Effects of Dietary Zearalenone on Oxidative Stress, Cell Apoptosis, and Tight Junction in the Intestine of Juvenile Grass Carp (Ctenopharyngodon idella)

Zearalenone (ZEA) is a prevalent mycotoxin with high toxicity in animals. In order to study its effect on juvenile grass carp (Ctenopharyngodon idella), six diets supplemented with different levels of ZEA (0, 535, 1041, 1548, 2002, and 2507 μg/kg diet) for 10 weeks were studied to assess its toxicity on intestinal structural integrity and potential mechanisms of action. Our report firstly proved that ZEA led to growth retardation and body deformity, and impaired the intestinal structural integrity of juvenile grass carp, as revealed by the following findings: (1) ZEA accumulated in the intestine and caused histopathological lesions; (2) ZEA resulted in oxidative injury, apoptosis, and breached tight junctions in the fish intestine, which were probably associated with Nuclear factor-erythroid 2-related factor 2 (Nrf2), p38 mitogen activated protein kinases (p38MAPK), and myosin light chain kinase (MLCK) signaling pathways, respectively. ZEA had no influence on the antioxidant gene levels of Kelch-like ECH associating protein 1 (Keap1)b (rather than Keap1a), glutathione-S-transferase (GST)P1, GSTP2 (not in the distal intestine (DI)), tight junctions occludin, claudin-c (not in the proximal intestine (PI)), or claudin-3c (not in the mid intestine (MI) or DI).

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Effects of Dietary Ochratoxin A on Growth Performance and Intestinal Apical Junctional Complex of Juvenile Grass Carp (Ctenopharyngodon idella)

Toxins ◽

10.3390/toxins13010011 ◽

2020 ◽

Vol 13 (1) ◽

pp. 11

Author(s):

Xin Liu ◽

Pei Wu ◽

Wei-Dan Jiang ◽

Yang Liu ◽

Jun Jiang ◽

...

Keyword(s):

Ochratoxin A ◽

Grass Carp ◽

Structural Integrity ◽

Fish Growth ◽

Ctenopharyngodon Idella ◽

Junctional Complex ◽

Distal Intestine ◽

Fish Intestine ◽

Apical Junctional Complex ◽

Proximal Intestine

Ochratoxin A (OTA) contamination widely occurs in various feed ingredients and food crops, potentially posing a serious health threat to animals. In this research, 1260 juvenile grass carp were separately fed with seven distinct experimental diets (0, 406, 795, 1209, 1612, 2003 and 2406 µg of OTA/kg of diet) for 60 consecutive days to evaluate OTA’s toxic effect on the intestinal apical junctional complex (including the tight junction (TJ) and the adherents junction (AJ)) and the underlying action mechanisms. Our experiment firstly confirmed that OTA caused fish growth retardation and disrupted the intestinal structural integrity. The detailed results show that OTA (1) depressed the feed efficiency, percentage weight gain and specific growth rate; (2) accumulated in the intestine; (3) caused oxidative damage and increased intestinal permeability; and (4) induced the RhoA/ROCK signaling pathway, destroying intestinal apical junctional complexes. Notably, OTA intervention did not result in changes in the gene expression of claudin-3c (in the proximal intestine (PI)), claudin-b and ZO-2b (in the mid intestine (MI) and distal intestine (DI)) in the fish intestine.

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Threonine deficiency decreased intestinal immunity and aggravated inflammation associated withNF-κBandtarget of rapamycinsignalling pathways in juvenile grass carp (Ctenopharyngodon idella) after infection withAeromonas hydrophila

British Journal Of Nutrition ◽

10.1017/s0007114517001830 ◽

2017 ◽

Vol 118 (2) ◽

pp. 92-108 ◽

Cited By ~ 37

Author(s):

Yu-Wen Dong ◽

Wei-Dan Jiang ◽

Yang Liu ◽

Pei Wu ◽

Jun Jiang ◽

...

Keyword(s):

G Protein ◽

Grass Carp ◽

Transforming Growth Factor ◽

Ctenopharyngodon Idella ◽

Mrna Levels ◽

Intestinal Immunity ◽

Distal Intestine ◽

Tnf Α ◽

Grass Carp Ctenopharyngodon Idella ◽

Proximal Intestine

AbstractThis study aimed to investigate the impacts of dietary threonine on intestinal immunity and inflammation in juvenile grass carp. Six iso-nitrogenous semi-purified diets containing graded levels of threonine (3·99–21·66 g threonine/kg) were formulated and fed to fishes for 8 weeks, and then challenged withAeromonas hydrophilafor 14 d. Results showed that, compared with optimum threonine supplementation, threonine deficiency (1) decreased the ability of fish against enteritis, intestinal lysozyme activities (except in the distal intestine), acid phosphatase activities, complement 3 (C3) and C4 contents and IgM contents (except in the proximal intestine (PI)), and it down-regulated the transcript abundances ofliver-expressed antimicrobial peptide(LEAP)-2A,LEAP-2B,hepcidin, IgZ, IgMandβ-defensin1(except in the PI) (P<0·05); (2) could up-regulate intestinal pro-inflammatory cytokinesTNF-α,IL-1β,IL-6, IL-8andIL-17DmRNA levels partly related toNF-κBsignalling; (3) could down-regulate intestinal anti-inflammatory cytokinetransforming growth factor(TGF)-β1,TGF-β2,IL-4/13A(notIL-4/13B) andIL-10mRNA levels partly by target of rapamycin signalling. Finally, on the basis of the specific growth rate, against the enteritis morbidity and IgM contents, the optimum threonine requirements were estimated to be 14·53 g threonine/kg diet (4·48 g threonine/100 g protein), 15.05 g threonine/kg diet (4·64 g threonine/100 g protein) and 15·17 g threonine/kg diet (4·68 g threonine/100 g protein), respectively.

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