Hepatic Antioxidant Enzyme Activities Research Articles

Effects of Replacing Fish Meal with Rubber Seed Cake on Growth, Digestive, Antioxidant and Protein Metabolism of Juvenile Asian Red-Tailed Catfish (Hemibagrus wyckioides)

An 8-week feeding trial was conducted to assess the impact of replacing fish meal (FM) with rubber seed cake (RSC) on growth performance, digestive enzyme activity of the gut, antioxidant capacity and protein metabolism-related parameters of plasma and liver in juvenile Asian red-tailed catfish (Hemibagrus wyckioides) with an average body weight of 3.21 g. Four isonitrogenous (41.08 ± 0.17) and isolipidic (10.07 ± 0.11) diets were formulated, incorporating RSC at a level of 0%, 15%, 30%, and 45% (w/w) to progressively replace FM. Dietary inclusion of 15–30% RSC did not significantly affect growth performance (p > 0.05). However, the replacement of FM with RSC resulted in linear reductions in intestinal trypsin and amylase activities, with a significant reduction in intestinal amylase activity observed at the 45% RSC inclusion level. Dietary inclusion of 30–45% RSC decreased plasma glutamate dehydrogenase and aspartate aminotransferase activities, but increased plasma adenosine monophosphate deaminase and hepatic γ-glutamyltransferase activities. This may indicate that the high substitution of FM by RSC may affect the homeostasis of amino acid metabolism. Dietary inclusion of 15% RSC did not affect serum and hepatic antioxidant enzyme activities; however, dietary inclusion of 45% RSC significantly increased plasma malondialdehyde level, but decreased catalase activity. Furthermore, dietary inclusion of 30–45% RSC significantly increased hepatic lactate dehydrogenase activity. These results demonstrated that replacing a portion of FM with RSC is feasible, and dietary inclusion of 15% RSC did not have significant adverse effects on growth performance, digestive function and antioxidant capacity of H. wyckioides.

Nutritional Composition and Effect of Loquat Fruit (Eriobotrya japonica L. var. Navela) on Lipid Metabolism and Liver Steatosis in High-Fat High-Sucrose Diet-Fed Mice.

Loquat (Eriobotrya japonica L.) is a popular fruit known for its sweet and slightly tangy flavor, which is widely consumed both fresh and in various processed forms. This study aimed to analyze the biochemical composition of loquat juice and investigate its metabolic benefits in mice fed a high-fat/high-sucrose diet (HFSD). Mice were fed either a standard diet or an HFSD and received or not the loquat juice at 4 or 8 mL/kg body weight for 8 weeks. Body weight, food efficiency ratio, plasma lipoprotein profile, plasma glucose, and lipid indices were monitored throughout the experiment. At the end of the experiment, additional assessments were performed, including lipid content measurements in liver, adipose tissue, bile, and feces; hepatic antioxidant enzyme activities (superoxide dismutase and catalase); hepatic malondialdehyde content; plasma biomarkers of liver injury; liver histology; and organ relative weight. Feeding mice with the HFSD resulted in a significant perturbation in lipid and glucose metabolism, obesity, liver steatosis, and oxidative stress-related enzymes. However, the concomitant administration of loquat juice significantly corrected this imbalance. Fresh loquat juice is low in fat and protein, moderately sugary, and energetically light; however, it is rich in minerals, vitamin C, and various phytochemicals compounds, such as phenolic acids, flavonoids, and carotenoids. The loquat juice could be considered a functional food and could be valorized through the extraction of active substances and their use as food supplements to prevent lipid metabolism disorders and the resulting health complications.

Phlorotannin Alleviates Liver Injury by Regulating Redox Balance, Apoptosis, and Ferroptosis of Broilers under Heat Stress.

Heat stress (HS) poses a great challenge to the poultry industry by inducing oxidative damage to the liver, endangering the health and production of broilers. As an important type of seaweed polyphenols, phlorotannin has been shown to have antioxidant properties. The present study evaluated the protective effects of dietary phlorotannin on HS-induced liver injury in broilers based on oxidative damage parameters. A total of 108 twenty-one days old male Arbor Acres plus (AA+) broilers were randomly divided into three groups: TN group (thermoneutral, 24 ± 1 °C, fed with basal diet), HS group (HS, 33 ± 1 °C for 8 h/day, fed with basal diet), and HS + phlorotannin group (HS + 600 mg/kg phlorotannin). Each group has six replicate cages with six birds per cage. The feeding experiment lasted 21 days. At the termination of the feeding experiment (42 days old), samples were collected for analysis of morphological and biochemical features. The results showed that HS decreased the liver index, serum albumin (ALB) content, hepatic antioxidant enzymes activities of catalase (CAT), total superoxide dismutase (T-SOD), glutathione S-transferase (GST), and glutathione peroxidase (GSH-Px) (p < 0.05), while increasing the hepatic histopathology score, apoptosis rate, and malondialdehyde (MDA) content (p < 0.05) in 42-day-old broilers. Compared with the HS group, dietary phlorotannin improved the activities of antioxidant enzymes (GST and GSH-Px) but decreased the histopathology score and apoptosis rate in the liver (p < 0.05). Moreover, HS down-regulated hepatic mRNA expression of CAT1, NQO1, HO-1, and SLC7A11 (p < 0.05), while up-regulated hepatic mRNA expression of Keap1, MafG, IκBα, NF-κB P65, IFN-γ, TFR1, ACSL4, Bax, and Caspase-9 (p < 0.05). Compared with HS group, dietary phlorotannin up-regulated hepatic mRNA expression of Nrf2, CAT1, MafF, GSTT1, NQO1, HO-1, GCLC, GPX1, TNF-α, Fpn1, and SLC7A11 (p < 0.05), while down-regulated hepatic mRNA expression of IκBα, Bax, Caspase-9, and TFR1 (p < 0.05). In conclusion, dietary supplementation of 600 mg/kg phlorotannin could alleviate HS-induced liver injury via regulating oxidative status, apoptosis, and ferroptosis in broilers; these roles of phlorotannin might be associated with the regulation of the Nrf2 signaling pathway.

