Increasing rates of commercialization and industrialization have led to the comprehensive evaluation of toxic effects of microplastics on crop plants. However, research on the impact of functionalized polystyrene nanoplastics on the toxicity of heavy metals remains limited. This study investigated the effects of polystyrene, carboxy-modified polystyrene, and amino-modified polystyrene on lead (Pb) toxicity in dandelion seedlings. The results showed that carboxy -modified polystyrene with a negative charge absorbed more Pb²⁺ than polystyrene and amino-modified polystyrene, and their maximum adsorption amounts were 5.328, 0.247, and 0.153 μg g⁻¹, respectively. The hydroponic experiment demonstrated that single amino-modified polystyrene was more toxic to dandelion seedlings than polystyrene and carboxy-modified polystyrene. The presence of Pb²⁺ was found to increase antioxidant enzymes (superoxide dismutase and catalase) and non-antioxidant enzymes (glutathione and ascorbic acid) activities in response to excessive reactive oxygen species in dandelion leaves and roots treated with polystyrene and carboxy-modified polystyrene, while it did not change much when amino-modified polystyrene was added. Interestingly, compared with single Pb²⁺, the addition of amino-modified polystyrene with positive charges induced an obvious decrease in the above parameters; however, they declined slightly in the treatments with polystyrene and carboxy-modified polystyrene despite a stronger adsorption capacity for Pb²⁺. Similarly, the bioactive compounds, including flavonoids, polyphenols, and polysaccharides in dandelion, showed a scavenging effect on O₂⁻ and H₂O₂, thereby inhibiting the accumulation and reducing medicinal properties. This study found that the effects of microplastics on the uptake, distribution, and toxicity of heavy metals depended on the nanoparticle surface charge.

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.

Evidence suggests that the invasion of Spartina alterniflora (S. alterniflora) poses potentially serious risks to the stability of coastal wetlands, an ecosystem that is extremely vulnerable to both biological and non-biological threats. However, the effects and mechanisms of sulfur (S) in mediating the growth and expansion of S. alterniflora are poorly understood, particularly when sediments are contaminated with cadmium (Cd). A 6-month greenhouse study was conducted to evaluate the mediating effect of S on Cd tolerance and growth of S. alterniflora. Treatments consisted of a factorial combination of three S rates (applied as Na₂SO₄; 0, 500, 1000 mg kg⁻¹ dry weight (DW), as S₀, S₅₀₀, and S₁₀₀₀) and four Cd rates (applied as CdCl₂; 0, 1, 2, 4 mg kg⁻¹ DW, as Cd₀, Cd₁, Cd₂, and Cd₄). Results showed that although the exogenous S supply obviously increased Cd accumulation in roots (up to 71.22 ± 6.43 mg kg⁻¹ DW) due to the decrease of Fe concentration in iron plaque (down to 4.02 ± 1.18 mg g⁻¹ DW), biomass reduction and oxidative stress in plant tissues were significantly alleviated. The addition of S significantly up-regulated the concentration of compounds related to Cd tolerance, including proline and glutathione. Therefore, the translocation of Cd was restricted, and plant growth was not impacted. The present study demonstrated that the exogenous sulfur supply could promote the growth of S. alterniflora and enhance its tolerance to Cd. Therefore, under the effects of S. alterniflora, the increased fluctuations of S pool caused by the release and deposition of S might further exacerbate S. alterniflora expansion in Cd contaminated coastal wetlands.

The main intent of the current research was to appraise if combined application of hydrogen sulfide (H₂S, 0.2 mM) and silicon (Si 2.0 mM) could improve tolerance of tomato plants to arsenic (As as sodium hydrogen arsenate heptahydrate, 0.2 mM) stress. Plant growth, chlorophylls (Chl), PSII maximum efficiency (Fv/Fm), H₂S concentration and L-cysteine desulfhydrase activity were found to be suppressed, but leaf and root As, leaf proline content, phytochelatins, malondialdehyde (MDA) and H₂O₂ as well as the activity of lipoxygenase (LOX) increased under As stress. H₂S and Si supplied together or alone enhanced the concentrations of key antioxidant biomolecules such as ascorbic acid, and reduced glutathione and the activities of key antioxidant system enzymes including catalase (CAT), superoxide dismutase (SOD), dehydroascorbate reductase (DHAR), glutathione reductase (GR), and glutathione S-transferase (GST). In comparison with individual application of H₂S or Si, the joint supplementation of both had better effect in improving growth and key biochemical processes, and reducing tissue As content, suggesting a putative collaborative role of both molecules in improving tolerance to As-toxicity in tomato plants.

