Glutamate Concentrations Research Articles

Calcium Involved in the Enrichment of γ-Aminobutyric Acid (GABA) in Broccoli Sprouts under Fructose Treatment.

The effect of fructose on γ-aminobutyric acid (GABA) content and its metabolic pathway in broccoli sprouts was investigated. The results demonstrated that the fructose treatment not only significantly increased the fresh weight, GABA, and glutamate contents in sprouts, but also promoted the activity of glutamic acid decarboxylase (GAD) and the expressions of BoGAD1 and BoGAD2. Meanwhile, fructose treatment inhibited the stem length of broccoli sprouts and enhanced the abscisic acid (ABA) production in comparison with the control. Ca2+, CaM contents, and BoCaM2 expression in broccoli sprouts were also stimulated after fructose treatment. Exogenous fructose increased inositol trisphosphate (IP3) content and activated the activity of phosphatidylinositol-specific phospholipase C (PI-PLC) and the expression of BoPLC2, contributing to Ca2+ influx into the cells. These results suggested that Ca2+ played an essential role in GABA enrichment under fructose treatment, which may be associated with GAD and PI-PLC.

One-carbon metabolism and related pathways in ruminal and small intestinal epithelium of lactating dairy cows.

Physiological and environmental stresses such as the transition into lactation and heat load contribute to gastrointestinal tract (GIT) dysfunction. The nonruminant gastrointestinal tract has mechanisms to cope with pro-oxidant and pro-inflammatory stressors arising from the gut lumen or within intestinal cells. One-carbon metabolism (OCM) contributes to anti-oxidant capacity via the production of glutathione (GSH) and taurine, and the synthesis of phospholipid, creatine, and the osmolyte glycinebetaine among others. A multipronged approach was used to assess the biological relevance of OCM and closely-related pathways on GIT function in dairy cows. Ruminal papillae (Rum) and scrapings from duodenum (Duo), jejunum (Jej), and ileum (Ile) were collected at slaughter from eight multiparous Holstein cows averaging 128 ± 12 d in milk and producing 39 ± 5 kg/d. A MIXED model ANOVA with preplanned orthogonal contrasts was used for statistical analysis. Methionine adenosyl transferase 1 activity (MAT) was ~10-fold greater (P < 0.01) and cystathionine β-synthase activity doubled in Rum vs. small intestine. Total glutathione peroxidase (GPX) activity was greatest (P = 0.03) in Ile, but similar to Rum. Activity and mRNA abundance of betaine-homocysteine S-methyltransferase were undetectable. There was a 2.5-fold greater protein abundance of GPX1 (P < 0.01) and a ~2-fold greater abundance of GPX3 (P < 0.01) in Rum vs. small intestine. Among the various amino acids (AA) with roles in OCM or closely-related pathways (e.g. creatine synthesis), concentrations of arginine, aspartate, glutamine, methionine, and serine were lower (P < 0.01) in Rum vs. small intestine. Unlike AA, concentrations of OCM-related intermediates S-5'-adenosyl-homocysteine (SAH), glycinebetaine, carnitine, creatine (CRE), and cysteinesulfinic acid were greater (P < 0.01) while taurine was lower in Rum vs. small intestine. Intermediates of the folate cycle were undetectable. The fact that S-adenosylmethionine (SAM) was undetectable while MAT activity and SAH were greater in Rum suggested that availability of SAM (a methyl donor) is a key determinant of flux through the folate and methionine cycles in the GIT. Except for adenosine, concentrations of glutamate, glycine, α-ketoglutarate, hypotaurine, and GSH were lowest in Ile. Together, the data underscored unique differences in activity of one-carbon metabolism and related pathways across sections of the GIT.

Ozone reduces ischemic damage after a stroke by regulating the autophagy of astrocytes.

