Intestinal Lipid Peroxidation Research Articles

Macleaya cordata isoquinoline alkaloids attenuate Escherichia coli lipopolysaccharide-induced intestinal epithelium injury in broiler chickens by co-regulating the TLR4/MyD88/NF-κB and Nrf2 signaling pathways.

This study sought to explore the effects and potential mechanisms of dietary supplementation with isoquinoline alkaloids (IA) from Macleaya cordata to alleviate lipopolysaccharide (LPS)-induced intestinal epithelium injury in broilers. A total of 486 1-day-old broilers were assigned at random to a control (CON) group, LPS group, and LPS+IA group in a 21-d study. The CON and LPS groups received a basal diet, while the LPS+IA group received a basal diet supplemented with 0.6 mg/kg IA. At 17, 19, and 21 days of age, the LPS and LPS+BP groups were injected intraperitoneally with LPS, and the CON group was intraperitoneally injected equivalent amount of saline solution. The results manifested that LPS injection caused intestinal inflammation and lipid peroxidation, disrupted intestinal barrier and function, and increased the abundance of harmful microorganisms. However, dietary IA supplementation alleviated LPS-induced adverse changes in intestinal morphology, apoptosis, mucosal barrier integrity, cecum microorganisms, and homeostasis disorder by decreasing inflammatory cytokines and enhancing antioxidant-related genes expressions; inhibited LPS-induced increases in TLR4 and NF-κB expressions and decreases in Nrf2 and GPX1 genes expressions. Our findings indicated that Macleaya cordata IA addition attenuated LPS-induced intestinal epithelium injury and disorder of intestinal homeostasis by enhancing the anti-inflammatory and antioxidant capacity of broiler chickens possibly via co-regulating TLR4/MyD88/NF-κB and Nrf2 signaling pathways.

Bifidobacterium longum GL001 alleviates rat intestinal ischemia-reperfusion injury by modulating gut microbiota composition and intestinal tissue metabolism.

Intestinal ischemia-reperfusion (IIR) injury leads to inflammation and oxidative stress, resulting in intestinal barrier damage. Probiotics, due to their anti-inflammatory and antioxidant properties, are considered for potential intervention to protect the intestinal barrier during IIR injury. Bifidobacterium longum, a recognized probiotic, has targeted effects on IIR injury, but its mechanisms of action are not yet understood. To investigate the mechanism of Bifidobacterium longum intervention in IIR injury, we conducted a study using a rat IIR injury model. The results showed that Bifidobacterium longum could alleviate inflammation and oxidative stress induced by IIR injury by suppressing the NF-κB inflammatory pathway and activating the Keap1/Nrf2 signaling pathway. Bifidobacterium longum GL001 also increased the abundance of the gut microbiota such as Oscillospira, Ouminococcus, Corynebacterium, Lactobacillus, and Akkermansia, while decreasing the abundance of Allobaculum, [Prevotella], Bacteroidaceae, Bacteroides, Shigella, and Helicobacter. In addition, Bifidobacterium longum GL001 reversed the changes in amino acids and bile acids induced by IIR injury and reduced the levels of DL-cysteine, an oxidative stress marker, in intestinal tissue. Spearman correlation analysis showed that L-cystine was positively correlated with Lactobacillus and negatively correlated with Shigella, while DL-proline was positively correlated with Akkermansia. Moreover, bile acids, cholic acid and lithocholic acid, were negatively correlated with Lactobacillus and positively correlated with Shigella. Therefore, Bifidobacterium longum GL001 may alleviate IIR injury by regulating the gut microbiota to modulate intestinal lipid peroxidation and bile acid metabolism.

PUFAs add fuel to Crohn’s disease-associated AIEC-induced enteritis by exacerbating intestinal epithelial lipid peroxidation