Ethanol Extract of Propolis Attenuates Liver Lipid Metabolism Disorder in High-Fat Diet-Fed SAMP8 Mice.

The prevalence of high-fat diet (HFD) consumption is increasing among middle-aged and older adults, which accelerates the aging process of this population and is more likely to induce lipid metabolism disorders. But the alleviation of ethanolic extract of propolis (EEP) on lipid metabolism disorders during aging remains unclear. This study assesseed the impact of EEP intervention (200 mgkg-1bw) on aging and lipid metabolism disorders in HFD-fed senescence accelerate mouse prone 8 (SAMP8) mice. Findings indicate that EEP ameliorates hair luster degradation and weight gain, reduces systemic inflammation and metabolism levels, enhances hepatic antioxidant enzyme activities, and improves the hepatic expression of senescence-associated secretory phenotype and aging-related genes in HFD-fed SAMP8 mice. Histological staining demonstrates that EEP improves hepatic lipid deposition and inflammatory cell infiltration. Transcriptomic and lipidomic analysis reveal that EEP promotes fatty acid β-oxidation by activating PPAR pathway, resulting in reduced hepatic lipid deposition, and attenuates bile acid (BA) accumulation by improving BA metabolism, which were ensured through qPCR validation of key genes and immunoblot validation of key proteins. CONCLUSIONS: EEP can regulate lipid metabolic dysregulation during aging accompanied by an HFD, potentially delaying the onset and progression of age-related diseases. This provides new approach for supporting healthy aging.

Prefeeding of berberine alleviates waterborne copper-induced hepatic oxidative stress, lipid deposition, and intestinal microbiota dysbiosis in yellow catfish (Pelteobagrus fulvidraco)

Copper (Cu) contamination is a common issue in aquaculture and normally leads to hepatic and intestinal damage in fish. Due to the effective lipid-lowering, antioxidative, and intestinal microbiota-maintaining properties of berberine (BBR), it has the potential to be a feed additive to diminish Cu toxicity in fish. This study aimed to determine whether berberine could alleviate hepatic and intestinal damage in yellow catfish (Pelteobagrus fulvidraco) caused by waterborne Cu2+ exposure. The fish with the same weight (2.65 ± 0.25 g) were assigned to four groups: a control group (Con) that received a control diet for nine weeks; a Cu group, a BBR100 group, and a BBR400 group that received the control diet, 100 mg/kg berberine, and 400 mg/kg berberine for eight weeks, respectively, and after that, they were exposed to 0.8 mg/L Cu2+ for an additional week. The BBR100 and BBR 400 groups had significantly higher weight gain than the Cu group, but significantly lower hepatic and serum total cholesterol and triglyceride levels, and berberine treatment significantly improved intestinal and hepatic histological damage (P < 0.05). Berberine treatment significantly increased intestinal complement 3 and complement 4 levels but distinctly regulated hepatic and intestinal antioxidant enzyme activities while significantly reducing malondialdehyde levels compared to those in the Cu group. In addition, pretreatment with berberine significantly increased the expression levels of intestinal farnesoid X receptor (fxr) and fibroblast growth factor 19, as well as hepatic fxr, and downregulated the expression of its downstream lipogenesis genes (srebp1c, fas, and pparγ). Based on 16S rDNA analysis, the abundances of some probiotic bacteria (e.g., Lactobacillus) were elevated, but the abundances of some pathogenic bacteria (e.g., Morganella) decreased in the BBR400 group. At KEGG level 3, the pathway related to “Pathogenic Escherichia coli infection” was significantly enriched in the Cu group but significantly lower enriched in the BBR100 group. These findings indicated that berberine alleviated waterborne copper-induced hepatic and intestinal damage mainly by activating the FXR pathway, reducing oxidative stress and lipid deposition, and maintaining intestinal microbiota homeostasis in yellow catfish.