Stroke is a common and damaging disease of brain tissue, and has high morbidity, disability, and mortality rates. Ozone (O3) is an isomer of oxygen and can be applied to ozonate the isolated blood in specific containers outside the body and return it to the body. O3 can also alter the activity and function of multiple cellular components, thus affecting blood viscosity and altering hemodynamics. However, the question of whether O3 has clinical value in the treatment of stroke requires further investigation. This study sought to evaluate the protective effect and possible mechanism of O3 in brain injury after stroke. First, oxygen-glucose deprivation/reoxygenation (OGD/R)-induced human glioblastoma cell (A172) and middle cerebral artery occlusion (MCAO) rat models were established. Second, the levels of the associated ribonucleic acids and proteins were analyzed using reverse-transcription real-time-quantitative polymerase chain reaction, Western Blot, or immunofluorescence assays. Third, the concentration of glutamate and lactate dehydrogenase (LDH) were assessed using enzyme-linked immunoassays. The results showed that glial fibrillary acidic protein was upregulated in the OGD/R A172 cells. O3 decreased LDH and increased glutamate levels in the OGD/R A172 cells, which suggests that O3 reduced brain damage in the in vitro stroke model. We also showed that O3 attenuated brain infarction in the in-vivo stroke model. Further, we found that O3 alleviated stroke-induced brain damage by reducing the apoptosis of astrocytes. Further, the B-cell lymphoma 2 inhibitor propofol alleviated stroke-induced brain damage. Thus, O3 notably alleviated stroke-induced brain damage by inhibiting the apoptosis of astrocytes in the OGD/R-induced human glioblastoma cell and MACO rat models.

Effects of Oxytocin on Glutamate Mediated Neurotoxicity in Neuroblastoma Cell Culture.

We aimed to investigate the effects of oxytocin on neurite growth, cell viability, cell proliferation and apoptosis to demonstrate its neuroprotective effect on glutamate induced neurotoxicity in human neuroblastoma SH-SY5Y cell culture. The effect of oxytocin on the toxic effects of glutamate in human neuroblastoma SH-SY5Y cell line with the Neurotoxicity Screening Test (NTT), apoptotic effects by Terminal Transferase dUTP Nick End Labeling (TUNEL) method and cell viability test by 3-(4.5-dimethylthiazol-2-yl)-2.5-diphenyltetrazolium bromide (MTT) method. In the NTT test; Neurotoxicity was induced by adding glutamate at a concentration of 32 μM to the cell culture. Oxytocin was added at 1, 3, 10, 30 and 100 μM concentrations and its effect on neurite elongation was investigated. It was demonstrated by TUNEL method that application of glutamate caused apoptosis. Afterwards, when glutamate and different doses of oxytocin were given, antiapoptotic effect was evaluated with the apoptotic index. Glutamate was found to have a dose-dependent neurotoxic effect and reduced neurite elongation by 50% at a concentration of 32 μM. It was shown that the inhibition of neurite elongation caused by glutamate decreased in a dose-dependent manner by applying oxytocin. Especially oxytocin was found to significantly reduce neurite inhibition and show a neuroprotective effect starting from 10 μM concentrations. The concentration at which glutamate reduces cell proliferation by 50% was determined as 54 μM in MTT. Subsequently, it was observed that the adverse effect of glutamate on cell proliferation significantly decreased with oxytocin administration, depending on the dose. It was found that different concentrations of glutamate have a significant toxic effect on cell proliferation and viability, glutamate inhibits neurite elongation in a dose-dependent manner; oxytocin reduces neurite inhibition caused by glutamate, has a neuroprotective effect, increases cell viability and has antiapoptotic effects.

Increased brain 1H-MRS glutamate and lactate signals following maximal aerobic capacity exercise in young healthy males: an exploratory study.

Physical exercise involves increased neuronal activity of many brain structures, but 1H-MRS investigations on the effects of human brain glutamate (Glu) concentrations on acute exercise have been sparse. Previous studies consistently found increases in brain lactate (Lac) concentrations following graded exercise up to 85% of the predicted maximal heart rate. However, the reported effects on brain concentrations of glutamine and glutamate were not consistent. This study aimed to determine the effect of acute intense graded maximal exercise on 1H-MRS signals related to concentrations of Glu, glutamate+glutamine (Glx), and Lac. Young adult males were randomly divided into two groups and subjected to 1H-MRS when resting (NE) or shortly after cessation of the intense graded exercise intended to pass the anaerobic threshold (E). 1H-MRS spectra were acquired from the large voxel encompassing the occipito-parietal cortex only once. Estimates of Glu, Glx, and Lac concentrations were calculated in institutional units by normalizing to a spectroscopic signal originating from creatine-containing compounds (Cr). Concentrations of Glu, Glx, and Lac were respectively 11%, 12.6%, and 48.5% higher in E than in NE (p < 0.001). The increased brain Lac signal in the exercising group indicated that in our experiment, vigorous exercise resulted in passing the anaerobic threshold and lactate apparently entered the brain. Concomitantly glutamate-related resonance signals from the vicinity of the occipito-parietal cortex were significantly increased; physiological mechanisms underlying these phenomena require further study. Future studies should evaluate whether the normalization rate of these concentrations is a marker of general physical fitness.

