effects of individual components and metabolites of PJ on antioxidant defense system of brain.

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