Microplastics are emergent contaminants threatening aquatic organisms including aquacultured fish. This study investigated the effects of high-density polyethylene (HDPE, 100 to 125 μm) on yellow perch (Perca flavescens) based on integrative evaluation including growth performance, nutritional status, nutrient metabolism, fish health, and gut microbial community. Five test diets (0, 1, 2, 4, or 8 g HDPE/100 g diet) containing 41% protein and 10.5% lipid were fed to juvenile perch (average body weight, 25.9 ± 0.2 g; n = 15) at a feeding rate of 1.5% to 2.0% body weight daily. The feeding trial was conducted in a flow-through water system for 9 wk with 3 tanks per treatment and 15 yellow perch per tank. No mortality or HDPE accumulation in the fish was found in any treatments. Weight gain and condition factor of fish were not significantly impacted by HDPE (P > 0.05). Compared to the control group, fish fed the 8% HDPE diet had significantly decreased levels of protein and ash (P < 0.05). In response to the increasing levels of HDPE exposure, the hepatosomatic index value, hepatocyte size, and liver glycogen level were increased, but lipid content was reduced in the liver tissues. Compared to the control treatment, fish fed the 8% HDPE diet had significant accumulations of total bile acids and different metabolism pathways such as bile acid biosynthesis, pyruvate metabolism, and carnitine synthesis. Significant enterocyte necrosis was documented in the foregut of fish fed the 2% or 8% HDPE diet; and significant cell sloughing was observed in the midgut and hindgut of fish fed the 8% HDPE diet. Fish fed the 2% HDPE diet harbored different microbiota communities compared to the control fish. This study demonstrates that HDPE ranging from 100 to 125 μm in feed can be evacuated by yellow perch with no impact on growth. However, dietary exposure to HDPE decreased whole fish nutrition quality, altered nutrient metabolism and the intestinal histopathology as well as microbiota community of yellow perch. The results indicate that extended exposure may pose a risk to fish health and jeopardize the nutrition quality of aquacultured end product. This hypothesis remains to be investigated further.

This study determined whether accumulated liver and visceral lipid in yellow perch can be alleviated by feeding an appropriate starch source. We compared the growth performance, nutritional composition and health of yellow perch fed a control diet (no added starch) and three diets with corn, potato or wheat starch (200 g/kg diet) to replace an equal proportion of fishmeal in the control diet. Dietary starch led to increased bulk density, hardness and gelatinization levels of feed pellets compared with the control diet. At the end of an 8‐week feeding, all fish fed the test diets had similar growth rates (p > .05). However, the wheat starch diet resulted in significantly enlarged livers and increased accumulation of lipid in the liver, viscera and whole body (p < .05). This diet also caused significantly higher levels of fasting glucose, aspartate aminotransferase and alkaline phosphatase activities in serum than the control diet. Liver cell diameters were larger, and Kupffer cell numbers were lower in the fish fed the wheat starch than those fed the control diet. Potato or corn starch had less impact on fish health and is considered to be an appropriate carbohydrate sources for yellow perch under the current testing conditions.

Two growth trials were conducted to determine the effect of feeding rate on the responses of a heat‐shock protein (hsp70) in the fry of Green Sturgeon Acipenser medirostris. Four tanks were randomly assigned to each feeding treatment: 2.5, 5.0, 7.5, 10.0, 12.5 and 15.0% of body weight/d in trial I and 2.0, 3.0, 4.0, 5.0, 6.0 and 7.0% of body weight/d for trial II. The fry were raised indoor at 18°C and fed a commercial salmonid soft‐moist diet. Densities were 50 fry/tank in trial I fed for 49 d posthatch (dph) and 30 fry/tank in trial II fed for 70 dph. At the end of 1 week of feeding, five fish from each tank were subjected to heat shock by increasing the water temperature from 18°C to 28°C at a rate of 4°C/h and then holding at 28°C thereafter for 4 h before tissue samples were collected. Heat shock induced significant changes in the levels of hsp70 in the liver and white muscle of fish in all feeding treatments. However, feeding rate treatments had no significant effect on the basal and heat‐shocked levels of hsp70 in the liver of these fish. The lowest feeding rate significantly depressed the induced level of hsp70 in the muscle of Green Sturgeon. A feeding rate of 10.0% of body weight/d is suggested for Green Sturgeon at 49 dph and 6.0% at 70 dph, based on their maximum responses of hsp70 in white muscle tissue. This study indicates that the response of hsp70 in the liver and muscle of Green Sturgeon is sensitive to heat‐shock stress. The effect of different feeding rates on the response of hsp70 is also tissue‐dependent. This variation should be considered when hsp70 is used as a biomarker to evaluate heat‐shock response.