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Chromium (Cr) is an element naturally occurring in rocky soils and volcanic dust. It has been classified as a carcinogen agent according to the International Agency for Research on Cancer. Therefore, this metal needs an accurate understanding and thorough investigation in soil–plant systems. Due to its high solubility, Cr (VI) is regarded as a hazardous ion, which contaminates groundwater and can be transferred through the food chain. Cr also negatively impacts the growth of plants by impairing their essential metabolic processes. The toxic effects of Cr are correlated with the generation of reactive oxygen species (ROS), which cause oxidative stress in plants. The current review summarizes the understanding of Cr toxicity in plants via discussing the possible mechanisms involved in its uptake, translocation and sub-cellular distribution, along with its interference with the other plant metabolic processes such as chlorophyll biosynthesis, photosynthesis and plant defensive system.

Nanotechnology now plays a revolutionary role in many applications; nanomaterials have experienced significant importance in both basic and applied sciences as well as in bio-nanotechnology. Zinc oxide nanoparticles (ZnO-NPs) have become one of the most important metal oxide NPs in biological applications due to their beneficial impacts. The purpose of this study was to explore the effects of ZnO-NPs in reducing Cd toxicity by studying the growth, photosynthesis reactions, antioxidant system, oxidative stress, and protein content in Lycopersicon esculentum (tomato). ZnO-NPs induced an upregulation of antioxidative enzymes which protect the photosynthetic apparatus in plants. Seeds of tomato were sown to create nursery. At 20 days after sowing (DAS), seedlings were transferred to soil pots. Varied concentrations (0.4, 0.6 or 0.8 mM) of Cd were applied to the soil after 24 and 25 DAS. Zinc (Zn; 50 mg/L) and ZnO-NPs (50 mg/L) treatments were given continuously for 5 days from 31 to 35 DAS and sampling took place at 45 DAS. The results indicate that a Cd-generated oxidative burst in the form of elevated hydrogen peroxide (H2O2) levels resulted in a decline in cell viability through enhanced activity of the antioxidant system and proline content; the data increased on follow-up treatment with ZnO-NPs. Foliar application of ZnO-NPs significantly enhanced plant height, fresh, and dry weight of plant, leaf area, SPAD chlorophyll, photosynthetic attributes, i.e., net photosynthetic rate (PN), transpiration rate (E), internal CO2 concentration (Ci), and stomatal conductance (gs). Application of ZnO-NPs reduced the adverse effects generated by Cd and increased protein content, activities of nitrate reductase and carbonic anhydrase over the control in both stressed and non-stressed plants. Additionally, microscopic studies showed a marked increase in stomatal aperture after ZnO-NPs treatment in the presence or absence of Cd. This was associated with decrease in malondialdehyde and superoxide radical (O2−) levels. The present study suggests that ZnO-NPs can be effectively used to reduce the toxicity of Cd in tomato plants and may also be suitable for testing on other crop species.

Based on the origin, we can classify different types of stress. Environmental factors, such as high light intensity, adverse temperature, drought, or soil salinity, are summarized as abiotic stresses and discriminated from biotic stresses that are exerted by pathogens and herbivores, for instance. It was an unexpected observation that overproduction of reactive oxygen species (ROS) is a common response to all kinds of stress investigated so far. With respect to applied aspects in agriculture and crop breeding, this observation allows using ROS production as a measure to rank the stress perception of individual plants. ROS are important messengers in cell signaling, but exceeding a concentration threshold causes damage. This requires fine-tuning of ROS production and degradation rates. In general, there are two options to control cellular ROS levels, (I) ROS scavenging at the expense of antioxidant consumption and (II) enzyme-controlled degradation of ROS. As antioxidants are limited in quantity, the first strategy only allows temporarily buffering of a certain cellular ROS level. This way, it prevents spells of eventually damaging ROS concentrations. In this review, we focus on the second strategy. We discuss how enzyme-controlled degradation of ROS integrates into plant metabolism. Enzyme activities can be continuously operative. Cellular homeostasis can be achieved by regulation of respective gene expression and subsequent regulation of the enzyme activities. A better understanding of this interplay allows for identifying traits for stress tolerance breeding of crops. As a side effect, the result also may be used to identify cultivation methods modifying crop metabolism, thus resulting in special crop quality.

