Glyphosate-induced lipid metabolism disorder contributes to hepatotoxicity in juvenile common carp

Liu, Jingbo; Dong, Chenyu; Zhai, Zhenzhen; Tang, Liang; Wang, Lin

doi:10.1016/j.envpol.2020.116186

Cited by 69 publications

(19 citation statements)

References 66 publications

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“…In hepatic tissues under exogenous CMN exposure, inflammatory cell infiltration (Figure 1A) can also be observed by other studies in aquatic and terrestrial animals exposed to xenobiotics. 36,37 Hepatic abnormalities with notable cytoplasmatic vacuolization were also observed by H&E staining and TEM observation, which could also be partially attributed to the dysregulation of "fat digestion and absorption" and "PPAR signaling pathway" (Figure 3A) pathways indicated by transcriptional profiles. 38 4.2.…”

Section: Discussionmentioning

confidence: 85%

ROS-Induced Hepatotoxicity under Cypermethrin: Involvement of the Crosstalk between Nrf2/Keap1 and NF-κB/iκB-α Pathways Regulated by Proteasome

Zhao

Wang

Liu

et al. 2021

Environ. Sci. Technol.

113

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Cypermethrin (CMN) is a man-made insecticide, and its abuse has led to potential adverse effects, particularly in sensitive populations such as aquatic organisms. The present study was focused on the toxic phenotype and detoxification mechanism in grass carp (Ctenopharyngodon idella) after treatment with waterborne CMN (0.651 μg/L) for 6 weeks in vivo or 6.392 μM for 24 h in vitro. In vivo, we describe the toxic phenotype of the liver of grass carp in terms of pathological changes, serum transaminase levels, oxidative stress indexes, and apoptosis rates. RNA-Seq analysis (2 × 3 cDNA libraries) suggested a compromise of proteasome and oxidative phosphorylation signaling pathways under CMN exposure. Thus, these two pathways were chosen for the in vitro study, which suggested that the CMN intoxicationinduced proteasome pathway caused hepatotoxicity in the liver cell line of grass carp (L8824 cells). Moreover, pretreatment with MG132, a proteasome inhibitor, displayed protection against the toxic effects of CMN by enhancing antioxidative and antiinflammatory capability by directly inhibiting the proteasomal degradation of nuclear factor erythroid-2 related factor (Nrf2) and IκB-α, thus turning on the transcription of downstream genes of Nrf2 and NF-κB, respectively. Taken together, these results suggest proteasome activity as a reason for CMN-induced hepatotoxicity.

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Section: Discussionmentioning

confidence: 85%

ROS-Induced Hepatotoxicity under Cypermethrin: Involvement of the Crosstalk between Nrf2/Keap1 and NF-κB/iκB-α Pathways Regulated by Proteasome

Zhao

Wang

Liu

et al. 2021

Environ. Sci. Technol.

113

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“…mL −1 caused an increase in ROS levels, although no other changes occurred in the remaining oxidative stress parameters analysed. This was probably due to the short exposure time, since recent studies, with longer exposure time to GBH and glyphosate at similar concentrations, and in different species, reported alterations of antioxidant enzymes’ action, secondary to high levels of ROS [ 32 , 87 , 88 , 89 ]. High levels of ROS are also associated with the induction of cell death [ 90 , 91 ] through the cellular damage caused by free radicals and the triggering of pro-apoptotic signals [ 92 ].…”

Section: Discussionmentioning

confidence: 99%

Inflammatory, Oxidative Stress, and Apoptosis Effects in Zebrafish Larvae after Rapid Exposure to a Commercial Glyphosate Formulation

