Soybean β-conglycinin induces inflammation and oxidation and causes dysfunction of intestinal digestion and absorption in fish

PLoS One. 2013;8(3):e58115. doi: 10.1371/journal.pone.0058115. Epub 2013 Mar 8.

Abstract

β-Conglycinin has been identified as one of the major feed allergens. However, studies of β-conglycinin on fish are scarce. This study investigated the effects of β-conglycinin on the growth, digestive and absorptive ability, inflammatory response, oxidative status and gene expression of juvenile Jian carp (Cyprinus carpio var. Jian) in vivo and their enterocytes in vitro. The results indicated that the specific growth rate (SGR), feed intake, and feed efficiency were reduced by β-conglycinin. In addition, activities of trypsin, chymotrypsin, lipase, creatine kinase, Na(+),K(+)-ATPase and alkaline phosphatase in the intestine showed similar tendencies. The protein content of the hepatopancreas and intestines, and the weight and length of the intestines were all reduced by β-conglycinin. β-Conglycinin increased lipid and protein oxidation in the detected tissues and cells. However, β-conglycinin decreased superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx) and glutathione reductase (GR) activities and glutathione (GSH) content in the intestine and enterocytes. Similar antioxidant activity in the hepatopancreas was observed, except for GST. The expression of target of rapamycin (TOR) gene was reduced by β-conglycinin. Furthermore, mRNA levels of interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β) genes were increased by β-conglycinin. However, β-conglycinin increased CuZnSOD, MnSOD, CAT, and GPx1b gene expression. In conclusion, this study indicates that β-conglycinin induces inflammation and oxidation, and causes dysfunction of intestinal digestion and absorption in fish, and finally reduces fish growth. The results of this study provide some information to the mechanism of β-conglycinin-induced negative effects.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, Plant / adverse effects*
  • Antigens, Plant / chemistry
  • Antigens, Plant / pharmacology
  • Carps / metabolism*
  • Cytokines / metabolism
  • Fish Diseases / chemically induced*
  • Fish Diseases / metabolism
  • Fish Diseases / pathology
  • Globulins / adverse effects*
  • Globulins / chemistry
  • Globulins / pharmacology
  • Glutathione / metabolism
  • Glycine max / chemistry*
  • Inflammation / chemically induced
  • Inflammation / metabolism
  • Inflammation / pathology
  • Inflammation / veterinary
  • Intestinal Absorption / drug effects*
  • Intestinal Diseases / chemically induced*
  • Intestinal Diseases / metabolism
  • Intestinal Diseases / pathology
  • Intestinal Mucosa / metabolism*
  • Intestines / pathology
  • Liver / enzymology
  • Liver / pathology
  • Oxidation-Reduction / drug effects
  • Oxidoreductases / metabolism
  • Seed Storage Proteins / adverse effects*
  • Seed Storage Proteins / chemistry
  • Seed Storage Proteins / pharmacology
  • Soybean Proteins / adverse effects*
  • Soybean Proteins / chemistry
  • Soybean Proteins / pharmacology

Substances

  • Antigens, Plant
  • Cytokines
  • Globulins
  • Seed Storage Proteins
  • Soybean Proteins
  • beta-conglycinin protein, Glycine max
  • Oxidoreductases
  • Glutathione

Grants and funding

This study was financially supported by the National Science Foundation of China (3087192), National Department Public Benefit Research Foundation (Agriculture) of China (2010003020) and Project supported by the Program for New Century Excellent Talents in University of Ministry of Education of China (NCET-08-0905). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.