Moxidectin is an antiparasitic drug belonging to the class of the macrocyclic lactones, subgroup mylbemicins. It is used worldwide in veterinary practice, but little is known about its potential environmental risks. Thus, we used the zebrafish embryo as a model system to study the potential effects of moxidectin on aquatic non-target organisms. The analyses were performed in two experimental sets (1) acute toxicity and apical endpoints were characterized, with biomarker assays providing information on the activity levels of catalase (CAT), glutathione S-transferase (GST), lactate dehydrogenase (LDH), and acetylcholinesterase (AChE); and (2) internal concentration and spatial distribution of moxidectin were determined using ultraperformance liquid chromatography quadrupole-time-of-flight mass spectrometry (UPLC-QToF-MS) and matrix-assisted laser desorption/ionization-MS imaging (MALDI-MSi). The acute toxicity to zebrafish embryos (96 hpf) appeared mainly as a decrease in hatching rates (EC50 = 20.75 μg/L). Z-DEVD-FMK solubility dmso It also altered the enzymatic activity of biomarker enzymes related to xenobiotic processing, anaerobic metabolism, and oxidative stress (GST, LDH, and CAT, respectively) and strongly accumulated in the embryos, as internal concentrations were 4 orders of magnitude higher than those detected in exposure solutions. MALDI-MSi revealed accumulations of the drug mainly in the head and eyes of the embryos (72 and 96 hpf). Thus, our results show that exposure to moxidectin decreases hatching success by 96 h and alters biochemical parameters in the early life stages of zebrafish while accumulating in the head and eye regions of the animals, demonstrating the need to prioritize this compound for environmental studies.1-Nitropyrene (1-NP) is one component of atmospheric fine particles. Previous report revealed that acute 1-NP exposure induced respiratory inflammation. This study aimed to investigate whether chronic 1-NP exposure induces pulmonary fibrosis. Male C57BL6/J mice were intratracheally instilled to 1-NP (20 μg/mouse/week) for 6 weeks. Diffuse interstitial inflammation, a-smooth muscle actin (a-SMA)-positive cells, a marker of epithelial-mesenchymal transition (EMT), and an extensive collagen deposition, measured by Masson staining, were observed in 1-NP-exposed mouse lungs. Pulmonary function showed that lung dynamic compliance (Cydn-min) was reduced in 1-NP-exposed mice. Conversely, inspiratory resistance (Ri) and expiratory resistance (Re) were elevated in 1-NP-exposed mice. Mechanistically, cell migration and invasion were accelerated in 1-NP-exposed pulmonary epithelial cells. In addition, E-cadherin, an epithelial marker, was downregulated, and vimentin, a-SMA and N-cadherin, three mesenchymal markers, were upregulated in 1-NP-exposed pulmonary epithelial cells. Although TGF-β wasn’t altered, phosphorylated Smad2/3 were enhanced in 1-NP-exposed pulmonary epithelial cells. Moreover, reactive oxygen species (ROS) were increased and endoplasmic reticulum (ER) stress was activated in 1-NP-exposed pulmonary epithelial cells. N-Acetylcysteine (NAC), an antioxidant, attenuated 1-NP-evoked excess ROS, ER stress and EMT in pulmonary epithelial cells. Similarly, pretreatment with NAC alleviated 1-NP-caused pulmonary EMT and lung fibrosis in mice. These results demonstrate that ROS-evoked ER stress contributes, at least partially, to 1-NP-induced EMT and pulmonary fibrosis.Loggerhead turtles (Caretta caretta) voluntarily ingest floating plastic debris and hence are chronically exposed to plastic additives, but very little is known about the levels of these compounds in their tissues. This work studied the presence of organophosphate esters (OPEs) on sea turtles collected from two different areas in the western Mediterranean, some of their prey and some floating plastic debris. OPEs were detected in all the samples analysed and ∑OPEs ranged from 12.5 to 384 ng/g wet weight (ww) in the turtles from the Catalan coasts, with a mean value of 21.6 ng/g ww, and from 6.08 to 100 ng/g ww in the turtles the Balearic Islands, with a mean value of 37.9 ng/g ww. Differences in ∑OPEs were statistically significant, but turtles from the two regions did not differ in their OPE profiles. As per turtle’s prey, ∑OPEs ranged from 4.55 to 90.5 ng/g ww. Finally, marine plastic litter showed ∑OPEs concentrations between 10.9 and 868 ng/g. Although most compounds were present in both potential sources of contamination, prey and plastic debris, the OPE profiles in loggerhead turtles and these sources were different. Some OPEs, such as tris(2-isopropylphenyl) phosphate (T2IPPP), tripropyl phosphate (TPP) and tris(2-butoxyethyl) phosphate (TBOEP), were detected in plastic debris and turtle muscle but not in their prey, thus suggesting that ingestion of plastic debris was their main source. Contrarily, the levels of triethyl phosphate (TEP), diphenyl cresyl phosphate (DCP), 2-isopropylphenyl diphenyl phosphate (2IPPDPP) and 4-isopropylphenyl diphenyl phosphate (4IPPDPP) in turtle muscle were much higher than in jellyfish, their main prey, thus indicating a biomagnification potential. Regular ingestion of plastic debris and contamination from their prey may explain why ∑OPEs in loggerhead turtles is much higher than the values reported previously for teleost fishes and marine mammals from the western Mediterranean.Plants in nature are protected against insect herbivory by a wide variety of specialized metabolites. Although insect herbivores generally tolerate the defensive metabolites of their preferred host plants, the presence of additional chemical defenses in otherwise closely related plant species can nevertheless provide resistance. This chemical resistance to insect herbivory can be enhanced by genetic engineering to increase the production of endogenous defensive metabolites, modify existing biochemical pathways, or move the biosynthesis of entirely new classes of specialized metabolites into recipient plants. However, current plant genetic engineering strategies are limited by insufficient knowledge of the biosynthetic pathways of plant specialized metabolism, unintended side-effects that result from redirecting plant metabolism, inadequate transgene construction and delivery methods, and requirements for tissue-specific production of defensive metabolites to enhance herbivore resistance.