Environmentally relevant concentrations of tralopyril affect carbohydrate metabolism and lipid metabolism of zebrafish (Danio rerio) by disrupting mitochondrial function

Chen, Xiangguang; Teng, Miaomiao; Zhang, Jie; Qian, Le; Duan, Manman; Wang, Zhao; Wang, Chengju

doi:10.1016/j.ecoenv.2021.112615

Cited by 19 publications

(6 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have suggested that these proteins are involved in carbohydrate metabolism (pentose phosphate pathway, glycolysis/gluconeogenesis, ascorbate and aldarate metabolism, fructose and mannose metabolism, pyruvate metabolism, glyoxylate and dicarboxylate metabolism, citrate cycle) 31‐33 . Furthermore, carbohydrate metabolism is an important aspect of energy production 34 . The above results indicate that T‐2 toxin likely causes disorders in energy metabolism in shrimp by inducing the down‐regulation of target proteins involved in carbohydrate metabolism.…”

Section: Discussionmentioning

confidence: 75%

“…[31][32][33] Furthermore, carbohydrate metabolism is an important aspect of energy production. 34 The above results indicate that T-2 toxin likely causes disorders in energy metabolism in shrimp by inducing the down-regulation of target proteins involved in carbohydrate metabolism. This, in turn, decreases the sarcoplasmic protein content in shrimp muscle, leading to a deterioration in shrimp muscle Myofibrillar proteins regulate the contraction of muscle fibers, including myosin, actin, and tropomyosin.…”

Section: Discussionmentioning

confidence: 83%

See 1 more Smart Citation

Protective mechanisms of three antioxidants against T‐2 toxin‐induced muscle protein deterioration in shrimp

Huang

Sun

et al. 2022

J Sci Food Agric

View full text Add to dashboard Cite

BACKGROUND: Quercetin (Q), tea polyphenols (TP), and rutin (R) are widely used plant-derived active ingredients. They possess antioxidant, anti-inflammatory, and anti-tumor properties, and can reduce the muscle damage caused by mycotoxins. However, few studies have examined the protective mechanisms of quercetin, tea polyphenols, and rutin on muscle quality. To elucidate their protective mechanisms, shrimp were exposed to both T-2 toxin and these three antioxidants for 20 days in a doseescalating trial. The changes in the protein composition of shrimp muscle were measured. The target proteins associated with T-2 and antioxidants were screened and identified by non-labeled quantitative proteomics. RESULTS:The T-2 toxin induced abnormal expression of 21 target proteins, leading to the deterioration of muscle proteins in shrimp. The three antioxidants ameliorated the T-2 toxin-induced damage to muscle proteins by increasing the sarcoplasmic and myofibrillar protein content and decreasing the alkali-soluble protein content. Quercetin had the strongest protective effect. The protective processes of these antioxidants involved the upregulation of target proteins involved in carbohydrate metabolism (enolase, malate dehydrogenase), protein translation (elongation factor 1-alpha and eukaryotic translation initiation factor 2 subunit alpha), and cytoskeleton component (actin 2, fast-type skeletal muscle actin 1). Quercetin regulated the largest number of target proteins, making it the best protective agent against T-2 toxin. CONCLUSION:The T-2 toxin (4.80-24.30 mg/kg feed) induced changes in target proteins and muscle composition of shrimp, leading to a deterioration in muscle proteins. Quercetin (2.00-32.00 g/kg feed) had significant protective effects against this deterioration in muscle protein in shrimp.

show abstract

Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 83%

Protective mechanisms of three antioxidants against T‐2 toxin‐induced muscle protein deterioration in shrimp

Huang

Sun

et al. 2022

J Sci Food Agric

View full text Add to dashboard Cite

show abstract

“…Since then, several studies have evaluated mitochondrial dysfunction, mainly by analyzing mitochondrial oxygen consumption for mitochondrial toxicity, such as the work of Bourdineaud et al [115], evaluating environmental pollutants; the work of Geffroy et al [116] and Ladhar et al [117], evaluating nanoparticles, already entering the area of nanotoxicology; the work of Bestman et al [118], also evaluating an organic compound for the manufacture of pesticides; and Cowie et al stating mitochondrial dysfunction of zebrafish caused by the pesticide Dieldrina [119]. Other studies have also evaluated pesticides using mitochondrial dysfunction as a method of toxicological analysis [49,53,54,[120][121][122][123][124][125][126][127][128][129][130][131][132][133].…”