Lotus seed protein ameliorates hepatic lipid metabolic disorders in high-fat diet-fed mice via activating the PPARα signaling pathway

Obesity, one of the prevalent chronic diseases globally, is a serious threat to human health. Dietary natural compounds intervention is an effective means to alleviate obesity. The objective of this study was to investigate the potential protective role of lotus seed protein (LSP) against obesity. The results of amino acid composition analysis indicated that LSP possessed a well-balanced distribution of amino acids and was rich in branched-chain amino acids (BCAAs). Meanwhile, LSP exhibited better ABTS radical scavenging, DPPH radical scavenging, hydroxyl radical scavenging, and Fe2+ chelating ability in vitro. In vivo, LSP intervention remarkably alleviated body weight gain, organ index gain, dyslipidemia, and hepatic lipid deposition in high-fat diet (HFD)-fed mice. Meanwhile, LSP enhanced hepatic antioxidant enzyme activities (superoxide dismutase (SOD) and catalase (CAT)) and decreased malondialdehyde (MDA) levels, subsequently alleviated liver injury. In addition, LSP intervention significantly improved insulin sensitivity and glucose tolerance in obese mice, thereby alleviating hyperglycemia and insulin resistance. At the molecular level, LSP intervention up-regulated the mRNA and protein expression of fatty acid oxidation-related genes (FATP1, CPT-1a, ACOX1) and down-regulated the mRNA and protein expression of lipid synthesis-related genes (SREBP-1c, ACC, SCD-1, FASN) by activating the PPARα signaling pathway, thereby promoting hepatic fatty acid oxidation and reducing lipogenesis. These results demonstrate that LSP has the potential as a dietary supplementation to prevent and ameliorate obesity.

Integrated biomarker-based ecological risks assessment of tadpole responses to tris(2-chloroethyl) phosphate, tris(1-chloro-2-propyl) phosphate, and their combined environmental exposure

Tris(2-chloroethyl) phosphate (TCEP) and tris(1-chloro-2-propyl) phosphate (TCPP) are common chlorinated organophosphorus flame retardants (OPFRs) used in industry. They have been frequently detected together in aquatic environments and associated with various hazardous effects. However, the ecological risks of prolonged exposure to these OPFRs at environmentally relevant concentrations in non-model aquatic organisms remain unexplored. This study investigated the effects of long-term exposure (up to 25 days) to TCEP and TCPP on metamorphosis, hepatic antioxidants, and endocrine function in Polypedates megacephalus tadpoles. Exposure concentrations were set at 3, 30, and 90 μg/L for each substance, conducted independently and in equal-concentration combinations, with a control group included for comparison. The integrated biomarker response (IBR) method developed an optimal linear model for predicting the overall ecological risks of TCEP and TCPP to tadpoles in potential distribution areas of Polypedates species. Results showed that: (1) Exposure to environmentally relevant concentrations of TCEP and TCPP elicited variable adverse effects on tadpole metamorphosis time, hepatic antioxidant enzyme activity and related gene expression, and endocrine-related gene expression, with their combined exposure exacerbating these effects. (2) The IBR value of TCEP was consistently greater than that of TCPP at each concentration, with an additive effect observed under their combined exposure. (3) The ecological risk of tadpoles exposed to the combined presence of TCEP and TCPP was highest in China's Taihu Lake and Vietnam's Hanoi than in other distribution locations. In summary, prolonged exposure to environmentally relevant concentrations of TCEP and TCPP presents potential ecological risks to amphibian tadpoles, offering insights for the development of policies and strategies to control TCEP and TCPP pollution in aquatic ecosystems. Furthermore, the methodology employed in establishing the IBR prediction model provides a methodological framework for assessing the overall ecological risks of multiple OPFRs.

Fermented agar by-product and sunflower cake mixture as feedstuff for European seabass (Dicentrarchus labrax)

Industrial agar production from red seaweeds such as Gelidium sp. generates large quantities of by-products (GBP), often discarded as waste. GBP and sunflower cake (SC) are under-valorized as feedstuff due to their high non-starch polysaccharide (NSP) content. Solid-state fermentation (SSF) may disrupt NSP and improve their nutritional value. This study evaluated the utilization of Aspergillus ibericus and Aspergillus niger for SSF of a GBP and SC mixture (1:1 ratio; Gmix). SSF with A. ibericus decreased neutral detergent fiber (NDF) content (P < 0.05) along with high β-glucosidase activity (P < 0.05). SSF with A. niger increased crude protein, reduced NDF and acid detergent fiber (ADF) content, and produced higher xylanase, cellulase, and protease activities (P < 0.05). A 63-day growth trial with European sea bass (Dicentrarchus labrax) juveniles tested four isoproteic and isolipidic diets (44 % protein; 16 % lipids): a control diet without Gmix and three diets incorporating 10 % Gmix unfermented (diet Gmix), fermented by A. ibericus (diet Gmix-ibericus), or by A. niger (diet Gmix-niger). The Gmix and Gmix-ibericus diets promoted similar growth to the control, but the Gmix-ibericus diet supported higher feed efficiency, nitrogen, and energy utilization than the control diet (P < 0.05). The Gmix-niger diet negatively affected overall growth, feed intake, and utilization. Plasma metabolite levels, hepatic antioxidant enzyme activities, and lipid peroxidation were similar among diets. However, the Gmix-ibericus diet reduced total and oxidized glutathione levels (P < 0.05). Overall, G-mix or Gmix-ibericus diets did not compromise European seabass performance or oxidative status, with the Gmix-ibericus diet enhancing feed utilization efficiency by 25 %. Further studies are needed to understand the negative impact of the Gmix-niger diet on the European seabass.

