Effect of Exogenous Treatment with Nitric Oxide (NO) on Redox Homeostasis in Barley Seedlings (Hordeum vulgare L.) Under Copper Stress

The protective mechanism of nitric oxide (NO) in regulating tolerance to Cu-induced toxicity in shoots of barley (Hordeum vulgare L.) was studied. The experiment consisted of four treatments based on additions to basal nutrient solutions (BNS): control (CTR), Cu (200 µM), SNP (500 µM), and Cu (200 µM) + SNP (500 µM) over a period of 10 days. Treatment with Cu significantly reduced seedling growth and photosynthetic efficiency concomitant with an increase in reactive oxygen species contents, lipid peroxidation markers, and antioxidant enzyme activities, indicating that Cu induced oxidative stress. Furthermore, growth inhibition of Cu-treated plants was associated with a reduction in photosynthetic pigments and maximum photosystem II efficiency as well as a strong decrease in levels of glutathione (GSH) and ascorbate (AsA). Addition of a nitric oxide (NO) donor, sodium nitroprusside (SNP), to the growth medium alleviated Cu toxicity by decreasing Cu uptake and enhancing antioxidant capacity, as indicated by increased contents of GSH and AsA. The application of SNP decreased oxidative stress and lipid peroxidation by suppressing lipoxygenase activity and enhancing some antioxidant enzyme activities. The results obtained indicate the potential of exogenously applied SNP in the management of metal toxicity. Hence, NO generating compounds have potential agronomical applications when cultivating in contaminated areas. Our findings indicate that NO can alleviate Cu toxicity by affecting the antioxidant defense system and maintaining the glutathione-ascorbate cycle status, suggesting that SNP treatment protects proteins against oxidation by regulating the cellular redox homeostasis.

Adaptive Responses of Citrus grandis Leaves to Copper Toxicity Revealed by RNA-Seq and Physiology

Copper (Cu)-toxic effects on Citrus grandis growth and Cu uptake, as well as gene expression and physiological parameters in leaves were investigated. Using RNA-Seq, 715 upregulated and 573 downregulated genes were identified in leaves of C. grandis seedlings exposed to Cu-toxicity (LCGSEC). Cu-toxicity altered the expression of 52 genes related to cell wall metabolism, thus impairing cell wall metabolism and lowering leaf growth. Cu-toxicity downregulated the expression of photosynthetic electron transport-related genes, thus reducing CO2 assimilation. Some genes involved in thermal energy dissipation, photorespiration, reactive oxygen species scavenging and cell redox homeostasis and some antioxidants (reduced glutathione, phytochelatins, metallothioneins, l-tryptophan and total phenolics) were upregulated in LCGSEC, but they could not protect LCGSEC from oxidative damage. Several adaptive responses might occur in LCGSEC. LCGSEC displayed both enhanced capacities to maintain homeostasis of Cu via reducing Cu uptake by leaves and preventing release of vacuolar Cu into the cytoplasm, and to improve internal detoxification of Cu by accumulating Cu chelators (lignin, reduced glutathione, phytochelatins, metallothioneins, l-tryptophan and total phenolics). The capacities to maintain both energy homeostasis and Ca homeostasis might be upregulated in LCGSEC. Cu-toxicity increased abscisates (auxins) level, thus stimulating stomatal closure and lowering water loss (enhancing water use efficiency and photosynthesis).

Copper Tolerance and Accumulation on Pelargonium graveolens L’Hér. Grown in Hydroponic Culture

Heavy metal contamination is a major health issue concerning the commercial production of medicinal and aromatic plants (MAPs) that are used for the extraction of bioactive molecules. Copper (Cu) is an anthropogenic contaminant that, at toxic levels, can accumulate in plant tissues, affecting plant growth and development. On the other hand, plant response to metal-induced stress may involve the synthesis and accumulation of beneficial secondary metabolites. In this study, hydroponically grown Pelargonium graveolens plants were exposed to different Cu concentrations in a nutrient solution (4, 25, 50, 100 μM) to evaluate the effects Cu toxicity on plant growth, mineral uptake and distribution in plants, some stress indicators, and the accumulation of bioactive secondary metabolites in leaf tissues. P. graveolens resulted in moderately tolerant Cu toxicity. At Cu concentrations up to 100 μM, biomass production was preserved and was accompanied by an increase in phenolics and antioxidant capacity. The metal contaminant was accumulated mainly in the roots. The leaf tissues of Cu-treated P. graveolens may be safely used for the extraction of bioactive molecules.

Tissue Distribution and Biochemical Changes in Response to Copper Accumulation in Erica australis L.

Copper uptake, accumulation in different tissues and organs and biochemical and physiological parameters were studied in Erica australis treated with different Cu concentrations (1, 50, 100 and 200 µM) under hydroponic culture. Copper treatments led to a significant reduction in growth rate, biomass production and water content in shoots, while photosynthetic pigments did not change. Copper treatments led to an increase in catalase and peroxidase activities. Copper accumulation followed the pattern roots > stems ≥ leaves, being roots the prevalent Cu sink. Analysis by scanning electron microscopy coupled with elemental X-ray analysis (SEM–EDX) showed a uniform Cu distribution in root tissues. On the contrary, in leaf tissues, Cu showed preferential storage in abaxial trichomes, suggesting a mechanism of compartmentation to restrict accumulation in mesophyll cells. The results show that the studied species act as a Cu-excluder, and Cu toxicity was avoided to a certain extent by root immobilization, leaf tissue compartmentation and induction of antioxidant enzymes to prevent cell damage.