Section: Application Of Zebrafish In Mitochondrial Toxicology Analysismentioning

confidence: 99%

Application of Zebrafish in Mitochondrial Dysfunction

Cristina Pereira,

V.L. Peixoto,

Viriato

2024

Zebrafish Research - An Ever-Expanding Experimental Model

View full text Add to dashboard Cite

This chapter provides an overview of the zebrafish (Danio rerio) as a model organism for studies of mitochondrial dysfunction. Zebrafish possess a genetic similarity with humans and have conserved mitochondrial genomes, rendering them a valuable research tool for examining the intricate mechanisms that govern mitochondrial processes at diverse developmental stages. The chapter explores several methods for evaluating mitochondrial health and function. Examples include in vitro cell culture and in vivo analysis in embryos, larvae, and adults. The chapter discusses the use of zebrafish models in toxicological research to investigate mitochondrial reactions to environmental stressors and xenobiotics. The importance of implementing standardized protocols, validating marker, integrating different omics data, and using in vivo and in vitro approaches to advance mitochondrial research will be highlighted. In summary, zebrafish are suitable for analyzing both mitochondrial function and dysfunction, as well as their impact on human health.

show abstract

“…Chlorfenapyr is a new insecticide derived from natural pyrroles secreted by Streptomyces spp., known as halogenated pyrroles. As a proinsecticide, chlorfenapyr gets metabolized to its active form, tralopyril, which disrupts mitochondrial oxidative phosphorylation, leading to cell death . According to reports, chlorfenapyr degraded slowly in soil, sediment, and water, with an average half-life of 1.0 year, 1.1 years, and 0.8 years, respectively .…”

Section: Introductionmentioning

confidence: 99%

“…As a proinsecticide, chlorfenapyr gets metabolized to its active form, tralopyril, 16 which disrupts mitochondrial oxidative phosphorylation, leading to cell death. 17 According to reports, chlorfenapyr degraded slowly in soil, sediment, and water, with an average half-life of 1.0 year, 1.1 years, and 0.8 years, respectively. 18 A 2020 survey of 1146 samples of 20 types of fruits and vegetables in the Incheon area of South Korea revealed that chlorfenapyr was the most frequently detected pesticide, present in 1.1% of the samples with concentrations ranging from 0.116 to 1.452 mg/kg.…”

Section: Introductionmentioning

confidence: 99%

Multifaceted Effects of Subchronic Exposure to Chlorfenapyr in Mice: Implications from Serum Metabolomics, Hepatic Oxidative Stress, and Intestinal Homeostasis

Xiong,

Ma,

et al. 2024

J. Agric. Food Chem.

View full text Add to dashboard Cite

As chlorfenapyr is a commonly used insecticide in agriculture, the health risks of subchronic exposure to chlorfenapyr remained unclear. This study aimed to extensively probe the health risks from subchronic exposure to chlorfenapyr at the NOAEL and 10-fold NOAEL dose in mice. Through pathological and biochemical examinations, the body metabolism, hepatic toxicity, and intestinal homeostasis were systematically assessed. After 12 weeks, a 10-fold NOAEL dose of chlorfenapyr resulted in weight reduction, increased daily food intake, and blood lipid abnormalities. Concurrently, this dosage induced hepatotoxicity and amplified oxidative stress in hepatocytes, a finding further supported in HepG2 cells. Moreover, chlorfenapyr resulted in intestinal inflammation, evidenced by increased inflammatory factors (IL-17a, IL-10, IL-1β, IL-6, IL-22), disrupted immune cells (RORγt, Foxp3), and compromised intestinal barriers (ZO-1 and occludin). By contrast, the NOAEL dose presented less toxicity in most evaluations. Serum metabolomic analyses unveiled widespread disruptions in pathways related to hepatotoxicity and intestinal inflammation, including NF-κB signaling, Th cell differentiation, and bile acid metabolism. Microbiomic analysis showed an increase in Lactobacillus, a decrease in Muribaculaceae, and diminished anti-inflammatory microbes, which further propelled the inflammatory response and leaded to intestinal inflammation. These findings revealed the molecular mechanisms underlying chlorfenapyr-induced hepatotoxicity and intestinal inflammation, highlighting the significant role of the gut microbiota.

show abstract

Environmentally relevant concentrations of tralopyril affect carbohydrate metabolism and lipid metabolism of zebrafish (Danio rerio) by disrupting mitochondrial function

Cited by 19 publications

References 42 publications

Protective mechanisms of three antioxidants against T‐2 toxin‐induced muscle protein deterioration in shrimp

Protective mechanisms of three antioxidants against T‐2 toxin‐induced muscle protein deterioration in shrimp

Application of Zebrafish in Mitochondrial Dysfunction

Multifaceted Effects of Subchronic Exposure to Chlorfenapyr in Mice: Implications from Serum Metabolomics, Hepatic Oxidative Stress, and Intestinal Homeostasis

Contact Info

Product

Resources

About