Effects of Dietary Glycinin on Oxidative Damage, Apoptosis and Tight Junction in the Intestine of Juvenile Hybrid Yellow Catfish, Pelteobagrus fulvidraco ♀ × Pelteobaggrus vachelli ♂.

The objective of this study was to examine the influences of glycinin for growth and intestinal structural integrity related to oxidative damage, apoptosis and tight junction of juvenile hybrid yellow catfish (Pelteobagrus fulvidraco ♀ × Pelteobaggrus vachelli ♂). Fish (initial weight, 1.02 ± 0.01 g) were fed diets containing five different levels of glycinin at 0%, 2%, 4%, 6%, and 8% for 8 weeks. The results demonstrated that dietary glycinin levels had a negative correlation with final weight, feed intake, protein efficiency ratio and survival rate of the experiment fish. When the level of dietary glycinin exceeded 4%, the structural integrity of the posterior intestine was observably impaired, characterized by disordered and exfoliated margin of intestinal villi, blurred and broken boundaries of tight junctions, damaged organelles and cell vacuolation. Levels of 4-8% dietary glycinin depressed the total antioxidant capacity and total superoxide dismutase activities of posterior intestine. Furthermore, a high level of dietary glycinin linearly and quadratically down-regulated the mRNA expressions of Claudin-1, Occludin and ZO-1, while it linearly and significantly up-regulated the mRNA expressions of Bax, Cyt C, Caspase 3, Caspase 9 and p53 in the posterior intestine. In conclusion, dietary 4-8% glycinin impaired the morphological structure of the posterior intestine by inducing oxidative stress and cell apoptosis, and eventually impeded the growth performance of juvenile hybrid yellow catfish.

Selenium attenuated food borne cadmium-induced intestinal inflammation in red swamp crayfish (Procambarus clarkii) via regulating PI3K/Akt/NF-κB pathway.

Selenium (Se), an indispensable micronutrient for living organisms, has been extensively studied for its heavy metal-detoxifying properties in diverse biological systems and tissues. Nevertheless, it is not entirely certain whether Se can effectively protect against Cadmium (Cd)-induced gut inflammation, especially in aquatic animals. In this study, we employed various approaches, including transcriptome profiling, histological examinations, assessment of antioxidant enzyme activities, and analysis of gut microbiota composition to investigate the effects on crayfish growth and intestinal health after exposure to dietary Cd (15 mg kg-1 diet) and Se (15 mg kg-1 diet) individually or in combination for 8 weeks. The results revealed that dietary Cd exposure resulted in reduced body weight and survival rates, along with an increased occurrence of intestinal inflammation. Nevertheless, Se supplementation proved effective in mitigating the adverse effects of Cd on growth and gut health. Se exhibited a remarkable ability to counteract the disruption of gut antioxidant abilities induced by dietary Cd, as evidenced by the observed increases in ROS and MDA contents, decrease in GSH levels, and inhibition of antioxidative enzyme activities. At the concentration of 6 mg kg-1 in the diet, Se was found beneficial for maintaining gut microbiota richness and diversity. Among them, Flavobacterium, Thermomonas, and Chloronema displayed a weak negative correlation with the rate of gut inflammation. Meanwhile, the levels of short chain fatty acids (SCFAs), including acetic acid (AA) and butanoic acid (BA), showed a significant increase in the Se-Cd group compared to the Cd-only group. Furthermore, transcriptome analysis exhibited significant responses of the PI3K/Akt and NF-κB pathways following crayfish exposure to dietary Se and Cd, either separately or in combination. In short, this study provides a new evidence regarding the molecular mechanisms through which Se could regulate the PI3K/Akt and NF-κB pathways, either directly or indirectly via ROS and SCFAs, thereby alleviating Cd-induced gut inflammation in crayfish.