Bioactive Peptides from Meretrix lusoria Enzymatic Hydrolysate as a Potential Treatment for Obesity in db/db Mice.

Obesity is acknowledged as a significant risk factor for cardiovascular disease, often accompanied by increased inflammation and diabetes. Bioactive peptides derived from marine animal proteins show promise as safe and effective anti-obesity agents by regulating adipocyte differentiation through the AMPK signaling pathway. Therefore, this study aims to investigate the anti-obesity and anti-diabetic effects of bioactive compounds derived from a Meretrix lusoria Protamex enzymatic hydrolysate (MLP) fraction (≤1 kDa) through a 6-week treatment (150 mg/kg or 300 mg/kg, administered once daily) in leptin receptor-deficient db/db mice. The MLP treatment significantly decreased the body weight, serum total cholesterol, triglycerides, and LDL-cholesterol levels while also exhibiting a beneficial effect on hepatic and serum marker parameters in db/db mice. A histological analysis revealed a reduction in hepatic steatosis and epididymal fat following MLP treatment. Furthermore, poor glucose tolerance was improved, and hepatic antioxidant enzyme activities were elevated in MLP-treated mice compared to db/db control mice. Western blot analysis showed an increased expression of the AMPK protein after MLP treatment. In addition, the expression of lipogenic genes decreased in db/db mice. These findings indicate that bioactive peptides, which are known to regulate blood glucose levels, lipid metabolism, and adipogenesis, could be beneficial functional food additives and pharmaceuticals.

Light perception and related alternation of physiological performance in spotted knifejaw Oplegnathus punctatus

Light is one of the main environmental factors that affects the behavior and physiology of fish. In the present study, the behavioral responses, retinal histology, hematological parameters (white blood cell [WBC], red blood cell [RBC], hemoglobin [Hb] hematocrit [Hct]), hepatic antioxidant enzyme (superoxide dismutase [SOD], catalase [CAT], and glutathione peroxidase [GSH-Px]) activity, aspartate-aminotransferase (AST) and alanine-aminotransferase (ALT) activities, malondialdehyde (MDA) content, histological alterations, apoptosis, and stress-related gene expression (hsp70, hsp90a, hsp90b) of spotted knifejaw were investigated under different light colors. The results showed that the residence time of spotted knifejaw plants significantly decreased under red and blue light stimuli but significantly increased under green light. Moreover, a positive and negative phototaxis of the spotted knifejaw under green and red lights was observed. However, retinal structure (relative thickness, cell number, and size) remained unchanged after red and green light treatment for 12 h. WBC and RBC numbers, Hb and Hct contents, hepatic SOD, CAT, GSH-Px, ALT and AST activities, and MDA levels were significantly increased after red and green light treatment for 12 h. Moreover, red and green light treatment caused hepatocyte vacuolization and nuclear migration and significantly increased the percentage of apoptotic cells. Hepatic hsp70, hsp90a, and hsp90b mRNA levels were significantly upregulated under red and green stimuli. Furthermore, the values of the above parameters under red light treatment were significantly greater than those under green light treatment. The aforementioned parameters nearly recovered to normal levels after the fish returned to normal light for 12 h. In conclusion, in spotted knifejaw, green light promoted attraction and red light avoidance, while red light could induce a more sensitive physiological response than green light. These findings expand the current knowledge on light perception and aid in the management of spotted knifejaw in captivity.

Acrylamide-Aggravated Liver Injury by Activating Endoplasmic Reticulum Stress in Female Mice with Diabetes.

Acrylamide (ACR) is a common industrial contaminant with endocrine-disrupting toxicity. Numerous studies have indicated that females and diabetics are more sensitive to environmental contaminants. However, it remains unknown whether female diabetics are susceptible to ACR-induced toxicity and its potential mechanisms. Thus, the female ACR-exposure diabetic Balb/c mice model was established to address these issues. Results showed that ACR could induce liver injury in normal mice and cause more serious inflammatory cell infiltration, hepatocyte volume increase, and fusion in diabetic mice liver. Meanwhile, ACR could lead to exacerbation of diabetic symptoms in diabetic mice by disturbing the glucose and lipid metabolism in the liver, which mainly manifests as the accumulation of liver glycogen and liver lipids, the reduction of the activity/content of glycolytic and metabolizing enzyme as well as pentose phosphatase, upregulation of the gene expression in fatty acid transporter and gluconeogenesis, and downregulation of the gene expression in fatty acid synthesis and metabolism. Moreover, ACR exposure could induce oxidative stress, inflammation, and endoplasmic reticulum stress in the liver by a decrease in hepatic antioxidant enzyme activity and antioxidant content, an increase in inflammatory factor levels, and a change in the related protein expression of endoplasmic reticulum stress (ERS) and apoptosis-related pathways in diabetic mice. Statistical analysis results revealed that ACR-induced liver injury was highly correlated with inflammation and oxidative stress, and ERS and diabetic mice had a higher risk of liver injury than normal mice. Overall results suggested that female diabetic mice easily suffer from ACR-induced toxicity, and the reason was that ACR could induce further damage to the liver by worsening the condition of inflammation, oxidative stress, and ERS in the liver.

