Plants detoxify toxic metal(loid)s by accumulating diverse metabolites. Beside scavenging excess reactive oxygen species (ROS) induced by metal(loid)s, some metabolites chelate metal(loid) ions. Classically, thiol-containing compounds, especially glutathione (GSH) and phytochelatins (PCs) are thought to be the major chelators that conjugate with metal(loid)s in the cytoplasm followed by transport and sequestration in the vacuole. In addition to this classical detoxification pathway, a role for secondary metabolites in metal(loid) detoxification has recently emerged. In particular, anthocyanins, a kind of flavonoids with ROS scavenging potential, contribute to enhanced arsenic tolerance in several plant species. Evidence is accumulating that, in analogy to GSH and PCs, anthocyanins may conjugate with arsenic followed by vacuolar sequestration in the detoxification event. Exogenous application or endogenous accumulation of anthocyanins enhances arsenic tolerance, leading to improved plant growth and productivity. The application of some plant hormones and signaling molecules stimulates endogenous anthocyanin synthesis which confers tolerance to arsenic stress. Anthocyanin biosynthesis is transcriptionally regulated by several transcription factors, including myeloblastosis (MYBs). The light-regulated transcription factor elongated hypocotyl 5 (HY5) also affects anthocyanin biosynthesis, but its role in arsenic tolerance remains elusive. Here, we review the mechanism of arsenic detoxification in plants and the potential role of anthocyanins in arsenic tolerance beyond the classical points of view. Our analysis proposes that anthocyanin manipulation in crop plants may ensure sustainable crop yield and food safety in the marginal lands prone to arsenic pollution.

Despite the large number of studies reporting the phytotoxicity of graphene-based materials, the effects of these materials on nutrient uptake in plants remain unclear. The present study showed that nitrate concentrations were significantly decreased in the roots of wheat plants treated with graphene oxide (GO) at 200–800 mg L⁻¹. Non-invasive microelectrode measurement demonstrated that GO could significantly inhibit the net NO₃⁻ influx in the meristematic, elongation, and mature zones of wheat roots. Further analysis indicated that GO could be trapped in the root vacuoles, and that the maximal root length and the number of lateral roots were significantly reduced. Additionally, root tip whitening, creases, oxidative stress, and weakened respiration were observed. These observations indicate that GO is highly unfavorable for vigorous root growth and inhibits increase in root uptake area. At the molecular level, GO exposure caused DNA damage and inhibited the expression of most nitrate transporters (NRTs) in wheat roots, with the most significantly downregulated genes being NRT1.3, NRT1.5, NRT2.1, NRT2.3, and NRT2.4. We concluded that GO exposure decreased the root uptake area and root activity, and decreased the expression of NRTs, which may have consequently suppressed the NO₃⁻ uptake rate, leading to adverse nitrate accumulation in stressed plants.

Because of its analgesic properties, acetaminophen (AAP) is widely used to relieve headache. AAP is generally considered safe for humans, but its effects on aquatic organisms are not well known. Here, we have hypothesis that effects of AAP on aquatic organisms would be environmental temperature dependent, because their physiological function depend on the temperature. To test this hypothesis, we used medaka (Oryzias latipes) as a model, because they can live at a wide range of temperatures (0–40 °C). We exposed medaka larvae to 0 (control), 50, or 150 mg/L of AAP at 15, 25 (optimal temperature), or 30 °C for 4 days. Egg yolk absorption was accelerated with raising temperature at any AAP dose. AAP exposure did not have biologically significant effects on survival ratio and body length of larvae at any tested temperature or dose, but heart rate decreased as the dose of AAP and environmental temperature increased. In addition, as the temperature increased, amount of ATP in individual larvae increased in control group, but decreased in AAP exposed group. Subsequently, exposure to 150 mg/L of AAP at 30 °C decreased the number of red blood cells in the gills; we used 150 mg/L of AAP in subsequent hematological and histological analyses. Hematological analysis showed that rising temperature increased the proportion of morphologically abnormal red blood cells in AAP-exposed larvae, suggesting that AAP induced anemia-like signs in larvae. Histological observation of the kidney, which is a hematopoietic organ in fish, revealed no abnormalities. However, in the liver, which is responsible for drug metabolism, the proportion of vacuoles increased with increasing temperature. Although the exposure concentration we tested was higher than environmentally relevant concentrations, our data indicated that rising temperature enhances the toxicity of AAP to medaka larvae, suggesting an ecological risk of AAP due to global warming.

