Abstract
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).
Highlights
Mycotoxins are defined as natural secondary metabolites found in a number of crops, including aflatoxin, zearalenone (ZEA), deoxynivalenol (DON), ochratoxin A (OTA), and T-2 toxin [1,2,3]
The ZEA ≥ 1041 μg/kg diet depressed the percentage of weight gain (PWG), specific growth rate (SGR), final body weight (FBW), feed intake (FI), feed efficiency (FE), intestinal length (IL), intestinal length index (ILI), intestinal weight (IW), and intestinal somatic index (ISI)
Our study showed that diets with a ZEA content ≥ 1041 μg/kg caused body malformation, such as body line irregularities, upward curvature of the tail, caudal fin deformity, operculum abnormality, and skeletal anomalies in juvenile grass carp
Summary
Mycotoxins are defined as natural secondary metabolites found in a number of crops, including aflatoxin, zearalenone (ZEA), deoxynivalenol (DON), ochratoxin A (OTA), and T-2 toxin [1,2,3]. Studies of the toxic effects of mycotoxins on fish have primarily been focused on growth inhibition and liver injury [4,5]. Reports of the toxic influence of mycotoxins on fish intestinal structure are scarce, and the following restrictions still remain: (1). Except for the previous study on DON from our lab [7], most other studies have only investigated the apparent morphology [8]; (2) The toxic effect on the intestine is different among various mycotoxins. In rainbow trout (Oncorhynchus mykiss), T-2 toxin-induced intestinal lesions (such as intestinal hemorrhage) occurred [9], whereas DON had no effect on the intestinal structure [10]. It is essential to systematically study the influence of other mycotoxins on fish intestinal structure and investigate their mechanisms of toxicity in depth
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