Sex differences in the acute effects of guanfacine on dACC glutamate concentrations in individuals with an alcohol use disorder

Sex differences in the acute effects of guanfacine on dACC glutamate concentrations in individuals with an alcohol use disorder

Hippocampal Glutamate, Resting Perfusion and the Effects of Cannabidiol in Psychosis Risk.

Preclinical and human data suggest that psychosis onset involves hippocampal glutamatergic dysfunction, driving hyperactivity and hyperperfusion in a hippocampal-midbrain-striatal circuit. Whether glutamatergic dysfunction is related to cerebral perfusion in patients at clinical high risk (CHR) for psychosis, and whether cannabidiol (CBD) has ameliorative effects on glutamate or its relationship with perfusion remains unknown. Using a double-blind, parallel-group design, 33 CHR patients were randomized to a single 600 mg dose of CBD or placebo; 19 healthy controls did not receive any drug. Proton magnetic resonance spectroscopy was used to measure glutamate concentrations in left hippocampus. We examined differences relating to CHR status (controls vs placebo), effects of CBD (placebo vs CBD), and linear between-group effects, such that placebo>CBD>controls or controls>CBD>placebo. We also examined group × glutamate × cerebral perfusion (measured using Arterial Spin Labeling) interactions. Compared to controls, CHR-placebo patients had significantly lower hippocampal glutamate (P =.015) and a significant linear relationship was observed across groups, such that glutamate was highest in controls, lowest in CHR-placebo, and intermediate in CHR-CBD (P =.031). Moreover, there was a significant interaction between group (controls vs CHR-placebo), hippocampal glutamate, and perfusion in the putamen and insula (P FWE =.012), with a strong positive correlation in CHR-placebo vs a negative correlation in controls. Our findings suggest that hippocampal glutamate is lower in CHR patients and may be partially normalized by a single dose of CBD. Furthermore, we provide the first in vivo evidence of an abnormal relationship between hippocampal glutamate and perfusion in the striatum and insula in CHR.

Effects of intrathecally administered interferon α on chronic constriction injury model rats' mechanical pain threshold and G protein expression in the spinal cord.

The aim of the study was to explore the analgesic mechanism of effects of intrathecally administered interferon a (IFN-a) on chronic constriction injury (CCI) model rats. 24 rats were divided into 6 groups, with 4 rats in each group, including the negative control group (Group N, no operation or treatment), the sham operation group (Group S, only the left sciatic nerve of the rats was exposed without ligation, 0.9% NaCl was intrathecally administered), and four experimental groups (CCI model was established first and then different drugs were intrathecally administered respectively), including 0.9% NaCl (Group C), IFN-a (Group CI), morphine (Group CM), and IFN-a combined with morphine (Group CIM). The mRNA levels of G proteins in both the spinal cord and dorsal root ganglia (DRG), as well as the content of amino acid and chemokine (C-X-C motif) ligand 6 (CXCL-6) in the cerebrospinal fluid were measured and analysed in each group. Intrathecal administration of IFN-a increased the mechanical pain threshold in CCI rats (33.32 ±1.36 vs. 21.08 ±1.59, p < 0.001), achieving the effect comparable to that of morphine (33.32 ±1.36 vs. 32.44 ±3.18, p > 0.05), increased the mRNA expression level of Gi protein (0.62 ±0.04 vs. 0.49 ±0.05, p = 0.006), and decreased the mRNA expression level of Gs protein in the spinal cord (1.80 ±0.16 vs. 2.06 ±0.15, p = 0.035) and DRG (2.11 ±0.10 vs. 2.79 ±0.13, p < 0.001). The intrathecal administration of both IFN-a and morphine can reduce the glutamate content in the cerebrospinal fluid (261.55 ±38.12 vs. 347.70 ±40.69, p = 0.012), but without any statistically significant difference in the content of CXCL-6 across all groups ( p > 0.05). Intrathecal injection of IFN-a improved the mechanical pain threshold in CCI rats, so we inferred that intrathecal administration of IFN-a had analgesic effects on neuropathic pain, possibly related to the activation of G-proteincoupled µ receptors in the spinal cord and the inhibition of glutamate release.