ABSTRACT Polyunsaturated fatty acids (PUFAs) have been shown to exacerbate Crohn’s disease (CD) by promoting lipid peroxidation (LPO) of intestinal epithelial cells (IECs). Dysbiosis of the gut microbiota may play a crucial role in this process. CD patients often exhibit an increased abundance of Escherichia coli (E. coli) in the gut, and the colonization of adherent-invasive E. coli (AIEC) is implicated in the initiation of intestinal inflammation in CD. However, the impact of AIEC on LPO remains unclear. In this study, we observed that AIEC colonization in the terminal ileum of CD patients was associated with decreased levels of glutathione peroxidase 4 (GPX4) and ferritin heavy chain (FTH) in the intestinal epithelium, along with elevated levels of 4-Hydroxynonenal (4-HNE). In vitro experiments demonstrated that AIEC infection reduced the levels of GPX4 and FTH, increased LPO, and induced ferroptosis in IECs. Furthermore, arachidonic acid (AA) and docosahexaenoic acid (DHA) supplementation in AIEC-infected IECs significantly aggravated LPO and ferroptosis. However, overexpression of GPX4 rescued AIEC-induced LPO and ferroptosis in IECs. Our results further confirmed that AIEC with AA supplementation, associated with excessive LPO and cell death in IECs, worsened colitis in the DSS mouse model and induced enteritis in the antibiotic cocktail pre-treatment mouse model in vivo. Moreover, treatment with ferrostatin-1, a ferroptosis inhibitor, alleviated AIEC with AA supplementation-induced enteritis in mice, accompanied by reduced LPO and cell death in IECs. Our findings suggest that AIEC, in combination with PUFA supplementation, can induce and exacerbate intestinal inflammation, primarily through increased LPO and ferroptosis in IECs.

ACSL4 is essential for radiation-induced intestinal injury by initiating ferroptosis

Lipid peroxidation-induced ferroptosis is a newly recognized type of programmed cell death. With the method of RNA sequencing, we found that irradiation (IR) markedly increased the expression of ferroptosis promotive genes, whereas reduced the expression of ferroptosis suppressive genes in murine intestine tissues, when compared with those of liver and lung tissues. By using ferroptosis inducer RSL-3 and inhibitor liproxstatin-1, we found that ferroptosis is essential for IR-induced intestinal injury. Acyl-CoA Synthetase Long-Chain Family Member 4 (ACSL4) is an important component for ferroptosis execution, and we found that ACSL4 expression was significantly upregulated in irradiated intestine tissues, but not in liver or lung tissues. Antibacterial and antifungal regents reduced the expression of ASCL4 and protected against tissue injury in irradiated intestine tissues. Further studies showed that troglitazone, a ACSL4 inhibitor, succeeded to suppresses intestine lipid peroxidation and tissue damage after IR.

Synthesis of salicylic acid phenylethyl ester (SAPE) and its implication in immunomodulatory and anticancer roles

Salicylic acid phenylethyl ester (SAPE) was synthesized by Zn(OTf)2-catalyzed selective esterification of salicylic acid and phenylethyl alcohol and studied for its role as an immunomodulatory and anticancer agent. Low toxicity and favorable physical, Lipinski-type, and solubility properties were elucidated by ADME-tox studies. Molecular docking of SAPE against COX-2 revealed favorable MolDockscore, rerank score, interaction energy, internal pose energy, and hydrogen bonding as compared to ibuprofen and indomethacin. An average RMSD of ~ 0.13 nm for the docked complex with stable dynamic equilibrium condition was noted during the 20 ns MD simulation. A low band gap predicting a strong binding affinity at the enzyme’s active site was further predicted by DFT analysis. The ester caused a reduction in the percentage of erythrocyte hemolysis and was shown to be non-cytotoxic against human lymphocytes, CaCo-2, and HepG-2 cells by the MTT assay. Moreover, it’s in vitro efficacy in inhibiting COX-2 enzyme under both LPS stimulated intestinal cells and direct sequestration assays was found to be higher than salicylic acid and indomethacin. The anticancer activity of SAPE was tested on the breast cancer cell line MCF-7, and potential efficacy was exhibited in terms of decreased cell viability. Flow cytometry analysis exhibited the arrest of the cell cycle at G1/G0 and S phases, during which induction of autophagic vesicle formation and decrease in mitochondrial membrane potential was observed owing to increased ROS production. Furthermore, at these phases, the onset of apoptosis along with DNA damage was also observed. Pre-treatment with SAPE in colitis-induced Wistar rats displayed low disease activity index and reduction in the extent of intestinal tissue disruption and lipid peroxidation. A marked increase of anti-oxidative enzymes viz., catalase, GGT, and GST, and a decrease of pro-inflammatory cytokines IL-6 and TNF-α in the intestinal tissue extracts of the treated groups was noted. The results of this study have sufficient credence to support that the synthesised ester (SAPE) be considered as an anti-oxidative and anti-inflammatory compound with therapeutic potential for the effective management of cancer.

