MicroRNA‐27a‐3p suppression of peroxisome proliferator‐activated receptor‐γ contributes to cognitive impairments resulting from sevoflurane treatment

Sevoflurane is the most widely used anaesthetic administered by inhalation. Exposure to sevoflurane in neonatal mice can induce learning deficits and abnormal social behaviours. MicroRNA (miR)‐27a‐3p, a short, non‐coding RNA that functions as a tumour suppressor, is up‐regulated after inhalation of anaesthetic, and peroxisome proliferator‐activated receptor γ (PPAR‐γ) is one of its target genes. The objective of this study was to investigate how the miR‐27a‐3p–PPAR‐γ interaction affects sevoflurane‐induced neurotoxicity. A luciferase reporter assay was employed to identify the interaction between miR‐27a‐3p and PPAR‐γ. Primary hippocampal neuron cultures prepared from embryonic day 0 C57BL/6 mice were treated with miR‐27a‐3p inhibitor or a PPAR‐γ agonist to determine the effect of miR‐27a‐3p and PPAR‐γ on sevoflurane‐induced cellular damage. Cellular damage was assessed by a flow cytometry assay to detect apoptotic cells, immunofluorescence to detect reactive oxygen species, western blotting to detect NADPH oxidase 1/4 and ELISA to measure inflammatory cytokine levels. In vivo experiments were performed using a sevoflurane‐induced anaesthetic mouse model to analyse the effects of miR‐27a‐3p on neurotoxicity by measuring the number of apoptotic neurons using the Terminal‐deoxynucleoitidyl Transferase Mediated Nick End Labeling (TUNEL) method and learning and memory function by employing the Morris water maze test. Our results revealed that PPAR‐γ expression was down‐regulated by miR‐27a‐3p following sevoflurane treatment in hippocampal neurons. Down‐regulation of miR‐27a‐3p expression decreased sevoflurane‐induced hippocampal neuron apoptosis by decreasing inflammation and oxidative stress‐related protein expression through the up‐regulation of PPAR‐γ. In vivo tests further confirmed that inhibition of miR‐27a‐3p expression attenuated sevoflurane‐induced neuronal apoptosis and learning and memory impairment. Our findings suggest that down‐regulation of miR‐27a‐3p expression ameliorated sevoflurane‐induced neurotoxicity and learning and memory impairment through the PPAR‐γ signalling pathway. MicroRNA‐27a‐3p may, therefore, be a potential therapeutic target for preventing or treating sevoflurane‐induced neurotoxicity.

     

Increased 4‐hydroxy‐2‐nonenal‐induced proteasome dysfunction is correlated with cardiac damage in streptozotocin‐injected rats with isoproterenol infusion

Increase in 4‐hydroxy‐2‐nonenal (4HNE) due to oxidative stress has been observed in a variety of cardiac diseases such as diabetic cardiomyopathy. 4HNE exerts a damaging effect in the myocardium by interfering with subcellular organelles like mitochondria by forming adducts. Therefore, we hypothesized that increased 4HNE adduct formation in the heart results in proteasome inactivation in isoproterenol (ISO)‐infused type 1 diabetes mellitus (DM) rats. Eight‐week‐old male Sprague Dawley rats were injected with streptozotocin (STZ, 65 mg kg^?1). The rats were infused with ISO (5 mg kg^?1) for 2 weeks by mini pumps, after 8 weeks of STZ injection. We studied normal control (n = 8) and DM + ISO (n = 10) groups. Cardiac performance was assessed by echocardiography and Millar catheter at the end of the protocol at 20 weeks. Initially, we found an increase in 4HNE adducts in the hearts of the DM + ISO group. There was also a decrease in myocardial proteasomal peptidase (chymotrypsin and trypsin‐like) activity. Increases in cardiomyocyte area (446 ± 32·7 vs 221 ± 10·83) (µm²), per cent area of cardiac fibrosis (7·4 ± 0·7 vs 2·7 ± 0·5) and cardiac dysfunction were also found in DM + ISO (P < 0·05) relative to controls. We also found increased 4HNE adduct formation on proteasomal subunits. Furthermore, reduced aldehyde dehydrogenase 2 activity was observed in the myocardium of the DM + ISO group. Treatment with 4HNE (100 μM) for 4 h on cultured H9c2 cardiomyocytes attenuated proteasome activity. Therefore, we conclude that the 4HNE‐induced decrease in proteasome activity may be involved in the cardiac pathology in STZ‐injected rats infused with ISO. Copyright © 2016 John Wiley & Sons, Ltd.     