Increasing attention has been brought to microplastics pollution recently, while emerging evidences indicate that nano-plastics degraded from microplastics are more of research significance owing to stronger toxicity. However, there is little study focused on the prevention of nano-plastics induced toxicity until now. Canidin-3-glucoside (C3G), a natural anthocyanin proved to possess multiple functions like antioxidant and intestinal tissue protection. Thus, we proposed whether C3G could act as a molecular weapon against nano-plastics induced toxicity. In Caco2 cell and Caenorhabditis elegans (C. elegans) models, we found that polystyrene (PS) nano-plastics exposure resulted in physiological toxicity and oxidative damage, which could be restored by C3G. More significantly in Caco2 cells, we observed that autophagy was activated via Sirt1-Foxo1 signaling pathway to attenuate PS induced toxicity after C3G intervention and further verified by adding autophagy inhibitor 3-Methyladenine (3-MA). Meanwhile, PS co-localization with lysosomes was observed, indicating the encapsulation and degradation of PS. In C. elegans, by detecting LGG-1/LC3 expression in GFP-targeted LGG-1 report gene (LGG-1:GFP) labeled transgenic DA2123 strain, the co-localization of LGG-1:GFP with PS was found as well, means that autophagy is involved in C3G’s beneficial effects. Furthermore, we were surprised to find that C3G could promote the discharge of PS from N2 nematodes, which reduces PS toxicity more directly.

Ionic liquids (ILs), also known as green solvents, are widely acknowledged in several fields, such as chemical separation, synthesis, and electrochemistry, owing to their excellent physiochemical properties. However, their poor biodegradability may lead to environmental and health risks, posing a severe threat to humans, thus requiring further research. In this study, the biotoxicities of the imidazolium-based ILs were evaluated in Tetrahymena pyriformis. Moreover, IL detoxification was investigated by addition of glutathione (GSH), cysteine, and nicotinamide adenine dinucleotide (NADH). Reactive oxygen species (ROS) initiated by different IL types caused damage to Tetrahymena, while glutathione, cysteine, and NADH eliminated ROS, achieving the detoxification purposes. Detoxification results showed that NADH exhibited the best detoxification ability, followed by glutathione and cysteine. Finally, RT-PCR results suggested that metallothionein might have participated in IL detoxification.

Cadmium (Cd) is a harmful heavy metal that can cause many health problems, while selenium (Se) is an essential nutrient for organisms that can protect them from heavy metal-induced damage. To explore the effects of Se on Cd-induced mitophagy in the liver, forty 3-month-old New Zealand white rabbits (2–2.5 kg), half male and half female, were randomly divided into four groups: the Control group, the Se (0.5 mg/kg body weight (BW)) group, the Cd (1 mg/kg BW) group and the Se+Cd group. After 30 days, the toxicity from Cd in the liver was assessed in terms of the nuclear xenobiotic receptor (NXR) response, oxidative stress and mitophagy. It was found that Cd decreased the activities of CYP450 enzymes and antioxidant enzymes and increased the contents of malondialdehyde (MDA) and hydrogen peroxide (H₂O₂) and also increased the consumption of reduced glutathione (GSH). Moreover, the mRNA levels of NXRs (CAR, PXR, AHR and Nrf2), some mitochondrial function factors (PGC-1α, Sirt1, Sirt3, Nrf1 and TFAM) and mitochondrial fusion factors (Mfn1, Mfn2 and OPA1) were downregulated, but the mRNA levels of other mitochondrial function factors (VDAC1, Cyt C and PRDX3), mitochondrial fission factors (Fis1 and MFF) and those in the PINK1/Parkin-mediated mitophagy pathway (p62, Bnip3 and LC3) were upregulated under Cd exposure. The protein expression levels of Nrf2, SOD2, PGC-1α, PINK1 and Parkin were consistent with the mRNA expression levels in the Cd group. Se alleviated the changes in the abovementioned factors induced by Cd. In conclusion, the results indicate that Cd can cause oxidative stress in rabbit livers by inhibiting NXRs and the antioxidation response leading to mitophagy, and these harmful changes caused by Cd can be alleviated by Se.