Application of Fermented Brewer’s Spent Grain Extract in Plant-Based Diets Improves Pre- and Post-mortem Oxidative Status of European Seabass (Dicentrarchus labrax)

In a previous study, it was shown that dietary supplementation with a carbohydrases and antioxidant-enriched extract (BSG-extract) produced by solid-state fermentation of brewer’s spent grain (BSG) improved nutrients digestibility, feed, and protein utilization of European seabass juveniles. This work aims to investigate the effect of this BSG-extract on liver and intestine oxidative status and muscle lipid peroxidation (LPO) of European seabass. A plant-based diet (55.4% plant feedstuffs; PF) was used as a control. Four test diets were formulated by supplementing the control diet with the BSG-extract (0.4 or 0.8% diet), added directly to the diet (BSG4 and BSG8 diets), or used to pre-treat the PF mixture of the control diet (PreBSG4 and PreBSG8 diets). European seabass juveniles (IBW 22 ± 1 g) were fed the experimental diets for 66 days until apparent satiety. In fish fed BSG-extract diets, compared to the control diet, intestinal LPO was reduced up to 29-40% ( p < 0.05 ); GPX, GR, and G6PD activities were increased compared to the control ( p < 0.05 ). In the liver, LPO was similar among diets, but except for catalase and G6PD, fish fed BSG-extract diets had higher antioxidant enzyme activities than the control ( p < 0.05 ). Except for the liver SOD activity, hepatic and intestinal antioxidant capacity was not affected by the dietary BSG-extract incorporation mode ( p > 0.05 ). After 72 h of storage at 4°C, muscle LPO was higher than at time 0 h. Compared to the control, BSG-extract reduced muscle LPO levels up to 30% at time 0 h in fish fed diets BSG4, BSG8, and PreBSG8 ( p < 0.008 ). Results indicate that dietary supplementation with BSG-extract increased the antioxidant level of diets, improved the intestine antioxidant capacity, and decreased LPO in European seabass juveniles’ muscle.

Dietary methionine hydroxy analogue supplementation benefits on growth, intestinal antioxidant status and microbiota in juvenile largemouth bass Micropterus salmoides

To study the possible impacts of dietary methionine hydroxy analogue (MHA) on growth, intestinal antioxidant status, and intestinal microbiota in juvenile largemouth bass (LMB) Micropterus salmoides (14.49–14.58 g), we conducted a feeding trial for 84-days. Four hundred and eighty fish were randomized into four dietary MHA treatments (0.0, 3.0, 6.0, and 9.0 g/kg diet). Results revealed that dietary MHA supplementation: (1) dramatically improved growth of juvenile LMB; (2) markedly decreased intestinal protein and lipid peroxidation, and increased intestinal antioxidant activities via Keap1/Nrf2 axis; (3) increased the richness and diversity of intestinal microbial community; (4) changed intestinal microbiota composition, increased the abundances of Proteobacteria, Bacteroidetes, and Actinobacteria, and decreased the abundances of Firmicutes and Cyanobacteria at the phylum level; increased the abundances of Bifidobacterium and Bacillus and decreased the abundance of Bacteroides at the genus level. Collectively, dietary MHA supplementation has potential benefits in growth, intestinal antioxidant capacity, and intestinal microbiota in LMB. The dietary optimal Met level of LMB (14.49–131.06 g) was recommended to be 14.49 g/kg diet, corresponding to 8.30 g/kg diet sourcing from basic diet and 4.19 g Met/kg diet sourcing from MHA based on specific growth rate.

Nicotinamide riboside relieves the severity of experimental necrotizing enterocolitis by regulating endothelial function via eNOS deacetylation