Enhancement of γ-aminobutyric acid and relevant metabolites in brown glutinous rice (Oryza sativa L.) through salt stress and low-frequency ultrasound treatments at pre-germination stage

In order to fortify γ-aminobutyric acid (GABA) of brown glutinous rice (BGR), pre-germination strategy was employed, and effects of low-frequency (28 kHz) ultrasound treatment combined with CaCl2 stress on the sprout length, germination rate, morphology, color, water, total polyphenol content (TPC), starch, protein, GABA contents and relevant metabolites were investigated. The germination rate would be inhibited under CaCl2 concentration ≥ 2.0 % during 24 h soaking without ultrasound treatment, and no significant difference was also observed combined with 9 h ultrasound treatment. Ultrasound treatment was beneficial to water absorption, TPC enrichment, energy metabolism, lipid metabolism and protein hydrolysis. Higher contents of GABA (3.29 folds), pyruvic acid (7.63 folds), glycerol (4.88 folds), glutamate (2.02 folds) and glucose (1.32 folds) were obtained due to the antagonistic effect between the 30 w ultrasound treatment and 2.0 % CaCl2 stress at the 9 h pre-germination, and energy, lipid and protein metabolomic pathways were all involved in the GABA accumulation.

Biochemical monitoring throughout all stages of rabies virus-like particles production by Raman spectroscopy using global models

This work aimed to quantify growth and biochemical parameters (viable cell density, Xv; cell viability, CV; glucose, lactate, glutamine, glutamate, ammonium, and potassium concentrations) in upstream stages to obtain rabies virus-like particles (rabies VLP) from insect cell-baculovirus system using on-line and off-line Raman spectra to calibrate global models with minimal experimental data. Five cultivations in bioreactor were performed. The first one comprised the growth of uninfected Spodoptera frugiperda (Sf9) cells, the second and third runs to obtain recombinant baculovirus (rBV) bearing Rabies G glycoprotein and matrix protein, respectively. The fourth one involved the generation of rabies VLP from rBVs and the last one was a repetition of the third one with cell inoculum infected by rBV. The spectra were acquired through a Raman spectrometer with a 785-nm laser source. The fitted Partial Least Square models for nutrients and metabolites were comparable with those previously reported for mammalian cell lines (Relative error < 15 %). However, the use of this chemometrics approach for Xv and CV was not as accurate as it was for other parameters. The findings from this work established the basis for bioprocess Raman spectroscopical monitoring using insect cells for VLP manufacturing, which are gaining ground in the pharmaceutical industry.

Parvalbumin in the metabolic pathway of glutamate and γ-aminobutyric acid: Influence on expression of GAD65 and GAD67

Parvalbumin-expressing neurons are a type of inhibitory intermediate neuron that play an important role in terminating seizures. The aim of the present study was to use lentiviral construction and packaging technology to overexpress and silence the parvalbumin gene in pheochromocytoma (PC12) cells, and to evaluate how parvalbumin influences the metabolic pathway involving glutamate and γ-aminobutyric acid (GABA). In this work, Immunofluorescence staining was used to verify the differentiation of PC12 cells into neurons after adding nerve growth factor (NGF). Western blotting and real-time quantitative polymerase chain reaction (qRT-PCR) were used to confirm lentivirus-mediated knockdown or overexpression of parvalbumin. Expression of parvalbumin, the 65-kDa GAD isoform (GAD65), and the 67-kDa GAD isoform (GAD67) in neuronal cells was examined at the mRNA and protein levels using qRT-PCR, western blotting and immunofluorescence staining, while intracellular glutamate and GABA levels were determined by high performance liquid chromatography (HPLC). We demonstrate that the expression of parvalbumin is associated with GAD65 and GAD67. Interestingly, overexpression of parvalbumin up-regulated GAD65 and GAD67, increased GABA concentration, and decreased glutamate concentration. Silencing of parvalbumin led to the opposite effects. Altogether, parvalbumin affected the expression of GAD65 and GAD67, thereby influencing the metabolic pathway involving glutamate and GABA.

