Due to the unreasonable use and discharge of the aquaculture industry, over standard of the antibiotics has been frequent in different types of water environments, causing adverse effects on aquatic organisms. Lycopene (LYC) is an esculent carotenoid, which is considered to be a strong antioxidant. This study was designed to explore the therapeutic effect of LYC on antibiotic (sulfamethoxazole (SMZ)) induced intestinal injury in grass carp Ctenopharyngodon idella. The 120 carps (the control, LYC, SMZ, and co-administration groups) were treated for 30 days. We found that treatment with LYC significantly suppressed SMZ-induced intestinal epithelial cell damage and tight junction protein destruction through histopathological observation, transmission electron microscopy and detection of related genes (Claudin-1/3/4, Occludin and zonula occludens (ZO)-1/2). Furthermore, LYC mitigated SMZ-induced dysregulation of oxidative stress markers, including elevated malondialdehyde (MDA) levels, and consumed super oxide dimutese (SOD), catalase (CAT) activities and glutathione (GSH) content. In the same treatment, LYC reduced inflammation and apoptosis by a detectable change in pro-inflammatory factors (tumor necrosis factor-alpha (TNF-β), interleukin (IL)-1β, IL-6 and IL-8), anti-inflammatory factors (transforming growth factor-beta (TGF-β) and IL-10) and pro-apoptosis related genes (p53, p53 upregulated modulator of apoptosis (PUMA), Bax/Bcl-2 ratio, caspase-3/9). In addition, activation of autophagy (as indicated by increased autophagy-related genes through AMPK/ATK/MTOR signaling pathway) under the stress of SMZ was also dropped back to the original levels by LYC co-administration. Collectively, our findings identified that LYC can serve as a protectant agent against SMZ-induced intestinal injury.

Frequency and intensity of wildfire occurrences are dramatically increasing worldwide due to global climate change, having a devastating effect on the entire ecosystem including plants. Moreover, distribution of fire-smoke can influence the natural environment over very long distances, i.e. hundreds of kilometres. Dry plant matter contains 0.1–0.9% (w/w) sulphur, which is mainly released during combustion into the atmosphere as sulphur dioxide (SO₂) resulting in local concentrations of up to 3000 nL L⁻¹. SO₂ is a highly hazardous gas, which enters plants mostly via the stomata. Toxic sulphite is formed inside the leaves due to conversion of SO₂. Plants as sessile organisms cannot escape from threats, why they evolved an impressive diversity of molecular defence mechanisms. In the present study, two recent wildfires in Germany were evaluated to analyse the effect of SO₂ released into the atmosphere on deciduous trees: the Meppen peat fire in 2018 and the forest fire close to Luebtheen in 2019. Collected leaf material from beech (Fagus sylvatica) and oak (Quercus robur) was examined with respect to detoxification of sulphur surplus due to the exposure to elevated SO₂. An induced stress reaction in both species was indicated by a 1.5-fold increase in oxidized glutathione. In beech leaves, the enzymatic activities of the sulphite detoxification enzymes sulphite oxidase and apoplastic peroxidases were increased 5-fold and a trend of sulphate accumulation was observed. In contrast, oaks did not regulate these enzymes during smoke exposure, however, the constitutive activity is 10-fold and 3-fold higher than in beech. These results show for the first time sulphite detoxification strategies of trees in situ after natural smoke exposure. Beech and oak trees survived short-term SO₂ fumigation due to exclusion of toxic gases and different oxidative detoxification strategies. Beeches use efficient upregulation of oxidative sulphite detoxification enzymes, while oaks hold a constitutively high enzyme-pool available.

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.

We investigated the in vitro effects of pyriproxyfen on ionic balance in the testis of the zebrafish by measuring ⁴⁵Ca²⁺ influx. In vivo pyriproxyfen treatment was carried out to study oxidative stress, and conduct morphological analysis of the testis and liver. Whole testes were incubated in vitro with/without pyriproxyfen (10⁻¹², 10⁻⁹ or 10⁻⁶ M; 30 min) and ⁴⁵Ca²⁺ influx determined. To study pyriproxyfen’s mechanism of action, inhibitors/activators of ionic channels or pumps/exchangers, protein kinase inhibitors or a calcium chelator were added 15 min before the addition of ⁴⁵Ca²⁺ and pyriproxyfen. We evaluated the in vivo effects of 7 day exposure to waterborne pyriproxyfen (10⁻⁹ M) on reactive oxygen species (ROS) formation, lipid peroxidation, and reduced glutathione content (GSH), glutathione S-transferase (GST), superoxide dismutase (SOD), catalase (CAT) and γ-glutamyltransferase (GGT) activity. Morphological analyses of the testis and liver were carried out after in vivo exposure of D. rerio to pyriproxyfen. Pyriproxyfen increased ⁴⁵Ca²⁺ influx by opening the voltage-dependent T-type channels (T-type VDCC), inhibiting sarco/endoplasmic reticulum ⁴⁵Ca²⁺-ATPase (SERCA) and the NCX exchanger (forward mode) and by mobilizing calcium from stores. The involvement of potassium channels and protein kinase C (PKC) was also demonstrated in pyriproxyfen-induced intracellular calcium elevation. In vivo pyriproxyfen treatment of D. rerio increased lipid peroxidation, decreased GSH content and increased GST activity in testes, in addition to increasing the number and size of spermatogonia cysts and inducing hepatocyte basophilia and dilation of blood vessels in the liver. The toxicity of pyriproxyfen is mediated by calcium overload, increased lipid peroxidation, and a diminished antioxidant capacity in the testis, due to GSH depletion, and altered spermatogenesis. The development of high basophilia in the liver suggests that pyriproxyfen may have estrogenic activity, possibly acting as an endocrine-disruptor. These findings indicate that these alterations may contribute to pyriproxyfen toxicity and spermatogenesis disruption.