Protective effects of antioxidant combination against D‐galactosamine‐induced kidney injury in rats

The protective effects of an antioxidant combination in kidney injury induced by the injection of D‐galactosamine (D‐GaIN) were examined in the present study. Sprague Dawley female rats were used and divided into four groups as follows: (1) animals injected physiological saline solution, intraperitoneally, (2) animals treated with the combination of ascorbic acid (100 mg kg^?1 day^?1), β‐carotene (15 mg kg^?1 day^?1), α‐tocopherol (100 mg kg^?1 day^?1), and sodium selenate (0.2 mg kg^?1 day^?1) for three days orally, (3) rats injected D‐GaIN (500 mg kg^?1) intraperitoneally as a single dose, and (4) animals treated with the antioxidant combination for three days, then injected D‐GaIN. The tissue and blood samples of animals were collected for morphological and biochemical evaluations. Histopathological injury in kidney tissues was observed together with a significant increase in tissue lipid peroxidation (LPO) level, myeloperoxidase (MPO), lactate dehydrogenase, catalase and superoxide dismutase (SOD) activities, and serum creatinine and urea levels, and a significant decrease in glutathione level and glutathione peroxidase activity in D‐GaIN injected rats. However, a decrease in the degenerative changes was detected in the kidney tissue of D‐GaIN + antioxidant group, and biochemical results showed reversed effects. In conclusion, it seems reasonable to conclude that the treatment of the antioxidant combination has a protective effect on D‐GaIN‐induced kidney injury of rats. Copyright © 2010 John Wiley & Sons, Ltd.     

BIOSYNTHESIS OF POLY‐3‐HYDROXYBUTYRATE (PHB) IN THE TRANSGENIC GREEN ALGA CHLAMYDOMONAS REINHARDTII1

A cell‐wall deficient strain of Chlamydomonas reinhardtii P. A Dang. CC‐849 was cotransformed with two expression vectors, p105B124 and pH105C124, containing phbB and phbC genes, respectively, from Ralstonia eutropha. The transformants were selected on Tris‐acetate‐phosphate media containing 10 μg · mL^?1 Zeomycin. Upon further screening, the transgenic algae were subcloned and maintained in culture. PCR analysis demonstrated that both phbB and phbC genes were successfully integrated into the algal nuclear genome. Poly‐3‐hydroxybutyrate (PHB) synthase activity in these transgenic algae ranged from 5.4 nmol · min^?1 · mg protein^?1 to 126 nmol · min^?1 · mg protein^?1. The amount of PHB in double transgenic algae was determined by gas chromatography–mass spectrometry (GC–MS) when comparing with PHB standard. In addition, PHB granules were observed in the cytoplasm of transgenic algal cells using TEM, which indicated that PHB was synthesized in transgenic C. reinhardtii. Hence, results clearly showed that producing PHB in C. reinhardtii was feasible. Further studies would focus on enhancing PHB production in the transgenic algae and targeting the chloroplast for PHB accumulation.     

Cd AND Zn TOLERANCE AND ACCUMULATION BY SEDUM JINIANUM IN EAST CHINA

Field survey, hydroponic culture, and pot experiments were carried out to examine and characterize cadmium (Cd) and zinc (Zn) uptake and accumulation by Sedum jinianum, a plant species native to China. Shoot Cd and Zn concentrations in S. jinianum growing on a lead/Zn mine area reached 103–478 and 4165–8349 mg kg^?1 (DM), respectively. The shoot Cd concentration increased with the increasing Cd supply, peaking at 5083 mg kg^?1 (DM) when grown in nutrient at a concentration of 100 μmol L^?1 for 32 d, and decreased as the solution concentration increased from 200 to 400 μmol L^?1. The shoot-to-root ratio of plant Cd concentrations was > 1 when grown in solution Cd concentrations ≤ 200 μmol L^?1. Foliar, stem, and root Zn concentrations increased linearly with the increasing Zn level from 1 to 9600 μmol L^?1. The Zn concentrations in various plant parts decreased in the order roots > stem > leaves, with maximum concentrations of 19.3, 33.8, and 46.1 g kg^?1 (DM), respectively, when plants were grown at 9600 μmol Zn L^?1 for 32 d. Shoot Cd concentrations reached 16.4 and 79.8 mg kg^?1 (DM) when plants were grown in the pots of soil with Cd levels of 2.4 mg kg^?1 and 9.2 mg kg^?1, respectively. At soil Zn levels of 619 and 4082 mg kg^?1, shoot Zn concentrations reached 1560 and 15,558 mg kg^?1 (DM), respectively. The results indicate that S. jinianum is a Cd hyperaccumulator with a high capacity to accumulate Zn in the shoots.     