BackgroundNicotinamide adenine dinucleotide (NAD+) is involved in regulating oxidative stress. Although NAD+ is associated with various health issues, its role in the intestinal microcirculation in necrotizing enterocolitis (NEC) remains to be confirmed. In the current study, we explored whether nicotinamide riboside (NR), a natural NAD + precursor, ameliorates the severity of NEC through endothelial nitric oxide synthase(eNOS) signaling. MethodsA mouse experimental NEC model was induced by formula gavage and hypoxia in full-term mouse pups. Intestinal endothelial cells (MIMECs) were isolated and subjected to stress using tumor necrosis factor (TNF)-α. NR was administered to assess the intestinal microcirculation and lipid peroxidation levels and to explore the involved signaling pathways. ResultsNAD + levels were reduced after induction of NEC stress, which was associated with intestinal injury. NR administration promoted NAD + levels, attenuated oxidative stress and relieved the symptoms of experimental NEC, which were relevant to increased intestinal microcirculatory perfusion through the sirtuin (SIRT) 1 pathway in experimental NEC mice. However, this improvement was not found in eNOS-knockout mice. Consistently, MIMECs exposed to TNFα showed decreased SIRT1 activity associated with increased eNOS acetylation, which could bring about endothelial dysfunction due to limited nitric oxide production. NR administration increased the NAD + content and repressed the production of reactive oxygen species (ROS) in MIMECs under TNFα stress. NR also promoted SIRT1 activity and accordingly suppressed the eNOS acetylation levels under TNFα stress. ConclusionThe current data indicate that NR administration improves the survival of experimental NEC mice via SIRT1-associated eNOS acetylation/deacetylation modulation, which is implicated in endothelial dysfunction. Although NR is commonly found in the human diet, it may also be a promising strategy for NEC treatment because of its pathogenic association with NEC.

Effects of dietary ARA, DHA, and carbohydrates levels on gilthead sea bream liver and intestine oxidative stress, tissue histomorphology, and gut microbiota

The present study aims evaluate the oxidative status, histomorphology of liver and intestine, and intestinal microbiota modulation of gilthead sea bream juveniles (initial body weight = 47.5 g) fed four isoproteic and isolipidic diets (47% protein; 18% lipids) with high or low gelatinized starch levels (20% or 5%; diets HS or LS, respectively) and different dietary ARA or DHA content (2.3/0.3 or 0/2.6, diets ARA or DHA, respectively).ARA-rich diets reduced liver and intestine lipid peroxidation (LPO) circa 12 and 66%, respectively. Dietary ARA also increased liver glutathione redox status (total, reduced (GSH) and oxidized glutathione (GSSG)) circa of 35% but only in the HS diets. Independently of dietary starch level, dietary ARA also reduced GSSG content (80 and 63 nmol g−1 tissue) and oxidative stress index (OSI) (8.7 and 7%) in the intestine. Fish fed DHA diets had increased hepatic superoxide dismutase (SOD) (749.1 and 489.1 U mg protein−1) and glutathione reductase (GR) (3.7 to 1.9 mU mg protein−1) activities. In the intestine, dietary ARA or DHA did not induce alterations in the activity of the antioxidant enzymes. Dietary starch improved liver OSI (1.5%), increased intestinal GSSG (80 and 128 nmol g−1 tissue), and decreased intestinal LPO values (104 nmol MDA g−1 tissue) in fish fed the DHA diets. Fish fed the HS diets had increased hepatic glucose-6-phosphate dehydrogenase (G6PDH) (171.4 and 166 mU mg protein−1), GR (2 and 3.71 mU mg protein−1), and glutathione peroxidase (GPX, only in DHA diets) (63.8 mU mg protein−1) activities, but decreased GR (27.2 and 27.6 mU mg protein−1) and SOD (2089.7 and 2158.8 U mg protein−1) activities in the intestine.Diet composition did not induce major histomorphological alterations in the distal intestine. Nevertheless, the HS diets, especially when combined with DHA, promoted hepatocyte hypertrophy and alterations in nuclei position.Compared to the DHA diets, in fish fed the ARA diets, mucosa bacterial profile had a reduced number of operational taxonomic units (10.3 and 12.0), richness (0.6 and 0.7), and diversity (2.2 and 2.3), and higher similarity between bacterial communities (85.0 and 80.4%).In conclusion, fish fed high dietary ARA presented lower hepatic and intestinal LPO and fewer hepatocyte morphological alterations than fish fed high DHA diets. Furthermore, interactive effects between dietary starch and DHA on liver and intestine GSH metabolism, antioxidant enzymes, LPO susceptibility, and liver histomorphology may be attenuated by a balanced ARA/DHA dietary ratio.

The Effect of Acute Oral Galactose Administration on the Redox System of the Rat Small Intestine.