Effects of Ethyl Acetate Fraction of Mangifera haden Seeds on Carbon Tetrachloride Induced Hepatotoxicity in Albino Rats

The present study investigated the effects of ethyl acetate fraction of Mangifera haden seeds on carbon tetrachloride-induced liver damage in wistar albino rats. The phytochemical compositions and acute toxicity studies of crude extract and Mangifera haden seed fraction were determined using standard methods. Albino rats (60) randomly grouped into twelve of five rats each were used for this study. Determination of total bilirubin and protein, lipid peroxidation, liver enzymes marker, antioxidant enzymes, glutathione, lipid profile analysis and histological examination were carried out using standard methods. Phytochemical constituents of crude extract and ethyl acetate fraction of Mangifera haden seed showed that they contain relative amount of flavonoids, phenolics, saponins, tannins, terpenoids, triterpenes, alkaloids and coumarins. Liver injury was induced with carbon tetrachloride (CCl4) at a dose of 1.0 ml/kg body weight of the animals. All the CCl4 intoxicated rats displayed hyperlipidemia as shown by their elevated levels of serum total cholesterol (TC), triacylglycerol (TAG), low density lipoprotein (LDL), and reduction in high density lipoprotein (HDL) levels. The administration of ethyl acetate fraction of Mangifera haden seeds significantly (P = 0.05) lowered the levels of serum TC, TAG, LDL, and increased HDL levels. The level of serum malondialdehyde (MDA) significantly (P = 0.05) increased in the CCl4 group as compared to the normal and treated groups. The elevated level of serum MDA decreased (P = 0.05) significantly at the treatment of rats with 200, 400 and 600 mg/kg of ethyl acetate fraction. The rats treated with CCl4 produced significant (P = 0.05) increase in serum ALT, AST and ALP when compared to the normal group. Animals treated with varying doses of ethyl acetate fraction produced significant (P = 0.05) reduction of serum ALT, AST and ALP activities when compared to the CCl4-untreated group. The activities of hepatic antioxidant enzymes (SOD, CAT and GPx) and glutathione concentration significantly (P = 0.05) decreased in CCl4­-untreated group compared to the normal group. The decreased activities of the antioxidant enzymes and glutathione concentration in CCl4 intoxicated rats were ameliorated/modulated more effectively in rats treated with 200, 400 and 600 mg/kg ethyl acetate fraction of Mangifera haden seed. Total bilirubin (TB) concentrations significantly (P = 0.05) increased in CCl4-untreated group when compared to the normal group. Oral treatment of rats with varying doses (200, 400, 600 mg/kg) of ethyl acetate fraction caused a significant (P = 0.05) decrease in the serum TB levels. Administration of CCl4 showed a reduction in serum total proteins. Treatment of the animals with 200, 400 and 600 mg/kg of ethyl acetate fraction caused significant (P = 0.05) increase in serum total potein. Histological examination showed hepatoprotective properties of plant’s fractions. The compounds found in the different fractions (ethyl acetate and n-hexane) of Mangifera haden seeds are 9-Octadecenoic acid (Z)-, methyl ester, (Z) –Oleic acid and so on. Therefore the medicinal importance of the plant is been established.

Improved traits of proximate composition, liver antioxidant capacity and feeding habits in diploid hybrids from female Micropterus salmoides × male Lepomis cyanellus