et al. 2021

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Glyphosate-based herbicides (GBH) are the most used herbicides in the world, carrying potentially adverse consequences to the environment and non-target species due to their massive and inadequate use. This study aimed to evaluate the effects of acute exposure to a commercial formulation of glyphosate, Roundup® Flex (RF), at environmentally relevant and higher concentrations in zebrafish larvae through the assessment of the inflammatory, oxidative stress and cell death response. Transgenic Tg(mpxGFP)i114 and wild-type (WT) zebrafish larvae (72 h post-fertilisation) were exposed to 1, 5, and 10 µg mL−1 of RF (based on the active ingredient concentration) for 4 h 30 min. A concentration of 2.5 µg mL−1 CuSO4 was used as a positive control. Copper sulphate exposure showed effectiveness in enhancing the inflammatory profile by increasing the number of neutrophils, nitric oxide (NO) levels, reactive oxygen species (ROS), and cell death. None of the RF concentrations tested showed changes in the number of neutrophils and NO. However, the concentration of 10 µg a.i. mL−1 was able to induce an increase in ROS levels and cell death. The activity of antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)), the biotransformation activity, the levels of reduced (GSH) and oxidised (GSSG) glutathione, lipid peroxidation (LPO), lactate dehydrogenase (LDH), and acetylcholinesterase (AChE) were similar among groups. Overall, the evidence may suggest toxicological effects are dependent on the concentration of RF, although at concentrations that are not routinely detected in the environment. Additional studies are needed to better understand the underlying molecular mechanisms of this formulation.

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“…Going a step further, our result showed the two main dominant phyla altogether comprise above 80% of all the bacterial sequences at the end of the experiment, which agrees with previous studies of gut microbial profiles in birds ( 70 , 71 ). The balance of Firmicutes and Bacteroidetes is measured as a ratio, Firmicutes / Bacteroidetes (F/B), which is a predictive marker reflecting gut microbiota dysbiosis ( 72 , 73 ). Besides, the increment of the F/B ratio induced by the contraction of Bacteroidetes and/or expansion of Firmicutes is tightly associated with fat accumulation and potential for obesity both in humans and other animals ( 74 , 75 ).…”

Section: Discussionmentioning

confidence: 99%

Gut Microbiota and Serum Metabolite Potential Interactions in Growing Layer Hens Exposed to High-Ambient Temperature

et al. 2022

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Emerging evidence has revealed the dysbiosis of gut microbiota contributes to development of metabolic diseases in animals. However, the potential interaction between gut microbiota and host metabolism in growing hens under metabolic disorder induced by chronic heat exposure (CHE) remains inconclusive. The aim of our study was to examine the potential association among the cecal microbiota community, physiological indicators, and serum metabolite profiles in CHE hens. One hundred and eighty Hy-Line Brown hens were randomly allocated into three groups: thermoneutral control (TN), heat stress (HS), and pair-fed (PF). The experiment lasted for 5 weeks, with the first 2 weeks serving as the adaptation period. Results showed that the expression level of heat shock protein 70 (HSP70) in both serum and cecal tissues was significantly increased in the HS group. Serum parameters analysis also revealed that CHE caused physiological function damage and metabolic disorders. These results suggest the experiment was successful, inducing chronic heat stress. 16S rRNA sequencing analysis showed that the CHE can clearly induce dysbiosis of the gut microbial community reflected in the increment of the F/B ratio. Besides, serum untargeted metabolomics revealed the relative concentrations of 40 metabolites were significantly altered in the HS group compared with the TN group. Pathway analysis showed that these metabolites were mainly involving the increased proteolysis rather than lipolysis, and this tendency could be a specific metabolic adaptation of the poultry. The pair-feed experiment showed that the above changes induced by CHE were partly independent from the reduction of feed intake. Mantel correlation analysis between gut microorganisms and physiological indicators showed that the phylum Firmicutes and Euryarchaeota have a potential interaction with a serum lipid parameter. Random forest analysis showed that both genus Faecalibacterium and Methanobrevibacter were important predictors of the CHE-induced lipid metabolism disorder. Taken together, our findings may contribute to a better understanding of the metabolic mechanisms underlying the energy metabolism imbalance caused by the CHE and provide novel insights into the host-microbes interactions and its effects on the metabolic adaptation of hens under chronic heat exposure.

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Glyphosate-induced lipid metabolism disorder contributes to hepatotoxicity in juvenile common carp

Cited by 69 publications

References 66 publications

ROS-Induced Hepatotoxicity under Cypermethrin: Involvement of the Crosstalk between Nrf2/Keap1 and NF-κB/iκB-α Pathways Regulated by Proteasome

ROS-Induced Hepatotoxicity under Cypermethrin: Involvement of the Crosstalk between Nrf2/Keap1 and NF-κB/iκB-α Pathways Regulated by Proteasome

Inflammatory, Oxidative Stress, and Apoptosis Effects in Zebrafish Larvae after Rapid Exposure to a Commercial Glyphosate Formulation

Gut Microbiota and Serum Metabolite Potential Interactions in Growing Layer Hens Exposed to High-Ambient Temperature

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