Protective effect of binaphthyl diselenide,a synthetic organoselenium compound,on 2‐nitropropane‐induced hepatotoxicity in rats

Organoselenides have been documented as promising pharmacological agents against a number of diseases associated with oxidative stress. Here we have investigated, for the first time, the potential antioxidant activity of binaphthyl diselenide ((NapSe)₂; 50 mg kg^?1, p.o.) against the 2‐nitropropane (2‐NP)‐induced hepatoxicity in rats, using different end points of toxicity (liver histopathology, plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatinine). In addition, in view of the association of oxidative stress with 2‐NP exposure, hepatic lipid peroxidation, ascorbic acid levels, δ‐aminolevulinate dehydratase (δ‐ALA‐D) and catalase (CAT) activities were evaluated. 2‐NP caused an increase of AST, ALT and hepatic lipid peroxidation. 2‐NP also caused hepatic histopathological alterations and δ‐ALA‐D inhibition. (NapSe)₂ (50 mg kg^?1) prevented 2‐NP‐induced changes in plasmatic ALT and AST activities and also prevented changes in hepatic histology, δ‐ALA‐D and lipid peroxidation. Results presented here indicate that the protective mechanism of (NapSe)₂ against 2‐NP hepatotoxicity is possibly linked to its antioxidant activity. Copyright © 2010 John Wiley & Sons, Ltd.     

Treatment with IFN‐γ prevents insulin‐dependent PKB,p70S6k phosphorylation and protein synthesis in mouse C2C12 myogenic cells

The purpose of the present study was to examine the potential effect of IFN‐γ (interferon‐γ) on the cellular content and phosphorylation of PKB (protein kinase B), p70^S6k (p70 S6 kinase) and MAPK (mitogen‐activated protein kinase), and on the ability of insulin to stimulate the glucose uptake and protein synthesis in mouse C2C12 myotubes. Insulin (100 nmol/l) stimulated glucose uptake in C2C12 myotubes by 203.4%. Glucose uptake in cells differentiated in the presence of IFN‐γ (10 ng/ml) was increased by 165.8% and was not further significantly modified by the addition of insulin (183.4% of control value). Insulin increased the rate of protein synthesis by 198.8%. The basal rate of protein synthesis was not affected by IFN‐γ; however, this cytokine abolished the insulin effect. Cellular levels of PKB, p70^S6k, p42^MAPK and p44^MAPK were not modified by IFN‐γ. Insulin caused the phosphorylation of PKB and the activation of p70^S6k, but not p42^MAPK and p44^MAPK. In cells differentiated in the presence of IFN‐γ, the insulin‐mediated PKB phosphorylation was significantly diminished, whereas the phosphorylation of p70^S6k was completely prevented. Pretreatment of C2C12 myogenic cells with IFN‐γ led to the marked increase in p42^MAPK phosphorylation. Exposure of C2C12 myoblasts to IFN‐γ impaired MyoD and myogenin expression and decreased the fusion index on the fifth day of differentiation. In conclusion, (i) IFN‐γ present in the extracellular environment during C2C12 myoblast differentiation prevents the stimulatory action of insulin on protein synthesis; (ii) IFN‐γ‐induced insulin resistance of protein synthesis in myogenic cells can be associated with the decreased phosphorylation of PKB and p70^S6k, as well as with the augmented basal phosphorylation of p42^MAPK; (iii) this cytokine effect can be partly explained by alterations in the differentiation process.     

PPAR‐β facilitating maturation of hepatic‐like tissue derived from mouse embryonic stem cells accompanied by mitochondriogenesis and membrane potential retention