Distant hybridization has been widely used as an effective strategy for improving fish germplasm. The largemouth bass (Micropterus salmoides, LB) is a popular fish worldwide due to its excellent performance in aquaculture, edibility, and sport fishing. However, the carnivorous nature of LB increases the cost and difficulty of culture and poses a threat to wild fishery resources. At present, there is a lack of research on improving the germplasm of LB. In this study, hybrid offspring (LG) were produced by crossing female LB and male green sunfish (Lepomis cyanellus, GS). The biological characteristics of the LG, such as muscle proximate composition, liver antioxidant enzyme activity, and pharyngeal tooth structure, were analyzed to evaluate their potential for aquaculture. The proximate composition analysis revealed that LG has a higher crude protein content of 20.07% compared to LB (18.1%) and GS (18.7%) (P < 0.05), and a lower crude fat content of 0.57% than LB (1.17%) (P < 0.05). Furthermore, LG had a significantly higher essential amino acid content (7.20%) than LB (6.43%) (P < 0.05), but not significantly different from GS (6.82%) (P > 0.05). In terms of fatty acid content, LG had significantly lower levels of saturated fatty acids (0.083%) compared to LB (0.153%) and GS (0.169%) (P < 0.05). Additionally, the amount of arachidonic acid (C20:4n6, ARA) in LG (0.058%) was significantly higher than LB (0.019%) and GS (0.043%) (P < 0.05). Regarding antioxidant enzyme activities in the liver, LG exhibited significantly higher superoxide dismutase (SOD) activity than LB and GS (P < 0.05). Electron microscopic observation of the pharyngeal tooth showed that the tooth number of LG (160.67 ± 3.93) was significantly lower than that of LB (181.67 ± 4.97) (P < 0.05) and significantly higher than that of GS (108.00 ± 3.58) (P < 0.05), while the tooth diameter of LG (0.076 ± 0.023) was significantly higher than that of LB (0.057 ± 0.016) (P < 0.05) and significantly lower than that of GS (0.108 ± 0.044) (P < 0.05). In conclusion, this study found that LG exhibited improved traits in proximate composition and hepatic antioxidant enzyme activity. The pharyngeal tooth characteristics indicated that LG may have different food selection and processing capabilities. This is the first report on biological characteristics in offspring produced from a distant hybridization between LB and GS, providing new insights into the genetic improvement and germplasm innovation of LB.

Structure and gene expression changes of the gill and liver in juvenile black porgy (Acanthopagrus schlegelii) under different salinities

Black porgy (Acanthopagrus schlegelii) is an important marine aquaculture species in China. It is an ideal object for the cultivation of low-salinity aquaculture strains in marine fish and the study of salinity tolerance mechanisms in fish because of its strong low-salinity tolerance ability. Gill is the main osmoregulatory organ in fish, and the liver plays an important role in the adaptation of the organism to stressful environments. In order to understand the coping mechanisms of the gills and livers of black porgy in different salinity environments, this study explored these organs after 30 days of culture in hypoosmotic (0.5 ppt), isosmotic (12 ppt), and normal seawater (28 ppt) at histologic, physiologic, and transcriptomic levels. The findings indicated that gill exhibited a higher number of differentially expressed genes than the liver, emphasizing the gill's heightened sensitivity to salinity changes. Protein interaction networks and enrichment analyses highlighted energy metabolism as a key regulatory focus at both 0.5 ppt and 12 ppt salinity in gills. Additionally, gills showed enrichment in ions, substance transport, and other metabolic pathways, suggesting a more direct regulatory response to salinity stress. The liver's regulatory patterns at different salinities exhibited significant distinctions, with pathways and genes related to metabolism, immunity, and antioxidants predominantly activated at 0.5 ppt, and molecular processes linked to cell proliferation taking precedence at 12 ppt salinity. Furthermore, the study revealed a reduction in the volume of the interlamellar cell mass (ILCM) of the gills, enhancing the contact area of the gill lamellae with water. At 0.5 ppt salinity, hepatic antioxidant enzyme activity increased, accompanied by oxidative stress damage. Conversely, at 12 ppt salinity, gill NKA activity significantly decreased without notable changes in liver structure. These results underscore the profound impact of salinity on gill structure and function, highlighting the crucial role of the liver in adapting to salinity environments.

Long-term dietary exposure to the non-steroidal anti-inflammatory drugs diclofenac and ibuprofen can affect the physiology of common carp (Cyprinus carpio) on multiple levels, even at “environmentally relevant” concentrations

The aim of the study was to evaluate the effects of emerging environmental contaminants, the non-steroidal anti-inflammatory drugs (NSAIDs) diclofenac (DCF) and ibuprofen (IBP), on physiological functions in juvenile common carp (Cyprinus carpio). Fish were exposed for 6 weeks, and for the first time, NSAIDs were administered through diet. Either substance was tested at two concentrations, 20 or 2000 μg/kg, resulting in four different treatments (DCF 20, DCF 2000, IBP 20, IBP 2000). The effects on haematological and biochemical profiles, the biomarkers of oxidative stress, and endocrine disruption were studied, and changes in RNA transcription were also monitored to obtain a comprehensive picture of toxicity. Fish exposure to high concentrations of NSAIDs (DCF 2000, IBP 2000) elicited numerous statistically significant changes (p < 0.05) in the endpoints investigated, with DCF being almost always more efficient than IBP. Compared to control fish, a decrease in total leukocyte count attributed to relative lymphopenia was observed. Plasma concentrations of total proteins, ammonia, and thyroxine, and enzyme activities of alanine aminotransferase (ALT), aspartate aminotransferase, and alkaline phosphatase (ALP) were significantly elevated in either group, as were the activities of certain hepatic antioxidant enzymes (superoxide dismutase, glutathione-S-transferase) in the DCF 2000 group. The transcriptomic profile of selected genes in the tissues of exposed fish was affected as well. Significant changes in plasma total proteins, ammonia, ALT, and ALP, as well as in the transcription of genes related to thyroid function and the antioxidant defense of the organism, were found even in fish exposed to the lower DCF concentration (DCF 20). As it was chosen to match DCF concentrations commonly detected in aquatic invertebrates (i.e., the potential feed source of fish), it can be considered “environmentally relevant”. Future research is necessary to shed more light on the dietary NSAID toxicity to fish.

