No abstract

An electrochemiluminescence (ECL) inhibition method combined with molecularly imprinted solid phase extraction (MISPE) was developed for quantitative determination of malachite green (MG) residues in fish. It was found that MG could strongly inhibit the ECL signal of luminol. Under the optimized conditions, the quenched ECL intensity versus the logarithm of the concentration of MG was in good linear relationship over a concentration range from 20 to 5000 ppt. The method detection limit was found to be about 6 ppt. Molecularly imprinted polymers (MIPs) were synthesized as solid phase extraction (SPE) sorbents, and MISPE was used for the selective extraction and purification of MG. By carrying out the oxidation reaction with 2,3-dichloro-5,6-dicyano-1,4-benzoquinone (DDQ), which could convert leucomalachite green (LMG) into MG, this method was successfully applied to determine MG residues in fish. A possible mechanism for the quenching effects of MG on luminol was also proposed.

The objective of this study was conducted to research the effects of β‐conglycinin in the diets on the growth performance, immunity function, antioxidant capacity and intestinal health of juvenile golden crucian carp (Carassius auratus). Five diets contained respectively (0, 20, 40, 60 and 80 g/kg) β‐conglycinin, and were used to feed juvenile golden crucian carp for 56 days. Final weight, weight gain and specific growth rate were significantly reduced by dietary β‐conglycinin (20–80 g/kg). Feed efficiency and protein efficiency were significantly reduced by dietary β‐conglycinin (40–80 g/kg). In hepatopancreas, the activities of T‐SOD, ACP, ALT and T‐AOC were significantly suppressed by dietary β‐conglycinin (20–80 g/kg). The activities of LZM, AKP, CAT and GPx were significantly reduced by dietary β‐conglycinin (40–80 g/kg). The activities of protease were significantly reduced and the content of MDA was significantly increased by dietary β‐conglycinin (60–80 g/kg). In proximal intestines, the activities of protease and CAT were significantly decreased by dietary β‐conglycinin (40–80 g/kg). In mid and distal intestines, the activities of protease and CAT were significantly inhibited by dietary β‐conglycinin (20–80 g/kg). In intestines, T‐AOC and GPx were significantly declined by dietary β‐conglycinin (20–80 g/kg). In proximal and mid intestines, the content of MDA were significantly increased by dietary β‐conglycinin (40–80 g/kg). In distal intestines, the content of MDA was significantly increased by dietary β‐conglycinin (20–80 g/kg). The expression of IGF‐I was significantly decreased and the expression of IL‐1β and TNF‐α was significantly increased by dietary β‐conglycinin (20–80 g/kg). The structural integrity of intestinal tissues were damaged by dietary β‐conglycinin (20–80 g/kg), the part of intestinal villus were shed, the part of epithelial cells were separated from lamina propria. Ultimately, these results suggested dietary β‐conglycinin should be <20 g/kg in formula feed of golden crucian carp.

No abstract

Pyroptosis, a type of programmed cell death that along with inflammation, is mainly regulated by two main pathways, cysteinyl aspartate specific proteinase (caspase)-1-induced canonical inflammatory pathway and caspase-11-induced non-canonical inflammatory pathway. The non-canonical inflammatory pathway-induced pyroptosis is a unique immune response in response to gram-negative (G − ) bacteria. It is induced by lipopolysaccharide (LPS) on the surface of G − bacteria. This activates caspase-11 which, in turn, activates a series of downstream proteins eventually forming protein pores on the cell membrane and inducing cell sacrificial processes. Caspase-11 belongs to the caspase family and is an homologous protein of caspase-1. It has the ability to specifically hydrolyze proteins, but it is still unclear how it regulates cell death caused by non-canonical inflammatory pathways. The present study describes a pathway that enables LPS to directly enter the cell and activate caspase-11, and the key role caspase-11 plays in the activation of pyroptosis and inflammation.