Neurotoxicity of xylazine in chicks

Despite the widespread use of xylazine in veterinary medicine, studies on its neurotoxicity are limited. So, our current study aims to reveal its neurotoxicity in chicks by determining the (LD50) of xylazine in Dixon's procedure. Moreover, it aims to study the effects of a small and repeated dose of xylazine on neurobehavioral test and the toxic doses of xylazine on the concentration of (glycine and glutamate) in the plasma of chicks and on the brain tissue after 60 and 90 minutes of injection. The LD50 of xylazine by injection into the chest muscle was 26.65 mg/kg. The injection of xylazine at a dose of 3 and 6 mg/kg in the chest muscle for three consecutive days caused an inhibition in motor activity within the open field as well as a significant elevation in the tonic immobility test response, injection of xylazine at doses 48.96 mg/kg ,60 and 90 minutes after the injection led to a significant increase in the glycine concentration as well as a significant decrease in glutamate after 90 minutes in the plasma of chicks, accompanied by histological variation in the brain tissue characterized by necrosis of neurons, vasogenic edema, neurophagia, cavities, infarction, necrosis of Purkinjean cell with decrees in the number of it. Our results revealed that xylazine had neurotoxic effects in chicks, represented by inhibition of neural behavior and motor activity within the open field, accompanied by a change in the concentration of glycine and glutamate in the plasma of chicks and histological variation in the brain tissue of chicks.

Effects of dietary β-alanine supplementation on growth performance, meat quality, carnosine content, amino acid composition and muscular antioxidant capacity in Chinese indigenous Ningxiang pig.

β-alanine has been demonstrated to improve carcass traits and meat quality of animals. However, no research has been found on the effects of dietary β-alanine in the meat quality control of finishing pigs, which are among the research focus. Therefore, this study aimed to evaluate the effects of dietary β-alanine supplementation on growth performance, meat quality, carnosine content, amino acid compositionand muscular antioxidant capacity of Chinese indigenous Ningxiang pigs. The treatments contained a basal diet (control, CON) and a basal diet supplemented with 600 mg/kg β-alanine. Each treatment group consisted of five pens, with five pigs per pen. Results showed that compared with CON, supplemental β-alanine did not affect the final body weight, average daily gain, average daily feed intake and the feed-to-gain ratio of pigs. Dietary β-alanine supplementation tended to increase the pH45 min (p = 0.071) while decreasing the shear force (p = 0.085) and the drip loss (p = 0.091). Moreover, it improved (p < 0.05) the activities of glutathione peroxidase and catalase and lessened (p < 0.05) malondialdehyde concentration. Added β-alanine in diets of finishing pigs could enhance the concentrations of arginine, alanine, and glutamate (p < 0.05) in the longissimus dorsi muscle and tended to raise the levels of cysteine, glycine and anserine (p = 0.060, p = 0.098 and p = 0.091respectively). Taken together, our results showed that dietary β-alanine supplementation contributed to the improvement of the carcass traits, meat qualityand anserine content, the amelioration of muscle antioxidant capacityand the regulation of amino acid composition in Chinese indigenous Ningxiang pigs.