The ameliorative mechanism of Lactiplantibacillus plantarum NJAU-01 against D-galactose induced oxidative stress: a hepatic proteomics and gut microbiota analysis.

Probiotic intervention is an effective strategy to alleviate oxidative stress-related diseases. Our previous studies found that Lactiplantibacillus plantarum NJAU-01 (NJAU-01) exhibited antioxidant effects in a D-galactose (D-gal)-induced aging mouse model. However, the underlying mechanism remains to be unveiled. This study was aimed to investigate the ameliorative effect and mechanism of NJAU-01 against oxidative stress induced by D-gal. The results showed that NJAU-01 could reverse the tendency of a slow body weight gain induced by D-gal. NJAU-01 relieved hepatic oxidative stress via increasing the hepatic total antioxidant capacity and antioxidant enzyme activities including superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT). Moreover, the malondialdehyde (MDA) level was reversed after NJAU-01 supplementation. The proteomic results showed that there were 201 differentially expressed proteins (DEPs) between NJAU-01 and D-gal groups. NJAU-01 regulated the expressions of glutathione S-transferase Mu 5 (Gstm5), glutathione S-transferase P2 (Gstp2) and NADH dehydrogenase 1α subcomplex subunit 7 (Ndufa7) related to oxidative stress, and autophagy protein 5 (Atg5) and plasma alpha-L-fucosidase (Fuca2) involved in autophagy, etc. 16S rDNA sequencing results showed that NJAU-01 supplementation could regulate the gut microbiota dysbiosis induced by D-gal via increasing the relative abundances of the phylum Firmicutes and the genus Lactobacillus and reducing the relative abundances of the phylum Bacteroidetes and the genera Lachnospiraceae_NK4A136_group as well as Prevotellaceae_UCG-001, etc.. Spearman correlation analysis results showed that the altered gut microbiota composition had a significant correlation with antioxidant enzyme activities and the DEPs related to oxidative stress. Overall, NJAU-01 alleviated hepatic oxidative stress induced by D-gal via manipulating the gut microbiota composition and hepatic protein expression profile.

The growth-promoting and lipid-lowering effects of berberine are associated with the regulation of intestinal bacteria and bile acid profiles in yellow catfish (Pelteobagrus fulvidraco)

Berberine has growth-promoting and lipid-lowering effects potentially through the regulation of intestinal microbiota and bile acid profiles. This experiment aimed to investigate the effect of dietary berberine on the intestinal microbiota-bile acid-farnesoid X receptor (FXR) axis in yellow catfish (Pelteobagrus fulvidraco). Fish (initial weight: 1.32 ± 0.26 g) were fed a control diet or a diet supplemented with 100 mg/kg (BBR100) or 400 mg/kg berberine (BBR400) for 60 days. The BBR400 group showed significant improvements in growth performance, hepatic antioxidant enzyme activities, intestinal lysozyme activity, cholic acid, ethylchenodeoxycholic acid, and hydroguinone carboxylic acid contents, along with significantly lower intestinal immunoglobulin M, complement 3, complement 4, serum total cholesterol (TCH), and triglyceride (TG) contents, compared to the control group (P < 0.05). In addition, both levels of berberine resulted in significant reductions in viscerosomatic index, hepatosomatic index, condition factor, hepatic TCH, TG, and malondialdehyde contents, as well as serum alanine aminotransferase activity and low-density lipoprotein cholesterol content. Berberine supplementation also significantly upregulated the expression of intestinal fxr and fibroblast growth factor 19, as well as hepatic fxr, short heterodimeric partners, and lipolysis genes, while inhibiting the expression of lipogenesis genes. Furthermore, berberine treatment improved intestinal histological parameters and increased the abundance of probiotic bacteria such as Ruegeria and Bifidobacterium, while reducing potential pathogenic bacteria such as Pseudomonas, Psychrobacter, Vibrio, and Pseudonocardia. Overall, this study suggests that berberine’s growth-promoting and lipid-lowering effects might be attributed to its modulation of intestinal microbiota, bile acid profile, and hepatic and intestinal FXR signaling.

Effects of Dietary Supplementation of Lacticaseibacillus Chiayiensis AACE3 on Hepatic Antioxidant Capacity, Immune Factors and Gut Microbiology in Nandan Yao Chicks.