Galactose is a ubiquitous monosaccharide with important yet incompletely understood nutritive and physiological roles. Chronic parenteral d-galactose administration is used for modeling aging-related pathophysiological processes in rodents due to its ability to induce oxidative stress (OS). Conversely, chronic oral d-galactose administration prevents and alleviates cognitive decline in a rat model of sporadic Alzheimer’s disease, indicating that galactose may exert beneficial health effects by acting in the gut. The present aim was to explore the acute time-response of intestinal redox homeostasis following oral administration of d-galactose. Male Wistar rats were euthanized at baseline (n = 6), 30 (n = 6), 60 (n = 6), and 120 (n = 6) minutes following orogastric administration of d-galactose (200 mg/kg). The overall reductive capacity, lipid peroxidation, the concentration of low-molecular-weight thiols (LMWT) and protein sulfhydryls (SH), the activity of Mn and Cu/Zn superoxide dismutases (SOD), reduced and oxidized fractions of nicotinamide adenine dinucleotide phosphates (NADPH/NADP), and the hydrogen peroxide dissociation rate were analyzed in duodenum and ileum. Acute oral administration of d-galactose increased the activity of SODs and decreased intestinal lipid peroxidation and nucleophilic substrates (LMWT, SH, NADPH), indicating activation of peroxidative damage defense pathways. The redox system of the small intestine can acutely tolerate even high luminal concentrations of galactose (0.55 M), and oral galactose treatment is associated with a reduction rather than the increment of the intestinal OS. The ability of oral d-galactose to modulate intestinal OS should be further explored in the context of intestinal barrier maintenance, and beneficial cognitive effects associated with long-term administration of low doses of d-galactose.

Pomegranate peel attenuates dextran sulfate sodium-induced lipid peroxidation in rat small intestine by enhancing the glutathione/glutathione disulfide redox potential.

The peel of the pomegranate fruit is rich in polyphenols with antioxidant properties. We investigated the preventive effect of pomegranate peel (PP) powder against dextran sulfate sodium (DSS)-induced lipid peroxidation in the small intestine of rats. Rats were allocated to four groups: CONT group, fed a standard rodent diet; DSS group, fed a standard rodent diet and treated with DSS; as well as PP1%+DSS and PP5%+DSS groups, fed a standard rodent diet supplemented with either 1% or 5% of PP powder and treated with DSS. Rats of the four groups consumed their diets for 25 days. Lipid peroxidation was determined by measuring malondialdehyde (MDA) concentrations in plasma and MDA contents in the small intestine and liver. Glutathione/glutathione disulfide (GSH/GSSG) redox status and antioxidant enzyme activities were determined in the small intestine and liver. MDA content was higher (P < 0.001) in the small intestines of the DSS group compared to the CONT group. MDA content was reduced (P < 0.001) in the small intestines of the PP1%+DSS and PP5%+DSS groups compared to the DSS group. GSH contents and GSH/GSSG ratios were higher (P < 0.001) in the small intestines of the PP5%+DSS group compared to the CONT, DSS and PP1%+DSS groups. The present study demonstrates that PP powder protects the small intestine against DSS-induced lipid peroxidation by enhancing the GSH/GSSG redox potential. Powder of PP is a promising agricultural by-product containing a mixture of bioactive polyphenols that can be used for the production of functional foods aimed at the prevention of oxidative stress-induced small intestine pathogenesis. © 2021 Society of Chemical Industry.

Physiological effects of stocking density on the fishPiaractus mesopotamicusfed with red seaweed (Pyropia columbina) and β‐carotene‐supplemented diets

This study aimed at investigating the physiological responses of Piaractus mesopotamicus exposed to high stocking density and the potential protective role of supplemented diets. Fish were fed with basal, red seaweed (Pyropia columbina) or β-carotene-supplemented diets for 90 days. Then, fish were distributed at low (1.5 g/L) and high (22 g/L) stocking densities for 15 days. Fish exposed to the high density showed increased hepatosomatic index, haemoglobin content and mean corpuscular haemoglobin concentration (all diets); decreased haematocrit, mean corpuscular volume (basal and seaweed) and white blood cells count (all diets) were observed. High density-exposed fish showed decreased plasmatic metabolites as well as the hepatic lipids content in basal and seaweed diets. Regarding oxidative stress, increased activity of glutathione S-transferase in high density-exposed fish muscle (all diets), and lower lipid peroxidation in liver (basal and β-carotene) and intestine (basal and seaweed) were evidenced. Interactions between diet and stocking density were recorded regarding the triglycerides (decrease in fish exposed to high density fed with basal and seaweed) and hepatic lipids (decrease in fish exposed to high density fed with basal). The major changes occurred in haematologic and metabolic parameters as strategies to cope with overcrowding stress. Fish response to stocking density was not affected by diets.