Due to increased use of agrochemicals and growing concerns about ecotoxicology, the development of new insecticides, moving away from those with neurotoxic and broad spectrum effects towards insecticides that are safer for the environment and nontarget beneficial species, has been a research priority. Novaluron stands out among these newer insecticides, is an insect growth regulator that is used for the control of insect pests in crops grown close to mulberry plantations. Mulberry serves as food for the silkworm Bombyx mori, which is a nontarget insect of great economic importance to silk production. We investigated the lethal and sublethal effects of Novaluron on the development of B. mori. Larvae were segregated into experimental groups: the control groups (CGs) and the treatment groups (TGs), which were treated with the Novaluron concentration of 0.15 mL/L. Following exposure, we analyzed: larval mortality, changes in the insect life cicle and cytotoxic effects on the midgut cells. This is the first report about the Novaluron’s effects on B.mori. We detected rupture in the integument, complete cessation of feeding, late development, incomplete ecdysis and production of defective cocoons. After 240 h of exposure, there was 100% mortality in TG larvae exposed in the 3rd instar and 20% mortality from larvae exposed in the 5th instar. Cytotoxic effects was observed, such as dilation of cells, emission of cytoplasmic protrusions, extreme rarefaction of the cytoplasm and nuclei, dilation of the endoplasmic reticulum in addition to changes in mitochondria, the presence of large digestive vacuoles and intercellular spaces and the presence of active caspase. Novaluron exposure impairs the midgut and may affect the physiological functions of this organ. Novaluron additionally compromises several phases of insect development, indicating the importance of toxicology studies that utilize different life stages of nontarget species to evaluate the safe use of insecticides.

The hydrocarbon phenanthrene is an organic compound commonly found in the environment. In aquatic ecosystems, it is highly toxic to organisms, although little is known about its effects on sediment-dwelling organisms. The purpose of this study was to evaluate phenanthrene effects on biochemical, histological, and ontogenetic levels in larvae of the sediment-dwelling invertebrate Chironomus sancticaroli at acute and chronic exposure. Lethal concentrations were estimated and toxicity (acute-96 h and chronic- 8 d) tests were performed at phenanthrene concentrations from 0.12 to 1.2 mg L⁻¹. At acute and chronic exposure, we evaluated acetylcholinesterase (AChE), alpha esterase (EST-α), and beta esterase (EST-β) activities as well as histological alterations. In the assays with chronic exposure, effects on larval development were estimated using antennae length (instar estimative) and body length (growth estimative). The EST-α showed a significantly increased activity after 48 h at acute exposure to high concentrations of phenanthrene, while EST-β activity was increased after 48 and 72 h at acute exposure at higher concentrations and at 0.12 mg L⁻¹ at chronic exposure. At acute exposure, the midgut showed alterations such as brush border disruption, gastric caeca regression, and lumen area reduction; the fat body showed nuclear alteration in the trophocytes, while the Malpighian tubules showed brush border reduction and the salivary glands were subject to cytoplasm vacuolation. At chronic exposure, the same alterations were observed, in addition to vacuolar coalescence in the trophocytes of the fat body. Regarding larval development, a reduction of body length was observed with increasing phenanthrene concentrations. Similarly, molting was delayed; in the control group, all larvae were in the fourth instar, while at higher phenanthrene concentrations, larvae were predominantly in the third instar. Phenanthrene had toxic effects on this chironomid, indicating risks for natural populations.

Microcystins (MCs) widely distributed in freshwaters have posed a significant risk to human health. Previous studies have demonstrated that exposure to MC-LR impairs pancreatic islet function, however, the underlying mechanisms still remain unclear. In the present study, we explored the role of endoplasmic reticulum (ER) impairment in β-cell dysfunction caused by MC-LR. The result showed that MC-LR modified ER morphology evidenced by increased ER amount and size at low doses (15, 30 or 60 μM) and vacuolar and dilated ER ultrastructure at high doses (100 or 200 μM). Also, insulin content showed increased at 15 or 30 μM but declined at 60, 100, or 200 μM, which was highly accordant with ER morphological alteration. Transcriptomic analysis identified a number of factors and several pathways associated with ER protein processing, ER stress, apoptosis, and diabetes mellitus in the cells treated with MC-LR compared with non-treated cells. Furthermore, MC-LR-induced ER stress significantly promoted the expression of PERK/eIF2α and their downstream targets (ATF4, CHOP, and Gadd34), which indicates that PERK-eIF2α-ATF4 pathway is involved in MC-LR-induced insulin deficiency. These results suggest that ER impairment is an important contributor to MC-LR-caused β-cell failure and provide a new insight into the association between MCs contamination and the occurrence of human diseases.

Although it was recently determined that silicon can alleviate cadmium (Cd) toxicity in rice, the effects of silicon properties and the molecular mechanisms are still unclear. Here, the effect of silica nanoparticles (SiNPs) on Cd toxicity in rice was examined using cells cultured in suspension in the presence or absence of SiNPs (19 nm, 48 nm and 202 nm). The results showed that the presence of SiNPs substantially enhanced the proportion of live cells to 95.4%, 78.6% and 66.2%, respectively, suggesting that the extent of alleviation of Cd toxicity decreased gradually with size of SiNPs. The morphological results showed that dramatic damage and severe structural changes in the organelle integrity of cells occurred in the absence of SiNPs, whereas the cells exposed to the SiNPs remained nearly intact even in the presence of high concentrations of Cd. Furthermore, the SiNPs accumulated on the surface of the rice cells. Using inductively coupled plasma mass spectroscopy, Cd accumulated preferentially in plant cells with cell walls. In addition, noninvasive microtest technology showed that the average Cd2+ influx in those treated with SiNPs (19 nm, 48 nm and 202 nm) decreased by 15.7-, 11.1- and 4.6-fold, respectively. The gene expression of Cd uptake and transport (OsLCT1 and OsNramp5) was inhibited by SiNPs, but the gene expression of Cd transport into vacuole (OsHMA3) and Si uptake (OsLsi1) was enhanced by the SiNPs. These results indicate that the presence of SiNPs increased at least 1.87-fold the Si uptake capacity and inhibited the Cd uptake capacity, which together resulted in the alleviation of the toxicity of Cd in rice. This study provided a molecular-scale insight into the understanding of the SiNPs-induced alleviation of the toxicity of Cd in rice.