The growing issue of antibiotic resistance has restrained the utilization of antibiotics as growth enhancers in the poultry industry. Probiotics are candidates for replacing antibiotics in the poultry industry. However, probiotics are strain-specific and their efficacy needs to be investigated before applying them. The aim of this study was to assess the positive effects of Lacticaseibacillus chiayiensis AACE3 on the health and gut microbiota of Nandan Yao chicks. The results showed that compared with the blank control (NC) and aureomycin (PC) groups, L. chiayiensis AACE3 increased final body weight (BW), villus height and improved the ratio of villus height to crypt depth in chicken jejunal tissues. L. chiayiensis AACE3 also increased the activity of hepatic antioxidant enzymes (SOD, CAT and T-AOC) and reduced hepatic oxidative damage (MDA). Furthermore, compared to NC, L. chiayiensis AACE3, the activity of intestinal digestive enzymes (i.e., α-amylase, lipase and trypsin) was increased. L. chiayiensis AACE3 upregulated the production of IgA and IgG and downregulated the production of IL-6, IL-1β and TNF-α in chicken serum. Moreover, supplementation of L. chiayiensis AACE3 enhances the diversity of gut microbes. At the phylum level, the abundance of Actinobacteriota and Proteobacteria decreased with L. chiayiensis AACE3 supplementation, while the abundance of Verrucomicrobiota and Bacteroidetes increased. At the genus level, there was an increase in the abundance of potential probiotics Akkermansia, Romboutsia, Subdoligranulum, and Lactobacillus. This study confirms that L. chiayiensis AACE3 is an excellent feed additive as an alternative to aureomycin and offers various advantages for the healthy growth of chickens during the brooding period by positively affecting their gut microbiome.

Genome-Wide and 16S rRNA Sequencing-Based Analysis on the Health Effects of Lacticaseibacillus paracasei XLK401 on Chicks.

Lacticaseibacillus paracasei, serves as a growth promoter used in the poultry industry, contributeing to broiler development. However, practical studies are needed to determine the probiotic potential and growth-promoting effects of specific L. paracasei strains. This study aims to determine whether L. paracasei XLK401 influences broiler chicken growth and the mechanisms involved. Notably, we identified several bile salt and acid tolerance-related genes (Asp23, atpD, atpA, atpH, and atpF) in L. paracasei XLK401. This bacterium demonstrates robust probiotic properties under acidic conditions (pH 2.0) and 0.3% bile salt conditions. It also contains a variety of antioxidant-related genes (trxA, trxB, and tpx), carbohydrate-related genes, gene-encoding glycosidases (e.g., GH and GT), and three clusters of genes associated with antimicrobial compounds. Supplementation with L. paracasei XLK401 significantly increased the body weight of the chicks. In addition, it significantly increased hepatic antioxidant enzyme activities (GSH-Px, SOD, and T-AOC) while significantly decreasing the levels of oxidative damage factors and inflammatory factors (MDA and IL-6), resulting in improved chick health. Improvements in body weight and health status were associated with significant increases in α-amylase activity and the remodeling of the host gut microbiota by L. paracasei XLK401. Among them, actinobacteria abundance in chicken intestines after feeding them L. paracasei XLK401 was significantly decreased, Bifidobacterium sp. abundance was also significantly decreased, and Subdoligranulum sp. abundance was significantly increased. This suggests that L. paracasei XLK401 can regulate the abundance of certain bacteria without changing the overall microbial structure. In addition, in the correlation analysis, Subdoligranulums sp. were positively correlated with SOD and negatively correlated with IL-1β and MDA. Overall, our study demonstrates that L. paracasei XLK401 effectively promotes healthy chick growth. This is made possible by the modulation of gut microbe abundance and the underlying probiotic effect of L. paracasei XLK401. Based on these findings, we postulate L. paracasei XLK401 as a potential efficient growth promoter in broiler farming.

Acrylamide-Induced Hepatotoxicity Through Oxidative Stress: Mechanisms and Interventions.

Significance: Acrylamide (AA) widely exists in the environment. Studies have demonstrated that AA has neurotoxicity and potential carcinogenicity in humans, and genotoxicity and severe hepatotoxicity in animals. As the critical metabolism organ, the liver is the primary attacking target of AA. This review summarizes the recent advances in hepatotoxicity mechanism through AA-induced oxidative stress in rodent livers and hepatic cell lines, and this is beneficial to assess the risks of AA exposure and explore effective intervention methods for AA hepatotoxicity. Recent Advances: Accumulating evidence has indicated that AA-induced oxidative stress is responsible for its hepatotoxicity. The changes in homological and biochemical indexes such as activities of hepatic antioxidant enzymes have been elucidated with the occurrence and development of oxidative stress. Also, the molecular mechanisms underlying AA-induced hepatotoxicity through oxidative stress have been mainly explained by apoptosis, inflammatory, and autophagic pathways. Critical Issues: This review is focusing on the molecular mechanism of hepatotoxicity through AA-induced oxidative stress, and this can provide a theoretical basis for the assessment of AA-induced health risk and finding potential intervention targets. Future Directions: Epigenetic modifications such as microRNAs (miRNAs) and modulation of the gut microbiome involved in the AA toxification pathway must be investigated, and they will provide novel insights to unravel the toxification mechanism and intervention strategy for AA hepatotoxicity. Antioxid. Redox Signal. 38, 1122-1137.