Effect of dexmedetomidine on ischemia-reperfusion injury of liver and kidney tissues in experimental diabetes and hepatic ischemia-reperfusion injury induced rats

Background: Reperfusion following ischemia can lead to more injuries than ischemia itself especially in diabetic patients. The aim of this study was to evaluate the effect of dexmedetomidine on ischemia-reperfusion injury (IRI) in rats with have hepatic IRI and diabetes mellitus.

Intestinal injury caused by Eimeria spp. impairs the phosphotransfer network and gain weight in experimentally infected chicken chicks.

Parasitic infections caused by protozoan belonging to genus Eimeria are considered important for the poultry industry, due to their severe intestinal lesions and high mortality rates, causing significant economic losses. Although several mechanisms of coccidiosis pathogenesis are known, the effects of this infection on intestinal enzymes linked to adenosine triphosphate (ATP) metabolism, as creatine kinase (CK), adenylate kinase (AK), and pyruvate kinase (PK), remain unknown. Thus, the aim of this study was to evaluate whether coccidiosis impairs enzymes linked ATP metabolism in the intestine of chicken chicks. For this, 42 animals that were 2days old were divided into two groups: uninfected (the negative control group) and experimentally infected on second day of life (the positive control group). On days 5, 10, and 15 post-infection (PI), fecal samples were collected for oocyst counts; intestinal tissue was collected in order to evaluate CK, AK, and PK activities, as well as parameters of the oxidative stress and histopathology. On days 10 and 15 PI, infected animals showed high counts of oocysts in fecal samples and intestinal lesions compared to the control group. Cytosolic CK activity was higher in infected animals on days 10 and 15 PI compared to the control group, while mitochondrial CK activity was lower on days 5, 10, and 15 PI. Also, AK activity was lower in infected animals on days 10 and 15 PI compared to control group, while no differences were observed between groups regarding PK activity. In relation to parameters of oxidative stress, intestinal lipid peroxidation and reactive oxygen species levels were higher in infected animals on days 10 and 15 PI compared to the control group, while non-protein thiol levels were lower on day 10 PI. On the 15th day, infected animals had lower body weight (P < 0.05). Based on this evidence, inhibition of mitochondrial CK activity causes an impairment of intestinal energetic homeostasis possibly through depletion on ATP levels, although the cytosolic CK activity acted as an attempt to restore the mitochondrial ATP levels through a feedback mechanism. Moreover, the impairment on energy metabolism appears to be mediated by excessive production of intestinal ROS, as well as oxidation of lipids and thiol groups.

Falcarinol Is a Potent Inducer of Heme Oxygenase-1 and Was More Effective than Sulforaphane in Attenuating Intestinal Inflammation at Diet-Achievable Doses.

Nuclear factor- (erythroid-derived 2) like 2 (Nrf2) is a transcription factor that regulates the expression of a battery of antioxidant, anti-inflammatory, and cytoprotective enzymes including heme oxygenase-1 (Hmox1, Ho-1) and NADPH:quinone oxidoreductase-1 (Nqo1). The isothiocyanate sulforaphane (SF) is widely understood to be the most effective natural activator of the Nrf2 pathway. Falcarinol (FA) is a lesser studied natural compound abundant in medicinal plants as well as dietary plants from the Apiaceae family such as carrot. We evaluated the protective effects of FA and SF (5 mg/kg twice per day in CB57BL/6 mice) pretreatment for one week against acute intestinal and systemic inflammation. The phytochemical pretreatment effectively reduced the magnitude of intestinal proinflammatory gene expression (IL-6, Tnfα/Tnfαr, Infγ, STAT3, and IL-10/IL-10r) with FA showing more potency than SF. FA was also more effective in upregulating Ho-1 at mRNA and protein levels in both the mouse liver and the intestine. FA but not SF attenuated plasma chemokine eotaxin and white blood cell growth factor GM-CSF, which are involved in the recruitment and stabilization of first-responder immune cells. Phytochemicals generally did not attenuate plasma proinflammatory cytokines. Plasma and intestinal lipid peroxidation was also not significantly changed 4 h after LPS injection; however, FA did reduce basal lipid peroxidation in the mesentery. Both phytochemical pretreatments protected against LPS-induced reduction in intestinal barrier integrity, but FA additionally reduced inflammatory cell infiltration even below negative control.