The accumulation of arsenic in crop plants has become a worldwide concern that affects millions of people. The major source of arsenic in crop plants is irrigation water and soil. In this study, Serendipita indica, an endophytic fungus, was used to investigate the protection against arsenic and its accumulation in the tomato plant. We found that inoculation of S. indica recovers seed germination, plant growth and improves overall plant health under arsenic stress. A hyper-colonization of fungus in the plant root was observed under arsenic stress, which results in reduced oxidative stress via modulation of antioxidative enzymes, glutathione, and proline levels. Furthermore, fungal colonization restricts arsenic mobilization from root to shoot and fruit by accumulating it exclusively in the root. We observed that fungal colonization enhances the arsenic bioaccumulation factor 1.48 times in root and reduces the arsenic translocation factor by 2.96 times from root to shoot and 13.6 times from root to fruit compared to non colonized plants. Further, investigation suggests that S. indica can tolerate arsenic by immobilizing it on the cell wall and accumulating it in the vacuole. This study shows that S. indica may be helpful for the reduction of arsenic accumulation in crops grown in arsenic-contaminated agriculture fields.

For the first time, we used targeted metabolome to investigate the effects of pH-aluminum (Al) interactions on energy-rich compounds and their metabolites (ECMs) and phytohormones in sweet orange (Citrus sinensis) roots. The concentration of total ECMs (TECMs) was reduced by Al-toxicity in 4.0-treated roots, but unaffected significantly in pH 3.0-treated roots. However, the concentrations of most ECMs and TECMs were not lower in pH 4.0 + 1.0 mM Al-treated roots (P4AR) than in pH 3.0 + 1.0 mM Al-treated roots (P3AR). Increased pH improved the adaptability of ECMs to Al-toxicity in roots. For example, increased pH improved the utilization efficiency of ECMs and the conversion of organic phosphorus (P) from P-containing ECMs into available phosphate in Al-treated roots. We identified upregulated cytokinins (CKs), downregulated jasmonic acid (JA), methyl jasmonate (MEJA) and jasmonates (JAs), and unaltered indole-3-acetic acid (IAA) and salicylic acid (SA) in P3AR vs pH 3.0 + 0 mM Al-treated roots (P3R); upregulated JA, JAs and IAA, downregulated total CKs, and unaltered MEJA and SA in P4AR vs pH 4.0 + 0 mM Al-treated roots (P4R); and upregulated CKs, downregulated JA, MEJA, JAs and SA, and unaltered IAA in P3AR vs P4AR. Generally viewed, raised pH-mediated increments of JA, MEJA, total JAs, SA and IAA concentrations and reduction of CKs concentration in Al-treated roots might help to maintain nutrient homeostasis, increase Al-toxicity-induced exudation of organic acid anions and the compartmentation of Al in vacuole, and reduce oxidative stress and Al uptake, thereby conferring root Al-tolerance. In short, elevated pH-mediated mitigation of root Al-stress involved the regulation of ECMs and phytohormones.

Arsenic (As) is recognized as a toxic metalloid and a severe threat to biodiversity due to its contamination. Soil and groundwater contamination with this metalloid has become a major concern. Large fractions of cultivable lands are becoming infertile gradually due to the irrigation of As contaminated water released from various sources. The toxicity of As causes the generation of free radicals, which are harmful to cellular metabolism and functions of plants. It alters the growth, metabolic, physiological, and molecular functions of the plants due to oxidative burst. Plants employ different signaling mechanisms to face the As toxicity like phosphate cascade, MAPK (Mitogen-Activated Protein Kinase), Ca-calmodulin, hormones, and ROS-signaling. The toxicity of As may significantly be reduced through various remediation techniques. Among them, the microbial-assisted remediation technique is cost-effective and eco-friendly. It breaks down the metalloid into less harmful species through various processes viz. biovolatilization, biomethylation, and transformation. Moreover, the adaptation strategies towards As toxicity are vacuolar sequestration, involvement of plant defense mechanism, and restricting its uptake from plant roots to above-ground parts. The speciation, uptake, transport, metabolism, ion dynamics, signaling pathways, crosstalk with phytohormones and gaseous molecules, as well as harmful impacts of the As on physiological processes, overall development of plants and remediation techniques are summarized in this review.