Relatively little is known about mitochondria metabolism in differentiating embryonic stem (ES) cells. Present research focused on several elements of cellular energy metabolism in hepatic‐like tissue derived from mouse ES cells. We demonstrated that mitochondrial location patterns and mitochondrial membrane potential (ΔΨ_m) existed in subsequent differentiation of the tissue. Mitochondriogenesis appeared at the early stage and kept a normal ΔΨ_m in differentiated mature hepatocytes. Peroxisome proliferator‐activated receptor‐α (PPAR‐α) expression was transitorily increased at the beginning, and kept a relatively low level later, which accompanied by expression of PPAR‐γ coactivator (PGC)‐1α, a master regulator of mitochondrial biogenesis. PPAR‐β expression showed robust up‐regulation in the late differentiation course. Enhanced co‐expressions of PPAR‐β and albumin with catalysis of UDP‐glucuronosyltransferases (UGTs) were observed at mature stage. While PPAR‐γ expression changed little before and after differentiation. Mitochondriogenesis could be accelerated by PPAR‐α specific agonist WY14643 and abolished by its antagonist GW6471 at the early stage. Neither of them affected mitochondrial ΔΨ_m and albumin generation in the differentiated hepatocytes. Furthermore, maturation of hepatic‐like tissue and mitochondriogenesis in hepatocyte could be efficiently stimulated by PPAR‐β specific agonist L165041 and abolished by PPAR‐β specific antagonist GSK0660, but not affected by PPAR‐γ specific agonist GW1929. In conclusion, the derived hepatic tissue morphologically possessed cellular energy metabolism features. PPAR‐α seemed only necessary for early mitochondriogenesis, while less important for ΔΨ_m retention in the mature tissue derived. The stimulation of PPAR‐β but not ‐γ enhanced hepatogenesis, hepatocytes maturation, and mitochondriogenesis. PPAR‐β took an important role in cellular energy metabolism of hepatogenesis. J. Cell. Biochem. 109: 498–508, 2010. © 2009 Wiley‐Liss, Inc.     

Bone‐marrow‐derived mesenchymal stem cells inhibit gastric aspiration lung injury and inflammation in rats

Gastric aspiration lung injury is one of the most common clinical events. This study investigated the effects of bone‐marrow‐derived mesenchymal stem cells (BMSCs) on combined acid plus small non‐acidified particle (CASP)‐induced aspiration lung injury. Enhanced green fluorescent protein (EGFP⁺) or EGFP^? BMSCs or 15d‐PGJ₂ were injected via the tail vein into rats immediately after CASP‐induced aspiration lung injury. Pathological changes in lung tissues, blood gas analysis, the wet/dry weight ratio (W/D) of the lung, levels of total proteins and number of total cells and neutrophils in bronchoalveolar lavage fluid (BALF) were determined. The cytokine levels were measured using ELISA. Protein expression was determined by Western blot. Bone‐marrow‐derived mesenchymal stem cells treatment significantly reduced alveolar oedema, exudation and lung inflammation; increased the arterial partial pressure of oxygen; and decreased the W/D of the lung, the levels of total proteins and the number of total cells and neutrophils in BALF in the rats with CASP‐induced lung injury. Bone‐marrow‐derived mesenchymal stem cells treatment decreased the levels of tumour necrosis factor‐α and Cytokine‐induced neutrophil chemoattractant (CINC)‐1 and the expression of p‐p65 and increased the levels of interleukin‐10 and 15d‐PGJ₂ and the expression of peroxisome proliferator‐activated receptor (PPAR)‐γ in the lung tissue in CASP‐induced rats. Tumour necrosis factor‐α stimulated BMSCs to secrete 15d‐PGJ₂. A tracking experiment showed that EGFP⁺ BMSCs were able to migrate to local lung tissues. Treatment with 15d‐PGJ₂ also significantly inhibited CASP‐induced lung inflammation and the production of pro‐inflammatory cytokines. Our results show that BMSCs can protect lung tissues from gastric aspiration injury and inhibit lung inflammation in rats. A beneficial effect might be achieved through BMSC‐derived 15d‐PGJ₂ activation of the PPAR‐γ receptor, reducing the production of proinflammatory cytokines.     

Ex vivo protective effects of nicotinamide and 3‐aminobenzamide on rat synaptosomes treated with Aβ(1–42)