Effect of partial dietary replacement of fishmeal by yellow mealworm (Tenebrio molitor) larvae meal on the innate immune response and intestinal antioxidant enzymes of rainbow trout (Oncorhynchus mykiss)

The present study investigated the effects of 25 and 50% dietary inclusion of yellow mealworm, Tenebrio molitor (TM), larvae on the intestinal antioxidant enzymes, lipid peroxidation and immune system of rainbow trout, Oncorhynchus mykiss. Fish were fed for 90 days with a control diet (TM0) or with 2 test diets (TM25 and TM50) where 35 and 67% of the fishmeal was replaced by TM larvae meal respectively. At the end of the growth trial, humoral immune parameters were assessed in the sera of the fish and the activities of antioxidant enzymes were measured in intestine homogenates. The present results show a strong increase of the activity of the antioxidant intestinal enzymes and reduction of lipid peroxidation. Increased trypsin inhibition and faster antibacterial activity of the serum were also detected. These evidences could be due to the physiological similarities between the exoskeleton of parasites and insects. The present findings reinforce the previous results which revealed a positive effect of the dietary TM on rainbow trout growth and further confirm its adequacy for fishmeal partial replacement in aquafeed.

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Cadmium (Cd) toxicity is influenced by dietary components, such as fiber and minerals. Garden egg, carrot and oat are rich sources of fiber. Thus, this study examines the effect of Solanum melongena (garden egg), Daucus carota (carrot) and oat-supplements on selected biochemical parameters in the plasma and tissues of cadmium-exposed rats. Twenty-five healthy male Wistar rats (140&plusmn;50 g) were distributed into five treatment groups in which rats in group one were not exposed to cadmium, and served as control while rats in group two were exposed to cadmium only in addition to their normal diet. Cadmium was administered by gastric intubation at a dose of 5 mg Cd/kg body weight as CdCl2. H2O was given three times a week for six weeks. Rats in Groups 3 to 5 were treated similarly with cadmium, but with their normal diet supplemented with 5% garden egg, carrot and oat, respectively. A significant (P&lt;0.05) increase was observed in alanine aminotransferase (ALT)/aspartate aminotransferase (AST) activity in the plasma/kidney of rats exposed to Cd, while a significant (P&lt;0.05) decrease was observed in liver ALT/AST activity. Likewise, the levels of liver, kidney and intestine alkaline phosphatase (ALP), superoxide dismutase (SOD) and lipid peroxidation were increased compared to the control. Conversely, feeding with garden egg, carrot and oat significantly (P&lt;0.05) reversed these effects of cadmium, compared to rats maintained on cadmium only. The results suggest that garden egg, carrot and oat contain bioactive/antioxidant properties which help in ameliorating cadmium toxicity.&nbsp;&nbsp; &nbsp; Key words: Cadmium, lipid peroxidation, dietary fiber, carrot.

Chronic exposure to low environmental concentrations and legal aquaculture doses of antibiotics cause systemic adverse effects in Nile tilapia and provoke differential human health risk

BackgroundAntibiotics used globally to treat human and animal diseases exist ubiquitously in the environment at low doses because of misuse, overdose and poor absorption after ingestion, coupled with their high-water solubility and degradation resistance. However, the systemic chronic effects of exposure to low environmental concentrations of antibiotics (LECAs) and legal aquaculture doses of antibiotics (LADAs) in fish and their human health risk are currently unknown. ObjectiveTo investigate the in vivo chronic effects of exposure to LECAs and LADAs using oxytetracycline (OTC) and sulfamethoxazole (SMZ) in Nile tilapia (Oreochromis niloticus) and their human health risk. MethodsTwenty O. niloticus weighing 27.73 ± 0.81 g were exposed to water containing LECAs (OTC at 420 ng/L and SMZ at 260 ng/L) and diets supplemented with LADAs (OTC 80 mg/kg/day and SMZ 100 mg/kg/day) for twelve weeks. General physiological functions, metabolic activities, intestinal and hepatic health were systemically evaluated. The possible human health risks of the consumption of the experimental Nile tilapia fillets in adults and children were assessed by using risk quotient. ResultsAfter exposure, we observed retarded growth performance accompanied by reduced nutrients digestibility, feed efficiency, organ indices, and lipid body composition in treated fish. Antibiotics distorted intestinal morphological features subsequently induced microbiota dysbiosis and suppressed intestinal tight junction proteins. Exposure of fish to LECAs and LADAs induced oxidative stress, suppressed innate immunity, stimulated inflammatory and detoxification responses, concomitantly inhibited antioxidant capacity and caused lipid peroxidation in intestine and liver organs. Both LECAs and LADAs enhanced gluconeogenesis, inhibited lipogenesis and fatty acid beta oxidation in intestine and liver organs. The exposure of fish to LECAs and LADAs induced anaerobic glycolytic pathway and affected intestinal fat catabolism in intestine while halted aerobic glycolysis, increased hepatic fat catabolism, and induced DNA damage in liver. The hazard risk quotient in children for fish treated with OTCD was >1 indicating human health risk. ConclusionOverall, both LECAs and LADAs impair general physiological functions, nutritional metabolism, and compromise fish immune system. Consumption of fish fed with legal OTC provokes health risk in children. Global stringent prohibition policy for use of antibiotics in aquaculture production and strategies to limit their release into the environment are urgently required to protect human health.