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.

The present study aimed to show that nickel and fluoride exhibited synchronized co-inhibited uptake in the aromatic rice cultivar, Gobindobhog, since bioaccumulation of the two elements was lower than that during individual stress, so that overall growth under combined stress was similar to control seedlings. On the contrary, lead and fluoride stimulated their co-uptake which triggered oxidative damages, NADPH oxidase activity, methylglyoxal accumulation, photosynthetic inhibition, membrane-protein damages, necrosis and genomic template degradation. Accumulation of proline, anthocyanins, non-protein thiols and phytochelatins was stimulated for systemic protection against reactive oxygen species (ROS) and xenobiotic-mediated injuries during lead-fluoride toxicity. ROS accumulation during nickel-fluoride stress was insignificant due to which enhanced accumulation of most antioxidants was not required. Glutathione depletion during combined lead-fluoride toxicity was due to its utilization in the glyoxalase cycle and also inhibition of glutathione reductase. However, the nickel-fluoride-treated sets maintained glutathione reserves and glyoxalase activity similar to those in control. Presence of fluoride ‘safeguarded’ the glutathione-utilizing enzymes like glutathione reductase, glutathione peroxidase and glutathione-S-transferase during dual lead-fluoride stress. This was because these enzymes showed higher activity compared to that under lead toxicity alone. Enzymatic antioxidants like superoxide dismutase, ascorbate peroxidase and guaiacol peroxidase were activated during lead-fluoride toxicity due to altered iron and copper homeostasis. Catalase activity was strongly inhibited, resulting in the inability to scavenge H₂O₂ and suppression of the fluoride-adaptable phenotype. However, none of the enzymatic antioxidants were inhibited during nickel-fluoride stress, which cumulatively allowed the seedlings to maintain normal physiology. Overall our findings holistically reveal the physiological plasticity of Gobindobhog in response to two different heavy metals under the influence of fluoride.

Hydrogen sulfide (H₂S) is well known as a gaseous signal in response to heavy metal stress, while methane (CH₄), the most prevalent greenhouse gas, confers cadmium (Cd) tolerance. In this report, the causal link between CH₄ and H₂S controlling Cd tolerance in alfalfa (Medicago sativa) plants was assessed. Our results observed that the administration of CH₄ not only intensifies H₂S metabolism, but also attenuates Cd-triggered growth inhibition in alfalfa seedlings, which were parallel to the alleviated roles in the redox imbalance and cell death in root tissues. Above results were not observed in roots after the removal of endogenous H₂S, either in the presence of either hypotaurine (HT; a H₂S scavenger) or DL-propargylglycine (PAG; a H₂S biosynthesis inhibitor). Using in situ noninvasive microtest technology (NMT) and inductively coupled plasma mass spectroscopy (ICP-MS), subsequent results confirmed the participation of H₂S in CH₄-inhibited Cd influx and accumulation in roots, which could be explained by reestablishing glutathione (GSH) pool (reduced/oxidized GSH and homoglutathione) homeostasis and promoting antioxidant defence. Overall, our results clearly revealed that H₂S operates downstream of CH₄ enhancing tolerance against Cd stress, which are significant for both fundamental and applied plant biology.

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.

It is estimated that approximately 0.4% of the total leachate produced in a landfill is destined for treatment plants, while the rest can reach the soil and groundwater. In this context, this study aimed to perform leachate toxicity evaluations through immune system cytotoxic assessments, genotoxic (comet assay) appraisals and antioxidant system (superoxide dismutase - SOD; catalase - CAT, glutathione-S-transferase - GST; reduced glutathione - GSH and metallothionein - MT) evaluations in Eisenia andrei earthworms exposed to a Brazilian leachate for 77 days. The leachate sample contained high organic matter (COD - 10,630 mg L⁻¹) and ammoniacal nitrogen (2398 mg L⁻¹), as well as several metals, including Ca, Cr, Fe, Mg, Ni and Zn. Leachate exposure resulted in SOD activity alterations and increased CAT activity and MT levels. Decreased GST activity and GSH levels were also observed. Antioxidant system alterations due to leachate exposure led to increased malondialdehyde levels as a result of lipid peroxidation after the 77 day-exposure. An inflammatory process was also observed in exposed earthworms, evidenced by increased amoebocyte density, and DNA damage was also noted. This study demonstrates for the first time that sublethal effect assessments in leachate-exposed earthworms comprise an important tool for solid waste management.

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.