The allelopathic interaction between plants is one of the elements that influences plant communities. It has been commonly studied by applying tissue extracts onto the acceptors or by treating them with isolated allelotoxins. Despite descriptive observations useful for agricultural practice, data describing the molecular mode of action of allelotoxins cannot be found. Due to the development of -omic techniques, we have an opportunity to investigate specific reactive oxygen species (ROS)-dependent changes in proteome or transcriptome that are induced by allelochemicals. The aim of our review is to summarize data on the ROS-induced modification in acceptor plants in response to allelopathic plants or isolated allelochemicals. We present the idea of how ROS are involved in the hormesis and plant autotoxicity phenomena. As an example of an -omic approach in studies of the mode of action of allelopatic compounds, we describe the influence of meta-tyrosine, an allelochemical exudated from roots of fescues, on nitration—one of nitro-oxidative posttranslational protein modification in the roots of tomato plants. We conclude that ROS overproduction and an induction of oxidative stress are general plants’ responses to various allelochemicals, thus modification in ROS metabolisms is regarded as an indirect mode of action of allelochemicals.

Main conclusion: Nitro/oxidative modifications of proteins and RNA nitration resulted from altered peroxynitrite generation are elements of the indirect mode of action of canavanine andmeta-tyrosine in plants Environmental conditions and stresses, including supplementation with toxic compounds, are known to impair reactive oxygen (ROS) and reactive nitrogen species (RNS) homeostasis, leading to modification in production of oxidized and nitrated derivatives. The role of nitrated and/or oxidized biotargets differs depending on the stress factors and developmental stage of plants. Canavanine (CAN) andmeta-tyrosine (m-Tyr) are non-proteinogenic amino acids (NPAAs). CAN, the structural analog of arginine, is found mostly in seeds of Fabaceae species, as a storage form of nitrogen. In mammalian cells, CAN is used as an anticancer agent due to its inhibitory action on nitric oxide synthesis.m-Tyr is a structural analogue of phenylalanine and an allelochemical found in root exudates of fescues. In animals,m-Tyr is recognized as a marker of oxidative stress. Supplementation of plants with CAN orm-Tyr modify ROS and RNS metabolism. Over the last few years of our research, we have collected the complex data on ROS and RNS metabolism in tomato (Solanum lycopersicumL.) plants exposed to CAN orm-Tyr. In addition, we have shown the level of nitrated RNA (8-Nitro-guanine) in roots of seedlings, stressed by the tested NPAAs. In this review, we describe the model of CAN andm-Tyr mode of action in plants based on modifications of signaling pathways induced by ROS/RNS with a special focus on peroxynitrite induced RNA and protein modifications.

Nitric oxide (NO) has been recognized as a gasotransmitter in the mainstream of plant research since the beginning of the 21st century. It is produced in plant tissue and the environment. It influences plant physiology during every ontogenetic stage from seed germination to plant senescence. In this review, we demonstrate the increased interest in NO as a regulatory molecule in combination with other signalling molecules and phytohormones in the information network of plant cells. This work is a summary of the current knowledge on NO action in seeds, starting from seed pretreatment techniques applied to increase seed quality. We describe mode of action of NO in the regulation of seed dormancy, germination, and aging. During each stage of seed physiology, NO appears to act as a key agent with a predominantly beneficial effect.

Hydrogen cyanide (HCN) occurs in living organisms and in the environment. This is a widely known poison but is also considered as a gasotransmitter. For most higher plants, microorganisms and animals HCN is toxic, especially at elevated concentrations. However, plants’ sensitivity to this compound is lower than animals’ due to the activity of an alternative oxidase in the mitochondrial respiration chain. All higher plants synthesize HCN as a co-product during the final step of ethylene biosynthesis, whilst some plant species release it from cyanogenic compounds, accumulated for diverse physiological purposes. This molecule is used as a toxic bomb against herbivores, as a source of nitrogen in N-deficient plants, or as a regulator of seed dormancy state. The toxicity of HCN is mainly due to the inhibition of the activity of several metalloenzymes: iron-containing enzymes, molybdoenzymes and enzymes that contain zinc or copper. HCN impacts cellular metabolism by modulation of the reactive oxygen species and reactive nitrogen species levels, and via modifications of proteins (S-cyanylation, oxidation). The aim of this work is to describe the dual (toxic and signalling) mode of cyanide action in plants at a cellular level.