Alzheimer's disease (AD) is the most common form of dementia and is characterized by the presence of senile plaques and neurofibrillary tangles, along with synaptic loss. The underlying mechanisms of AD are not clarified yet, but oxidative stress and mitochondrial dysfunction are important factors. Overactivation of poly(adenosine diphosphate ribose) polymerase‐1 (PARP‐1) enzyme has been known to cause neuroinflammation and cell death in neurodegenerative processes. The aim of the present study was to investigate the protective effects of the PARP‐1 inhibitors, 3‐aminobenzamide (3‐AB) and nicotinamide (NA), against amyloid β peptide (1–42) (Aβ(1–42))‐induced oxidative damage and mitochondrial reduction capacity on isolated synaptosomes. Rats were injected intraperitoneally with 3‐AB (30–100 mg kg^?1), NA (100–500 mg kg^?1) or with saline for 7 days. Synaptosomes were incubated with 10–30 μM Aβ(1–42) or saline for 6 h at 37 °C. Ex vivo Aβ(1–42) treatment significantly induced oxidative stress and mitochondrial dysfunction in synaptosomes of the saline group, while synaptosomes of 3‐AB and NA groups showed significant decreases in lipid peroxidation, reactive oxygen species production and protein oxidation. Moreover, both NA and 3‐AB were able to improve the mitochondrial reduction capacity against Aβ(1–42). These data suggest that NA and 3‐AB may have protective effects in neurodegenerative processes because of the reduced levels of oxidative stress and the improvement of mitochondrial function. Copyright © 2014 John Wiley & Sons, Ltd.     

Cistanches alleviates sevoflurane‐induced cognitive dysfunction by regulating PPAR‐γ‐dependent antioxidant and anti‐inflammatory in rats

This study aimed to investigate the protective effects and underlying mechanisms of cistanche on sevoflurane‐induced aged cognitive dysfunction rat model. Aged (24 months) male SD rats were randomly assigned to four groups: control group, sevoflurane group, control + cistanche and sevoflurane + cistanche group. Subsequently, inflammatory cytokine levels were measured by ELISA, and the cognitive dysfunction of rats was evaluated by water maze test, open‐field test and the fear conditioning test. Three days following anaesthesia, the rats were killed and hippocampus was harvested for the analysis of relative biomolecules. The oxidative stress level was indicated as nitrite and MDA concentration, along with the SOD and CAT activity. Finally, PPAR‐γ antagonist was used to explore the mechanism of cistanche in vivo. The results showed that after inhaling the sevoflurane, 24‐ but not 3‐month‐old male SD rats developed obvious cognitive impairments in the behaviour test 3 days after anaesthesia. Intraperitoneal injection of cistanche at the dose of 50 mg/kg for 3 consecutive days before anaesthesia alleviated the sevoflurane‐induced elevation of neuroinflammation levels and significantly attenuated the hippocampus‐dependent memory impairments in 24‐month‐old rats. Cistanche also reduced the oxidative stress by decreasing nitrite and MDA while increasing the SOD and CAT activity. Moreover, such treatment also inhibited the activation of microglia. In addition, we demonstrated that PPAR‐γ inhibition conversely alleviated cistanche‐induced protective effect. Taken together, we demonstrated that cistanche can exert antioxidant, anti‐inflammatory, anti‐apoptosis and anti‐activation of microglia effects on the development of sevoflurane‐induced cognitive dysfunction by activating PPAR‐γ signalling.     

Influence of kolaviron and vitamin E on ethylene glycol monoethyl ether‐induced haematotoxicity and renal apoptosis in rats

The present study investigated the protective effects of kolaviron, a biflavonoid from the seed of Garcinia kola, and vitamin E on ethylene glycol monoethyl ether (EGEE)‐induced haematotoxicity and renal apoptosis in male rats. EGEE was administered at a dose of 200 mg kg^?1 alone or simultaneously administered with kolaviron (100 and 200 mg kg^?1) and vitamin E (50 mg kg^?1) for 14 days. Results of haematological examination showed that white blood cells, platelets, neutrophils and mean corpuscular haemoglobin concentration were significantly lower, whereas lymphocytes were increased in EGEE‐exposed rats compared with those in the control. Administration of EGEE caused a significant decrease in the superoxide dismutase and catalase activities as well as in the glutathione level but significantly increased glutathione Stransferase activity and levels of hydrogen peroxide and lipid peroxidation in kidneys of rats compared with those in the control. Also, EGEE‐treated rats showed significant elevation in the serum urea and creatinine with marked increase in the frequency of terminal deoxynucleotidyl transferase‐mediated dUTP nick end labelling assay‐positive apoptotic cells in the tubular epithelial cells in comparison with the control. Co‐administration with kolaviron or vitamin E exhibited chemoprotective effects against EGEE‐mediated haematotoxicity, augmented renal antioxidant status and prevented the induction of renal apoptosis. Copyright © 2013 John Wiley & Sons, Ltd.     

