High lipid diets (HLD) and high plant-protein diets (HPD) exhibit potential fishmeal-saving effects but negatively impact liver health and growth performance in fish. We hypothesized that HLD and HPD impair liver health in pearl gentian groupers (Epinephelus fuscoguttatus♂ × Epinephelus lanceolatus♀) through the modulation of intestinal microbiota and bile acid (BA) metabolism. Four diet groups were tested: control diet (CD, 46.21% crude protein, 9.48% crude lipid), HLD (46.37% crude protein, 16.70% crude lipid), HPD (46.50% crude protein, 9.38% crude lipid), and high lipid-high plant-protein diet (HLPD, 46.54% crude protein, 16.67% crude lipid). A total of 300 fish (average body weight = 15.22 ± 0.03 g) were randomly divided into 4 diet treatments (ensuring 3 tanks replicates of each diet treatment, each tank containing 25 fish). After an eight-week feeding period, the HLD and HPD significantly decreased the final body weight (FBW), weight gain rate (WGR), specific growth rate (SGR) and feed intake (FI) in comparison to CD group, with HLPD exacerbating these indicators (P < 0.05). Compared to CD group, the content of total cholesterol (T-CHO) and triglyceride (TG) in liver and serum were significantly increased in HLD group (P < 0.05). Compared to HPD group, the content of T-CHO in liver was significantly decreased, the content of TG in liver and serum were significantly increased in HLPD group (P < 0.05). HLD, HPD, and HLPD impaired liver health by inducing histological damage, inflammation, and oxidative stress. Compared to CD group, the mRNA relative expression of bile salt export pump (bsep) and multidrug resistance protein 3 (mdr3) were significantly increased in HLD group, whereas the mRNA relative expression of sterol-27-hydroxylase (cyp27a1), microsomal epoxide hydrolase (meh), apical sodium-dependent bile acid transporter (asbt), multidrug resistance-associated protein 3 (mrp3), farnesoid X receptor (fxr) and G protein-coupled bile acid receptor 5 (tgr5) were significantly decreased (P < 0.05). Compared to CD group, the mRNA relative expression of mdr3, asbt, mrp3, organic anion transporters 1 (oatp1), meh, fxr and tgr5 were significantly decreased in HPD group (P < 0.05). In summary, HLD affects intestinal microbiota, BA metabolism, and lipid metabolism, leading to lipid deposition and liver damage. HPD regulates gut microbiota, BA metabolism, inflammatory responses, and BA receptor expression, impairing grouper liver health. HLPD synergistically combines the adverse effects of HLD and HPD on grouper liver health.

Phaeocystis globosa blooms frequently in the Beibu Gulf of China. This species has a distinct life cycle that includes colonies and solitary cells. Colonies are formed during a bloom, while solitary cells are produced between blooms. Information about the abundance of solitary cells and other picophytoplankton in the northern Beibu Gulf is limited. To elucidate phytoplankton variation trends during periods of frequent P. globosa blooms and to determine the main physiochemical factors affecting phytoplankton distribution, four cruises were conducted between November 2018 and April 2019. Seawater was collected, and water temperature, salinity, and nutrient concentrations were simultaneously determined. Redundancy analysis was performed to understand the relationship between environmental factors and phytoplankton assemblages. Seven phytoplankton clusters were present during the cruises. Picophytoplankton abundance (including Synechococcus and Picoeukaryote groups I and II) dominated during the four cruises. Synechococcus abundance was restricted by the low temperatures in winter, decreasing from November to February and increasing in April. Picoeukaryote I abundance was almost unaffected by low temperatures and was mainly affected by nutrient concentration. P. globosa solitary cell abundance increased from November to January and decreased in February and April, and phosphorus was the key factor affecting P. globosa blooms. This is the first study to reveal the abundance and distribution of P. globosa solitary cells in this area.

Dunaliella salina is currently one of the most commercially valuable microalgae species in the world. In reponse to selenite, D. salina is a microalgae with a high selenium content, thereby increasing its value, which is crucial for increasing its economic value as a nutrional supplement. However, the effects of selenite on D. salina are still unclear, and its molecular mechanism of the response to selenite stress is also elusive. Here, in order to study the effects of selenite on D. salina and the corresponding regulatory mechanism, we characterized the physiological phenotypes of D. salina under different selenite concentrations and carried out a quantitative proteomic study. The results showed that the effective concentration for 50% growth inhibition (EC₅₀) of the algae was 192.7 mg/L after 11 days of cultivation. When selenite concentration was lower than 100 mg/L, selenite did not hinder the growth of D. salina in the early stage, but shortened the cell growth cycle, although cell growth was significantly inhibited when the concentration of selenium was higher than 250 mg/L. Bioaccumulation experiments showed that the content of intracellular selenium in D. salina cells reached the highest level under the treatment with 50 mg/L selenite, and the contents of total selenium and organic selenium in D. salina cells were 499.77 μg/g and 303.01 μg/g (dry weight), respectively. Proteomic analysis revealed that a series of proteins related to stress responses, amino acid metabolism and energy production pathways were profoundly altered by the selenite treatment. Glutathione peroxidase (GPX7), a selenium-containing protein, was identified in the group given the selenium treatment. Moreover, proteins involved in photoreactions and oxidative phosphorylation were significantly upregulated, indicating that D. salina effectively balanced the energy demand and energy production under selenite stress. This study provides novel insights into the responses to selenite of D. salina, a microalgae candidate as a biological carrier of selenium and would be helpful for the development of industrial strains rich in selenium.

Microcystin-LR (MC-LR), a prevalent and highly potent cyanobacterial toxin, is generated during the outbreaks of these blooms. Despite its prevalence, there is a scarcity of information regarding the chronic effects and underlying molecular mechanisms of MC-LR at environmentally relevant concentrations on muscular toxicity in fish. Hence, we assessed the muscular toxicity of chronic MC-LR exposure via histological and biochemical analyses and delved into the underpinning mechanisms via holistic multi-omics approaches of gut microbiome, serum metabolome, muscle transcriptome and metabolome in Nile tilapia. After 60 days of MC-LR exposure, 30 μg/L MC-LR exposure significantly triggered muscular toxicity, as illustrated by decreased nutrient value, reduced myofiber diameter and sarcomere length, and diffuse dissolution of myofibrils. Transcriptomic and metabolomic analyses of muscle revealed that MC-LR exposure altered antioxidant status, protein turnover, amino acid metabolism, nucleotide synthesis and breakdown, and lipid metabolism regulation, leading to oxidative stress, inflammation response, apoptosis, decreased protein deposition and inhibited myofiber growth of Nile tilapia. Furthermore, MC-LR exposure perturbed the intestinal microbiota composition and compromised the integrity of the intestinal barrier, resulting in increased toxicity-related metabolites such as lipopolysaccharide (LPS), phenol and phenylacetic acid entering the muscle through the bloodstream, promoting muscle injury. These results provided new insight into the underlying biomolecular mechanisms and potential roles of the gut-muscle axis in MC-LR-induced muscular toxicity in aquatic animals.