Arsenite [As(III)] toxicity causes impeded growth, inadequate productivity of plants and toxicity through the food chain. Using various chemical residues for priming is one of the approaches in conferring arsenic tolerance in crops. We investigated the mechanism of abscisic acid (ABA)-induced As(III) tolerance in rice genotypes (cv. Swarna and Swarna Sub1) pretreated with 10 μM of ABA for 24 h and transferred into 0, 25 and 50 μM arsenic for 10 days. Plants showed a dose-dependent bioaccumulation of As(III), oxidative stress indicators like superoxide, hydrogen peroxide, thiobarbituric acid reactive substances and the activity of lipoxygenase. As(III) had disrupted cellular redox that reflecting growth indices like net assimilation rate, relative growth rate, specific leaf weight, leaf mass ratio, relative water content, proline, delta-1-pyrroline-5-carboxylate synthetase and electrolyte leakage. ABA priming was more protective in cv. Swarna Sub1 than Swarna for retrieval of total glutathione pool, non-protein thiols, cysteine, phytochelatin and glutathione reductase. Phosphate metabolisms were significantly curtailed irrespective of genotypes where ABA had moderated phosphate uptake and its metabolizing enzymes like acid phosphatase, alkaline phosphatase and H⁺/ATPase. Rice seedlings had regulated antioxidative potential with the varied polymorphic expression of those enzymes markedly with antioxidative enzymes. The results have given the possible cellular and physiological traits those may interact with ABA priming in the establishment of plant tolerance with As(III) over accumulation and, thereby, its amelioration for oxidative damages. Finally, cv. Swarna Sub1 was identified as a rice genotype as a candidate for breeding program for sustainability against As(III) stress with cellular and physiological traits serving better for selection pressure.

It is widely recognized that apex predators, such as large sharks with highly migratory behavior, are particularly vulnerable to pollution, mainly due to biomagnification processes. However, in highly impacted areas, mesopredator sharks with resident behavior can be as vulnerable as apex sharks. In this context, this study evaluated cadmium (Cd), mercury (Hg), lead (Pb), and rubidium (Rb) concentrations, as well as the potentially protective effects of selenium (Se) and the behavior of two non-enzymatic biomarkers, metallothionein (MT) and reduced glutathione (GSH), employing the Atlantic nurse shark Ginglymostoma cirratum as a study model and compared the results with other resident benthic sharks, as well as highly mobile apex sharks. Muscle tissue samples from 28 nurse sharks opportunistically sampled from the Brazilian Amazon Coast were analyzed. Lower metal concentrations were observed for Pb, Rb and Se in the rainy season, while statistically significant correlations between metals were observed only between Hg and Cd and Pb and Se. Molar ratio calculations indicate potential protective Se effects against Pb, but not against Cd and Hg. No associations between MT and the determined metals were observed, indicating a lack of detoxification processes via the MT detoxification route. The same was noted for GSH, indicating no induction of this primary cellular antioxidant defense. Our results indicate that benthic/mesopredator sharks with resident behavior are, in fact, as impacted as highly mobile apex predators, with the traditional detoxification pathways seemingly inefficient for the investigated species. Moreover, considering the studied population and other literature data, pollution should be listed as a threat to the species in future risk assessments.

Hydrogen peroxide (H₂O₂), as a common disinfectant, has been extensively used in aquaculture. The toxicity of high ambient H₂O₂ for gills and liver of fish has received attention from many researchers. However, whether H₂O₂ exposure induced brain injury and neurotoxicity has not been reported in fish. Therefore, this study aimed to explore the potential mechanism of H₂O₂ toxicity in brain of common carp via transcriptome analysis and biochemical parameter detection. The fish were exposed to 0 (control) and 1 mM of H₂O₂ for 1 h per day lasting 14 days. The results showed that H₂O₂ exposure caused oxidative damage in brain evidenced by decreased glutathione (GSH), total antioxidant capacity (T-AOC) and nicotinamide adenine dinucleotide (NAD⁺) levels, and increased formation of malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Meanwhile, H₂O₂ exposure reduced 5-hydroxytryptamine (5-HT) level, and down-regulated tryptophan hydroxylase 1 (tph1a), tph2, 5-hydroxytryptamine receptor 1A-beta (htr1ab) and htr2b expression in brain. Transcriptome analysis showed that H₂O₂ exposure up-regulated 604 genes and down-regulated 1209 genes in brain. Go enrichment displayed that the differently expressed genes (DEGs) were enriched mainly in cellular process, single-organism process, metabolic process, and biological regulation in the biological process category. Further, KEGG enrichment indicated that H₂O₂ exposure led to dysregulation of neurotransmitter signals including depression of glutamatergic synapse, GABAergic synapse and endocannabinoid signaling. Also, we found the alteration of three key pathways including calcium, cAMP and HIF-1 in brain after H₂O₂ exposure. In conclusion, our data indicated that H₂O₂ exposure induced oxidative damage and neurotoxicity, possibly related to dysregulation of neurotransmitters and calcium, cAMP and HIF-1 signaling pathways, which may adversely affect learning, memory and social responses of common carp. This study provided novel insight into biological effects and underlying mechanism of H₂O₂ toxicity in aquatic animal, and contributed to proper application of H₂O₂ in aquaculture.