Comparative Biochemistry and Physiology C-toxicology & Pharmacology最新文献

Nanopolystyrene (NP) and phoxim (PHO) are pervasive environmental contaminants that pose a significant threat to the health of aquatic organisms, prompting widespread concern among researchers and the public alike. The hepatopancreas play important roles in the Chinese mitten crab (Eriocheir sinensis), such as digestion, absorption and detoxification. This study assessed the hepatopancreatic toxicity caused by the exposure of Eriocheir sinensis to environmentally relevant concentrations of NP and/or PHO. After a 21-day exposure period, NP (1.0 × 10¹⁰ particles/L) and PHO (24 μg/L) exposure resulted in reduced number of blister-like, resorptive, and fibrillar cells and an elevation in lipid droplets within the hepatopancreas compared to the control group. Furthermore, trypsin and lipase activity decreased, amylase activity increased, and a significantly decrease in the expression of digestion-related genes, including CHT, CarL, and CarB, suggested impairment in both digestive and metabolic functions. The marked upregulation of key genes, including PPARγ, GYK, PEPCK, and SCD, as well as key metabolites such as 4-methylzymosterol-carboxylate, zymosterone, lathosterol, 7-dehydro-desmosterol, vitamin D2, 24-methylene-cycloartanol, 5-dehydroepisterol, and sitosterol in the lipid metabolic pathway, showed that the peroxisome proliferator-activated receptor (PPAR) and steroid biosynthesis signaling pathways were highly affected by exposure to NP and/or PHO. These findings indicated that exposure to NP and/or PHO might adversely affect the hepatopancreatic physiological homeostasis in E. sinensis by causing tissue damage and interfering with digestive and metabolic functions. Our results provide ecotoxicological insights into the effects of nanopolystyrene and/or phoxim exposure on the digestive function of Eriocheir sinensis.

Glyphosate, a pesticide commonly found in aquatic ecosystems, affects this habitat and nontarget organisms such as fish. The increase in water temperature, linked to factors such as climate change, poses a considerable threat. Despite extensive ecotoxicological research, we still do not know the real individual and specific consequences of continued exposure to glyphosate and high temperatures, simulating a scenario where the aquatic environment remains contaminated and temperatures continue to rise. Therefore, in this study, we examined the effects of exposure to environmentally relevant concentrations of glyphosate, active ingredient glyphosate (GAI), and glyphosate-based herbicide (GBH) in combination with high temperature (34 °C) in adult zebrafish (Danio rerio). The fish were acclimated to 28 or 34 °C for 96 h. The exposure to 225 and 450 μg L^-1 (GBH or GAI) at 28 or 34 °C for 7 days. We analyzed behavioral endpoints (anxiety-like response, sociability, and aggressivity) and biochemical biomarkers of the brain and muscle (oxidative stress). Anxiety-like responses and decreased sociability were disrupted by the combination of glyphosate and high temperature. Furthermore, there is a decrease in Acetylcholinesterase activity in the brain, and an increase in Lipid Peroxidation, Protein Carbonylation, Acetylcholinesterase activity, and Glutathione S-Transferase activity in the muscle. These results demonstrated oxidative stress, anxiety-like behavior and decreased sociability caused by glyphosate and high temperature. We concluded that the combined effects of glyphosate and high temperature affected redox homeostasis and behavior, emphasizing that the field of glyphosate pollution should be carefully considered when evaluating the effects of climate change.

Higher antioxidant defenses in marine than terrestrial mammals allow them to cope with oxidative stress associated with diving-induced ischemia/reperfusion. Does this adaptation translate to inherent resistance to other stressors? We analyzed oxidative stress indicators in cells derived from human and California sea lion (Zalophus californianus) skeletal muscle upon exposure to di (2-ethylhexyl) phthalate (DEHP). Human abdominal muscle biopsies were collected from healthy women undergoing planned cesarean surgery. California sea lion samples were collected postmortem from stranded animals. Skeletal muscle cells derived from each species were exposed to 1 mM DEHP for 13 days (n = 25) or maintained under control (untreated) conditions (n = 25). Superoxide radical (O₂^•-) production, oxidative damage and antioxidant enzyme activities were measured using spectrophotometric methods. Gene expression was analyzed by RT-qPCR. DEHP exposure increased O₂^•- production and superoxide dismutase (SOD) activity in both species. Glutathione S-transferase (GST) activity and protein carbonyl levels increased in human but not in California sea lion cells. In contrast, glutathione peroxidase (GPx) and catalase (CAT) activities increased in California sea lion but not in human cells exposed to DEHP. In human cells, DEHP increased microsomal GST1 and GST (κ, μ, θ, ω, and ᴢ), while suppressing 8-oxoguanine DNA glycosylase (OGG1), CAT, glutathione reductase (GR), and nuclear factor erythroid 2-related factor 2 (NRF2) expression, suggesting increased oxidative stress and phase two detoxification processes. In California sea lion cells, DEHP increased OGG1, NRF2, GPx2 and SOD3 expression, suggesting activation of antioxidant defenses, which potentially contribute to maintaining redox homeostasis, avoiding oxidative damage.