Multiple mechanistic action of Rosmarinus officinalis L. extract against ethanol effects in an acute model of intestinal damage

The high levels of oxidative stress and inflammation can be present in the etiology of degenerative intestinal pathologies associated with ethanol ingestion. The Rosmarinus officinalis L. has exhibited several physiological and medicinal activities. In this investigation, we intended to clarify, for the first time, the antioxidant and anti-inflammatory effects of ethanolic extract of Rosmarinus officinalis L. (eeRo) against an acute damage induced by ethanol, specifically in the small intestine of rats. The rats were treated three times, at every 24 h, with eeRo at 500–1000 mg/kg or vehicle, oral gavage. All groups got a single dose of ethanol (2 ml/kg), oral gavage, after 36 h of fasting and 1 h after the last dose of eeRo or vehicle administration. We performed the mensuration of oxidative stress profile in lipid peroxidation in serum and intestine; Na+/K+ ATPase, catalase, and superoxide dismutase activities assays only in intestine; and anti-inflammatory evidences of eeRo in myeloperoxidase activity assay only in the intestine. The eeRo was able to protect the animals against the lipid peroxidation in serum and intestine. It prevented the reduction in Na+/K+ ATPase and catalase levels induced by ethanol in the intestine. In addition, eeRo increased the superoxide dismutase activity when compared to control and protected the intestine against elevations in myeloperoxidase activity caused by ethanol. Our results suggested that eeRo exerted a significant intestinal protective effect by antioxidant and anti-inflammatory mechanisms. Thus, the eeRo represented a promising agent against intestinal lesions induced by ethanol.

Glutamate attenuates lipopolysaccharide-induced oxidative damage and mRNA expression changes of tight junction and defensin proteins, inflammatory and apoptosis response signaling molecules in the intestine of fish

The present study explored the possible preventive effects of dietary glutamate (Glu) on LPS-induced oxidative damage, mRNA expression changes of tight junction (TJ) and defensin proteins, inflammatory and apoptosis response signaling molecules in fish intestine. Young Jian carp were fed five diets supplemental graded levels of Glu (0, 4, 8, 16 and 32 g kg−1 diet) for 63 days. The results indicated that Glu supplementation depressed LPS induced the production of reactive oxygen species (ROS) and severe oxidative damage (lipid peroxidation and protein oxidation) in fish intestine, which was partially due to the increased glutathione (GSH) content and antioxidant enzyme activities including superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione-S-transferase (GST), and glutathione reductase (GR) (P < 0.05). Further investigations indicated that Glu supplementation caused elevation of those antioxidant enzyme activities are related to the up-regulation of corresponding antioxidant enzymes and the related signaling factor Nrf2 mRNA levels (P < 0.05). Meanwhile, Glu pre-treatment significantly suppressed LPS-induced COX-2 and inflammatory cytokines mRNA expression and down-regulated NF-κB p65 and MAPK p38 transcription. Furthermore, pre-treatment with Glu prevented LPS induced apoptosis-related gene expression (caspase 3 and 9, P < 0.05). Lastly, Glu supplementation also attenuated LPS induced intestinal barrier function-related gene TJ proteins (ZO-1, occludin1, claudin2, 3, and 7), β-defensin1 and 3 mRNA expressions decreasing (P < 0.05). Taken together, the present results showed Glu could attenuate LPS induced the oxidative damage by Nrf2 signal pathway and depress LPS induced inflammation response (cytokines, COX-2, NF-κB p65, and MAPK p38), apoptosis (caspase3 and 9), and barrier function (ZO-1, occludin1, claudin2, 3 and 7, and β-defensin 1 and 3)-related gene expression changes of fish intestine.