Reactive oxygen species (ROS) such as hydrogen peroxide and superoxide are produced in plants in response to many biotic and abiotic stressors, and they can enhance stress adaptation in certain circumstances or mediate symptom development in others. The roles of ROS in plant-pathogen interactions have been extensively studied, but far less is known about their involvement in plant-insect interactions. A growing body of evidence, however, indicates that ROS accumulate in response to aphids, an economically damaging group of phloem-feeding insects. This review will cover the current state of knowledge about when, where, and how ROS accumulate in response to aphids, which salivary effectors modify ROS levels in plants, and how microbial associates influence ROS induction by aphids. We will also explore the potential adaptive significance of intra- and extracellular oxidative responses to aphid infestation in compatible and incompatible interactions and highlight knowledge gaps that deserve further exploration.

Funding Information: This study was financed by national funds from FCT—Fundação para a Ciência e a Tecnologia, I.P., under the scope of the project UID/50006/2023 of the Associate Laboratory for Green Chemistry-LAQV REQUIMTE. Publisher Copyright: © 2025 by the authors. Floridoside (2-O-D-glycerol-α-D-galactopyranoside) is a natural product typically found in red algae. It serves as the algae’s carbon reserve and is produced as a protective response against osmotic and heat stress. Both floridoside and its acylated derivatives have been associated with modulating redox homeostasis and inflammatory responses. Therefore, we aimed to evaluate whether the newly synthesized floridoside phosphotriesters (1b–1d, 1f–1h) and acylated floridoside derivative (1e) can modulate the oxidative burst in stimulated human neutrophils. Synthetic strategies included the glycosylation of the thioglycoside donor with glycerol derivatives, having NIS/TfOH as the promoter. Phosphorylation was achieved with POCl3 in the presence of pyridine. The compounds were analysed for their cytotoxicity, with 1b and 1h being cytotoxic at 50 μM, while the others showed no cytotoxicity in the tested concentrations. The detection of the neutrophils’ oxidative burst was performed using multiple probes [luminol, aminophenyl fluorescein (APF), and Amplex Red (AR)] to evaluate reactive species levels. Compound 1e prevented the oxidative burst in activated human neutrophils (IC50 = 83 ± 7 μM). All the other tested compounds were ineffective in inhibiting APF and AR oxidation under the present experimental conditions. These findings highlight the potential of floridoside-based derivatives as candidates for targeting inflammatory pathways.

Floridoside (2-O-D-glycerol-α-D-galactopyranoside) is a natural product typically found in red algae. It serves as the algae’s carbon reserve and is produced as a protective response against osmotic and heat stress. Both floridoside and its acylated derivatives have been associated with modulating redox homeostasis and inflammatory responses. Therefore, we aimed to evaluate whether the newly synthesized floridoside phosphotriesters (1b–1d, 1f–1h) and acylated floridoside derivative (1e) can modulate the oxidative burst in stimulated human neutrophils. Synthetic strategies included the glycosylation of the thioglycoside donor with glycerol derivatives, having NIS/TfOH as the promoter. Phosphorylation was achieved with POCl3 in the presence of pyridine. The compounds were analysed for their cytotoxicity, with 1b and 1h being cytotoxic at 50 μM, while the others showed no cytotoxicity in the tested concentrations. The detection of the neutrophils’ oxidative burst was performed using multiple probes [luminol, aminophenyl fluorescein (APF), and Amplex Red (AR)] to evaluate reactive species levels. Compound 1e prevented the oxidative burst in activated human neutrophils (IC50 = 83 ± 7 μM). All the other tested compounds were ineffective in inhibiting APF and AR oxidation under the present experimental conditions. These findings highlight the potential of floridoside-based derivatives as candidates for targeting inflammatory pathways.

Macrophages are cells of the innate immune system and represent an important component of the first-line defense against pathogens and tumor cells. Here, their diverse functions in inflammation and tumor defense are described, and the mechanisms, tools, and activation pathways and states applied are presented. The main focus is on the role and origin of reactive oxygen species (ROS), the important signal pathways TLR/NF-κB, and the M1/​​M2 polarization of macrophages. Graphical abstract