Chemical Synthesis of 3D Graphene‐Like Cages for Sodium‐Ion Batteries Applications

Sodium (Na) super ion conductor structured Na₃V₂(PO₄)₃ (NVP) is extensively explored as cathode material for sodium‐ion batteries (SIBs) due to its large interstitial channels for Na⁺ migration. The synthesis of 3D graphene‐like structure coated on NVP nanoflakes arrays via a one‐pot, solid‐state reaction in molten hydrocarbon is reported. The NVP nanoflakes are uniformly coated by the in situ generated 3D graphene‐like layers with the thickness of 3 nm. As a cathode material, graphene covered NVP nanoflakes exhibit excellent electrochemical performances, including close to theoretical reversible capacity (115.2 mA h g^?1 at 1 C), superior rate capability (75.9 mA h g^?1 at 200 C), and excellent cyclic stability (62.5% of capacity retention over 30000 cycles at 50 C). Furthermore, the 3D graphene‐like cages after removing NVP also serve as a good anode material and deliver a specific capacity of 242.5 mA h g^?1 at 0.1 A g^?1. The full SIB using these two cathode and anode materials delivers a high specific capacity (109.2 mA h g^?1 at 0.1 A g^?1) and good cycling stability (77.1% capacity retention over 200 cycles at 0.1 A g^?1).     

EFFECT OF INDOLE-3-ACETIC ACID,KINETIN, AND ETHYLENEDIAMINETETRAACETIC ACID ON PLANT GROWTH AND UPTAKE AND TRANSLOCATION OF LEAD,MICRONUTRIENTS, AND MACRONUTRIENTS IN ALFALFA PLANTS

Alfalfa plants germinated and grown for 15 d in soil containing 80 mg Pb kg^?1 were treated with ethylenediaminetetraacetic acid (EDTA) at 0.8 mM and indole-3-acetic acid-kinetin (IAA-KN) at 100 μM. Fifteen days after the treatment application, the concentration of lead (Pb), macronutrients, and micronutrients was determined using inductively coupled plasma/optical emission spectroscopy. The chlorophyll content and plant growth were also measured. Roots of plants exposed to Pb alone, Pb–EDTA, and Pb–EDTA-IAA-KN had 160, 140, and 150 mg Pb kg^?1 DW, respectively. Pb was not detected in the stems of plants exposed to Pb alone; however, stems of plants treated with EDTA and EDTA–IAA-KN had 78 and 142 mg Pb kg^?1 DW, respectively. While the Pb concentration in leaves of plants treated with EDTA and EDTA–IAA-KN was 92 and 127 mg kg^?1 DW, respectively. In addition, EDTA and EDTA–IAA-KN significantly increased the translocation of zinc and manganese to leaves. The x-ray absorption spectroscopic studies demonstrated that Pb(II) was transported from roots to leaves without a change in the oxidation state.     

Effect of dietary dextrin levels on the growth performance,blood chemistry,body composition,hepatic triglicerides and glycogen of Lebranche mullet juveniles (Mugil liza Valenciennes 1836, Mugilidae)

The effects of increasing levels of dietary dextrin on growth performance, body composition, blood chemistry and hepatic triglycerides and glycogen levels were evaluated for juvenile Lebranche mullet, Mugil liza Valenciennes 1836, Mugilidae). Five diets were formulated to be isonitrogenous (350 g kg^?1) and isolipidic (6 g kg^?1) with increasing dextrin levels (D150: 150 g kg^?1; D200: 200 g kg^?1; D250: 250 g kg^?1; D300: 300 g kg^?1; D350: 350 g kg^?1). The experimental diets were offered to the fish for 34 days, four times per day, until apparent satiation. Each treatment was tested in triplicate, with nine fish per tank (mean weight 4.69 ± 0.31 g). Fish were reared in a recirculating aquatic system of 15 fibreglass tanks each containing 50 L of saltwater. Growth parameters and body composition of the mullets were not significantly affected (P > 0.05) by the dietary treatments. Plasma glucose concentration declined (P < 0.05) when dietary dextrin increased from D250 to D300, but recovered to the previous values (in reference to D150 and D200) when fish were fed with D350. Glycated haemoglobin, plasma proteins, triglycerides and cholesterol showed no significant differences among these treatments. Hepatic glycogen reached a maximum in treatment D250, followed by D350, D200 and D300, with the lowest concentration of liver glycogen found in D150 (P < 0.05). The concentration of liver triglycerides showed an increase (P < 0.05) in treatments D300 and D350 compared with D200. In conclusion, Mugil liza juveniles can be fed diets with high levels of dietary dextrin with no deleterious effects to their growth or plasma biochemistry, hepatic glycogen or triglycerides.