In real environments, multiple pollutants often coexist, so studying the impact of a single pollutant does not fully reflect the actual situation. Cycloxaprid, a new neonicotinoid pesticide, poses significant ecological risks due to its unique mechanism and widespread distribution in aquatic environments. Additionally, the ecological effects of microplastics, another common environmental pollutant, cannot be overlooked. This study explored the ecotoxicological effects of cycloxaprid and microplastics, both alone and in combination, on Penaeus vannamei over 28 days. The results revealed significant physiological impacts, with notable changes in the shrimp immune system and hepatopancreatic energy and lipid metabolism. Key findings include alterations in hemocyanin, nitric oxide, and phenol oxidase levels, along with disturbances in Na⁺/K⁺-, Ca²⁺-, and Mg²⁺-ATPase activities. Additionally, neural signaling disruptions were evidenced by fluctuations in acetylcholine, dopamine, and acetylcholinesterase levels. Transcriptomic analysis revealed the profound influence of these pollutants on gene expression and metabolic processes in the hepatopancreas and nervous system. This comprehensive assessment underlines the potential growth impacts on shrimp and underscores the ecological risks of cycloxaprid and microplastics, offering insights for future risk assessments and biomarker identification.

The skin and gut microbiota are crucial to amphibians. Triadimefon (TF), a widely used triazole fungicide, controls crop diseases and regulates growth, with uncertain effects on amphibian microbiota. Contamination, typically involving mixed chemicals at low concentrations, including cadmium (Cd) and TF, may detrimentally affect amphibian growth, survival, and microbiota health in both the skin and gut, but few research has examined these consequences. This research examines the impact of Cd and TF on Rana dybowskii tadpoles, focusing on survival, body mass, and microbiome changes over 28 days across four groups: control, Cd, TF, and Cd + TF groups. Results showed significant reductions in survival and body mass in Cd and TF-treated groups, with the combination group being the most affected. Microbiota analysis revealed significant dysbiosis in both gut and skin microbiomes under pollutant stress, with a marked microbiota and a shift in dominant microbial communities. Function prediction analysis based on the microbiome composition highlighted significant differences across various biological pathways, including metabolism, immune system, environmental adaptation, and disease resistance. These alterations suggest that pollutant exposure compromises the tadpoles' ability to maintain homeostasis and resist pathogens. In conclusion, this study reveals the detrimental effects of Cd and TF on the survival, growth, and microbiomes of R. dybowskii tadpoles, indicating significant environmental and health risks.

Atenolol is a widely prescribed β₁-cardioselective blocker. We studied atenolol effects on cardiac and renal development in day 18 (D18) chicken embryos. Embryos were dosed with atenolol (3 μg atenolol/g estimated embryo mass) for three days during one of the mesonephric kidney stage (D7-D9), mesonephric-metanephric stage (D11-D13), or metanephric stage (D15-D17), and then sampled on D18. Wet embryo body mass in atenolol-treated groups was reduced at D18 (P < 0.01). Wet heart mass of atenolol-treated embryos was significantly (P < 0.01) reduced in the mesonephric stage on D18. Similarly, kidney mass in atenolol-treated mesonephric and metanephric stages was significantly reduced at D18. Nephron density was 40 % lower following atenolol treatment during the mesonephros stage. Individual glomerular areas of mesonephric- and metanephric-treated stages were significantly larger (P < 0.01) than controls, but overall glomerular area was reduced in the meso- and meso-metanephros populations. Collectively, these data suggest that chronic atenolol treatment results in major renal remodeling and that the mesonephros renal stage (D7-D9), is the critical window for effects of atenolol on renal morphology. Acute atenolol application at D11 through D19 had no effect on mean arterial blood pressure or heart rate, even though these variables were acutely altered as early as Day 15 by isoproterenol. Collectively, these data suggest that the morphological effects of atenolol were not the result of altered perfusion. Further experiments are required to determine if reduced embryo, cardiac and renal masses are specific to chronic atenolol treatment, or whether other β blockers might have similar effects.

Di(2-ethylhexyl) phthalate (DEHP) is a plasticizer used in various industrial and consumer products. It is not covalently bound within these products and leaches out during repeated use, heating, or cleaning. Main routes of environmental DEHP pollution are through the industrial and municipal wastewaters, which pollute aquatic environments. The reproductive system of adult fish is known to be vulnerable to DEHP exposure; however, the effects of early-life exposure to DEHP on reproductive function in adult zebrafish (Danio rerio) females are less studied. To evaluate the impact of early-life exposure to DEHP on freshwater female fish reproduction, zebrafish embryos were exposed to DEHP at 0, 10, 100, and 1000 nmol/L from 5 h post-fertilization (hpf) to 120 hpf (larval stage) and then raised to adulthood in clean water. DEHP decreased the number of released eggs and the fertilization rate after mating with unexposed males. Bodyweight and length, the weight of the ovaries, and the gonadosomatic index were decreased in adult female zebrafish following early-life exposure to DEHP. Histological analysis of the ovaries revealed that DEHP inhibited oogenesis. Serum 17β-estradiol levels were significantly reduced. DEHP inhibited gene expression of all three nuclear estrogen receptors in the ovaries, namely esr1, esr2a, and esr2b, and two gonadotropin receptors, fshr and lhr. These results suggest that transient early-life exposure to environmentally relevant concentrations of DEHP can inhibit the reproduction of adult female zebrafish.