The Arabidopsis immune receptor FLS2 perceives bacterial flagellin epitope flg22 to activate defenses through the central cytoplasmic kinase BIK1. The heterotrimeric G proteins composed of the non-canonical Gα protein XLG2, the Gβ protein AGB1, and the Gγ proteins AGG1 and AGG2 are required for FLS2-mediated immune responses through an unknown mechanism. Here we show that in the pre-activation state, XLG2 directly interacts with FLS2 and BIK1, and it functions together with AGB1 and AGG1/2 to attenuate proteasome-mediated degradation of BIK1, allowing optimum immune activation. Following the activation by flg22, XLG2 dissociates from AGB1 and is phosphorylated by BIK1 in the N terminus. The phosphorylated XLG2 enhances the production of reactive oxygen species (ROS) likely by modulating the NADPH oxidase RbohD. The study demonstrates that the G proteins are directly coupled to the FLS2 receptor complex and regulate immune signaling through both pre-activation and post-activation mechanisms. Living cells need to be able to detect changes in their environment and respond accordingly. This ability involves signals from outside of the cell triggering changes to the activity inside the cell. Heterotrimeric G proteins are important for this kind of signaling in a wide range of organisms. In animals and fungi, these proteins directly work with a specific class of receptor proteins called G protein-coupled receptors (or GPCRs for short). Plants also have heterotrimeric G proteins, but it remains unclear whether they similiarly work with GPCRs. Plants detect invading microbes by using receptors that are completely different from GPCRs. For example, a receptor called FLS2 from the model plant Arabidopsis senses a telltale protein produced by bacteria, and then passes the signal to another protein called BIK1 to activate the plant’s defenses. Heterotrimeric G proteins are required for this process, but the underlying mechanisms remain unknown. Liang, Ding et al. now show that heterotrimeric G proteins regulate FLS2-controlled defenses by directly interacting with FLS2 and BIK1. Heterotrimeric G proteins also enhance defenses in at least two different ways. Firstly, in the absence of an infection, heterotrimeric G proteins stabilize the BIK1 protein to ensure that it is ready to respond. Secondly, if FLS2 does detect the telltale bacterial protein, BIK1 marks one of the heterotrimeric G proteins with a phosphate group. This then allows the G protein to boost the activity of another plant enzyme that is vital for defense signaling. In the future, it will be important to work out how activation of FLS2 leads to the activation of heterotrimeric G proteins. Furthermore, heterotrimeric G proteins are likely to regulate additional plant proteins when defenses are activated, and further studies are needed to identify these proteins.

Cadmium (Cd) is considered to be one of the most toxic pollutants persistent in soil for thousands of years and is ranked on seventh position among all environmental pollutants. The higher concentration of Cd in plants inhibits their growth and metabolism and further enters the food chain. Cd toxicity initiates redox actions in plants by inducing oxidative stress through the production of free radicals. It alters mineral uptake by disturbing water potential or affects the microbial population in soils, opening and closing of stomata, transpiration, photosynthesis, antioxidant levels, sugar metabolism and productivities. It also causes chlorosis, mineral deficiencies, inhibition of nitrate reductase activity and ammonia assimilation in several plant species. The plants have adopted a number of mechanisms to facilitate reduction in the amount of ROS. They possess series of antioxidative defence responses to scavenge reactive oxygen species (ROS) levels. Furthermore, specific mechanisms such as such as efflux, immobilization, stabilization, complexation, sequestration and detoxification are generally observed to combat the Cd stresses. Moreover, endogenous phytohormonal signalling during stressed conditions within plants has also been focussed. Cd stimulates various hormonal signalling pathways and regulates many physiological processes in plants that in turn ameliorate Cd stress. Strikingly, phytohormones play an imperative role during signal transduction pathway along with regulating overall growth and development of plants under toxic conditions. Moreover, plant hormones boost antioxidant activities and plummet oxidative damage from plants along with maintaining cellular homeostasis. This review encompasses the ecotoxicological aspects of Cd within plants and plant responses to tackle such adversities.

Adverse effect of nanoparticles may include impairment of phagocyte function. To identify the effect of nanoparticle size on uptake, cytotoxicity, chemotaxis, cytokine secretion, phagocytosis, oxidative burst, nitric oxide production and myeloperoxidase release, leukocytes isolated from human peripheral blood, monocytes and macrophages were studied. Carboxyl polystyrene (CPS) particles in sizes between 20 and 1,000 nm served as model particles. Twenty nanometers CPS particles were taken up passively, while larger CPS particles entered cells actively and passively. Twenty nanometers CPS were cytotoxic to all phagocytes, ≥500 nm CPS particles only to macrophages. Twenty nanometers CPS particles stimulated IL-8 secretion in human monocytes and induced oxidative burst in monocytes. Five hundred nanometers and 1,000 nm CPS particles stimulated IL-6 and IL-8 secretion in monocytes and macrophages, chemotaxis towards a chemotactic stimulus of monocytes and phagocytosis of bacteria by macrophages and provoked an oxidative burst of granulocytes. At very high concentrations, CPS particles of 20 and 500 nm stimulated myeloperoxidase release of granulocytes and nitric oxide generation in macrophages. Cytotoxic effect could contribute to some of the observed effects. In the absence of cytotoxicity, 500 and 1,000 nm CPS particles appear to influence phagocyte function to a greater extent than particles in other sizes.