The effect of copper and manganese on phytoplankton in the Grand River (southern Ontario), Lake Erie and Pacific Ocean ecosystems

With the increased use and loading of metals into the environment, the accumulation of toxic metals by phytoplankton has become a concern. Trace metal interactions with phytoplankton are of particular interest due to the influence of phytoplankton on the biogeochemical cycling of metals in aquatic systems. The study of the accumulation of metals and their toxicity in phytoplantkon is also of interest since phytoplankton lie at the base of many aquatic food webs. Toxic metals therefore have the potential to disrupt food webs and may have important implications on aquatic ecosystems. This study has chosen to focus on the response of phytoplankton to two trace metals in particular: copper (Cu) and manganese (Mn). Although both Cu and Mn are essential elements for phytoplankton, Cu is of particular interest as a toxicant. A number of laboratory studies have suggested that there exists a physiological interaction between Cu and Mn, and that Cu toxicity can be decreased in the presence of high concentrations of Mn. However, few studies have examined the effects of these metals on phytoplankton in their natural environments. The significance of this study is that it is one of the first to examine whether the importance of Cu toxicity and the interaction between Cu and Mn observed in the laboratory is also observable under natural conditions. Short-term bioassays were conducted in order to observe the response of phytoplankton from the Grand River (Southern Ontario) and Lake Erie to additions of various concentrations of eu and Mn under natural conditions. Similar long-term bioassay experiments were also conducted in the Pacific Ocean. Experiments in the Grand River and the Pacific Ocean revealed no significant decrease in phytoplankton biomass or in photosynthetic efficiency with the addition of various concentrations of Cu and Mn. In Lake Erie, phytoplankton biomass was only adversely affected following relatively high additions of Cu of 60 nM, and only under certain conditions. These results seem to indicate that under the tested conditions, Cu toxicity may not be of particular concern to the phytoplankton of the Grand River, Lake Erie and Pacific Ocean ecosystems.

The effect of copper and manganese on phytoplankton in the Grand River (southern Ontario), Lake Erie and Pacific Ocean ecosystems

With the increased use and loading of metals into the environment, the accumulation of toxic metals by phytoplankton has become a concern. Trace metal interactions with phytoplankton are of particular interest due to the influence of phytoplankton on the biogeochemical cycling of metals in aquatic systems. The study of the accumulation of metals and their toxicity in phytoplantkon is also of interest since phytoplankton lie at the base of many aquatic food webs. Toxic metals therefore have the potential to disrupt food webs and may have important implications on aquatic ecosystems. This study has chosen to focus on the response of phytoplankton to two trace metals in particular: copper (Cu) and manganese (Mn). Although both Cu and Mn are essential elements for phytoplankton, Cu is of particular interest as a toxicant. A number of laboratory studies have suggested that there exists a physiological interaction between Cu and Mn, and that Cu toxicity can be decreased in the presence of high concentrations of Mn. However, few studies have examined the effects of these metals on phytoplankton in their natural environments. The significance of this study is that it is one of the first to examine whether the importance of Cu toxicity and the interaction between Cu and Mn observed in the laboratory is also observable under natural conditions. Short-term bioassays were conducted in order to observe the response of phytoplankton from the Grand River (Southern Ontario) and Lake Erie to additions of various concentrations of eu and Mn under natural conditions. Similar long-term bioassay experiments were also conducted in the Pacific Ocean. Experiments in the Grand River and the Pacific Ocean revealed no significant decrease in phytoplankton biomass or in photosynthetic efficiency with the addition of various concentrations of Cu and Mn. In Lake Erie, phytoplankton biomass was only adversely affected following relatively high additions of Cu of 60 nM, and only under certain conditions. These results seem to indicate that under the tested conditions, Cu toxicity may not be of particular concern to the phytoplankton of the Grand River, Lake Erie and Pacific Ocean ecosystems.

Copper Toxicity Is Not Just Oxidative Damage: Zinc Systems and Insight from Wilson Disease

Essential metals such as copper (Cu) and zinc (Zn) are important cofactors in diverse cellular processes, while metal imbalance may impact or be altered by disease state. Cu is essential for aerobic life with significant functions in oxidation-reduction catalysis. This redox reactivity requires precise intracellular handling and molecular-to-organismal levels of homeostatic control. As the central organ of Cu homeostasis in vertebrates, the liver has long been associated with Cu storage disorders including Wilson Disease (WD) (heritable human Cu toxicosis), Idiopathic Copper Toxicosis and Endemic Tyrolean Infantile Cirrhosis. Cu imbalance is also associated with chronic liver diseases that arise from hepatitis viral infection or other liver injury. The labile redox characteristic of Cu is often discussed as a primary mechanism of Cu toxicity. However, work emerging largely from the study of WD models suggests that Cu toxicity may have specific biochemical consequences that are not directly attributable to redox activity. This work reviews Cu toxicity with a focus on the liver and proposes that Cu accumulation specifically impacts Zn-dependent processes. The prospect that Cu toxicity has specific biochemical impacts that are not entirely attributable to redox may promote further inquiry into Cu toxicity in WD and other Cu-associated disorders.