Effects of Fishmeal Substitution with Mealworm Meals (Tenebrio molitor and Alphitobius diaperinus) on the Growth, Physiobiochemical Response, Digesta Microbiome, and Immune Genes Expression of Atlantic Salmon (Salmo salar).

A 12-week growth trial was conducted to assess the effects of mealworm meals, as a substitution for fishmeal, on the growth, physiobiochemical responses, digesta microbiome, and immune-related genes expression of Atlantic salmon (Salmo salar). Twenty Atlantic salmon parr (38.5 ± 0.1 g, initial weight) were stocked into each of 16 tanks in a recirculating aquaculture system. A fishmeal-based diet (100% FM) was used as the control treatment and was compared with three test diets where: (1) fishmeal was partially (50%) replaced with defatted mealworm meal, Tenebrio molitor (50% DMM), (2) fishmeal was fully replaced with defatted mealworm meal (100% DMM), and (3) fishmeal was partially replaced with whole lesser mealworm meal, Alphitobius diaperinus (50% WMM). All substitutions were done on a crude protein basis. Each of the four experimental diets was evaluated in quadruplicate tanks as part of randomized design. The results indicated that Atlantic salmon showed high survival (greater or equal to 98.8%), and no significant difference in final growth, feed efficiency, feces stability and condition indices. Hepatosomatic index was lower in fish fed 100% DMM and 50% WMM when compared to fish fed the control diet (100% FM). Whole-body proximate and amino acid compositions were not statistically different between treatments, while essential fatty acids, including linolenic, eicosapentaenoic acid, and homo-a-linolenic, were lower in fish fed 100% DMM. Plasma parameters (total protein, alanine aminotransferase, alkaline phosphatase, and total iron-binding capacity), hepatic peroxide, and antioxidant enzymes were not significantly affected by dietary substitutions, whereas plasma immunoglobulin M showed significantly higher levels in fish fed 50% DMM and 100% DMM when compared to fish fed the control diet (100% FM). The inclusion of mealworm meals significantly impacted the overall microbiome composition but not the richness and evenness of the salmon digesta microbiomes compared to control. The most common genus in all treatments was Pseudomonas, which has been previously shown to have both commensal and pathogenic members. The relative expressions of growth (IGF-I) and protein synthesis (TIPRL) were not significantly different between the treatments, whereas immunoglobulin genes (IgM, IgD, and IgT) were significantly upregulated in fish fed the DMM diets when compared to fish fed the control diet. Overall, this study suggests that the mealworm meals tested could be suitable alternatives to fishmeal in the diet of Atlantic salmon.

The effects of fish meal substitution by clam meal on the growth and health of Florida pompano (Trachinotus carolinus).

A 12-week feeding trial was conducted to evaluate the effects of fish meal (FM) substitution by clam meal (CM, at 10%, 20% and 30% of the diet) on the growth, feed utilization, hepatic antioxidant enzymes, plasma parameters, fatty acid and amino acid composition, and gut microbiome of juvenile Florida pompano, Trachinotus carolinus. The results indicated that: (1) juveniles fed 10% and 20% CM had a significantly higher final weight than the group fed the control (0% CM); and the control group also showed significantly lower weight gain, feed intake, protein retention value, whole-body crude protein and total amino acids composition, but higher hepatosomatic index and whole-body crude fat; (2) hepatic peroxide content and superoxide dismutase activity were not significantly affected by the substitution of CM, but it did affect glutathione peroxidase activity, with higher levels found in fish fed 30% CM compared to 0% and 10% CM; (3) plasma total protein, alkaline phosphatase, alanine aminotransferase, and immunoglobulin M showed no significant differences among the treatments; (4) there were no significant differences among treatments in terms of fatty acids composition and microbial diversity. Overall, this study concluded that CM has comparable benefit in the diet of Florida pompano as FM does.

The effect of emodin on cytotoxicity, apoptosis and antioxidant capacity in the hepatic cells of grass carp (Ctenopharyngodon idellus).

We determined the effect of emodin on the lactate dehydrogenase (LDH) release, superoxide dismutase (SOD), glutathione (GSH), total antioxidant capacity (T-AOC), reactive oxygen species (ROS), mitochondria membrane potential (ΔΨm), and apoptosis in the hepatic cells of grass carp (Ctenopharyngodon idellus). Cultured cells were treated with different concentrations of emodin (0.04-25 µg/ml) for 24 h. We found that the cytotoxic effect of emodin was mediated by apoptosis, and that this apoptosis occurred in a dose-dependent manner. Emodin (1-25 µg/ml) significantly induced apoptosis accompanying by ΔΨm disruption and ROS generation and significantly reduced the SOD activities and T-AOC compared to the control. Thus, the oxidative effect of emodin may be attributed to the loss of the cell's ability to maintain the activity of its radical-scavenging enzymes. GSH was also significantly higher after 0.2-1 µg/ml emodin exposure, indicating that cells failed to maintain their redox balance when compensating for the increased oxidative stress. Our results suggest that emodin (1-25 µg/ml) exerts its cytotoxic effects via apoptosis by directly affecting the mitochondria.

Effect of heat stress and recovery on viability, oxidative damage, and heat shock protein expression in hepatic cells of grass carp (Ctenopharyngodon idellus).

In this study, we investigated the effects of hyperthermia and recovery on cell viability, lactate dehydrogenase (LDH) activity, superoxide dismutase (SOD) activity, malondialdehyde (MDA), total antioxidant capacity (T-AOC), and heat shock protein (HSP60, 70, and 90) mRNA expression in the hepatic cells of the grass carp, Ctenopharyngodon idellus. Triplicate groups of cultured cells were exposed to 30, 32, or 34 °C for 0.5 h and then immediately incubated at 27 °C in 5 % CO2 for 6, 12, 24, or 48 h. Hyperthermia stress greatly reduced cell viability and increased LDH release. Cell damage declined after recovery. Hyperthermia stress increased the lipid peroxide levels and reduced the antioxidant capacity (e.g., reduced SOD and T-AOC) of the cells. However, oxidative damage declined as the recovery period increased, and the levels of MDA, SOD, and T-AOC were restored. After cells were exposed to 32 °C, the expression of HSP60 after recovery for 1, 2, and 4 h (P < 0.05), the expression of HSP70 after recovery for 0.5 and 1 h (P < 0.01), and the expression of HSP90 throughout recovery were significantly higher (P < 0.01) than the prestress levels. During the recovery period, the variations in HSP gene expression reflected the transition period from a state of cellular growth to one of the cellular repairs. In conclusion, hyperthermia depresses cell viability, induces oxidative damage, and increases HSP expression, which plays an important role during hyperthermic stress in grass carp hepatic cells.