Effect of Carbon Sources on Glutamate Production from Corynebacterium glutamicum 2262

A comparative study between natural and synthetic environments is carried out by realizing six fermentation experiments in batch culture. The objective of this study is to consider the effect of carbon sources on growth and the production of glutamic acid by Corynebacterium glutamicum 2262. The difference between the culture media lies in the carbon source. Two natural environments of date juice, one of which is treated with invertase to hydrolyse sucrose with a concentration of total sugars of 88 g/L. Four synthetic media with a concentration of 34 g/L sugars: medium containing mixed sugars (glucose + fructose + sucrose) with rates proportional to that of date juice, the other three media are composed of a single sugar (either glucose, fructose, or sucrose). The results showed that Corynebacterium glutamicum is able to use the three sugars whether they are single or mixed, although the best results of glutamate production (8.41 g/L) are obtained on the mixture of three sugars, which explains the interest and valorisation of date waste. On the other hand, the date juice-based media are shown to have a glutamate concentration of 7.98 g/L during the hydrolysis of sucrose of date juice.

Fused in sarcoma undergoes cold denaturation: Implications for phase separation.

The mediation of liquid-liquid phase separation (LLPS) for fused in sarcoma (FUS) protein is generally attributed to the low-complexity, disordered domains and is enhanced at low temperature. The role of FUS folded domains on the LLPS process remains relatively unknown since most studies are mainly based on fragmented FUS domains. Here, we investigate the effect of metabolites on full-length (FL) FUS LLPS using turbidity assays and differential interference contrast (DIC) microscopy, and explore the behavior of the folded domains by nuclear magnetic resonance (NMR) spectroscopy. FL FUS LLPS is maximal at low concentrations of glucose and glutamate, moderate concentrations of NaCl, Zn2+ , and Ca2+ and at the isoelectric pH. The FUS RNA recognition motif (RRM) and zinc-finger (ZnF) domains are found to undergo cold denaturation above 0°C at a temperature that is determined by the conformational stability of the ZnF domain. Cold unfolding exposes buried nonpolar residues that can participate in LLPS-promoting hydrophobic interactions. Therefore, these findings constitute the first evidence that FUS globular domains may have an active role in LLPS under cold stress conditions and in the assembly of stress granules, providing further insight into the environmental regulation of LLPS.

A mean-field model of glutamate and GABA synaptic dynamics for functional MRS

Advances in functional magnetic resonance spectroscopy (fMRS) have enabled the quantification of activity-dependent changes in neurotransmitter concentrations in vivo. However, the physiological basis of the large changes in GABA and glutamate observed by fMRS (>10%) over short time scales of less than a minute remain unclear as such changes cannot be accounted for by known synthesis or degradation metabolic pathways. Instead, it has been hypothesized that fMRS detects shifts in neurotransmitter concentrations as they cycle from presynaptic vesicles, where they are largely invisible, to extracellular and cytosolic pools, where they are detectable. The present paper uses a computational modelling approach to demonstrate the viability of this hypothesis. A new mean-field model of the neural mechanisms generating the fMRS signal in a cortical voxel is derived. The proposed macroscopic mean-field model is based on a microscopic description of the neurotransmitter dynamics at the level of the synapse. Specifically, GABA and glutamate are assumed to cycle between three metabolic pools: packaged in the vesicles; active in the synaptic cleft; and undergoing recycling and repackaging in the astrocytic or neuronal cytosol. Computational simulations from the model are used to generate predicted changes in GABA and glutamate concentrations in response to different types of stimuli including pain, vision, and electric current stimulation. The predicted changes in the extracellular and cytosolic pools corresponded to those reported in empirical fMRS data. Furthermore, the model predicts a selective control mechanism of the GABA/glutamate relationship, whereby inhibitory stimulation reduces both neurotransmitters, whereas excitatory stimulation increases glutamate and decreases GABA. The proposed model bridges between neural dynamics and fMRS and provides a mechanistic account for the activity-dependent changes in the glutamate and GABA fMRS signals. Lastly, these results indicate that echo-time may be an important timing parameter that can be leveraged to maximise fMRS experimental outcomes.

Polylactic acid microplastics induce higher biotoxicity of decabromodiphenyl ethane on earthworms (Eisenia fetida) compared to polyethylene and polypropylene microplastics

Decabromodiphenyl ethane (DBDPE) and microplastics (MPs), such as fossil-based polymers polyethylene (PE), polypropylene (PP), and bio-based plastics polylactic acid (PLA) are abundant in e-waste dismantling areas. However, the information on the effects of DBDPE combined with MPs (DBDPE-MPs) on earthworms is still limited. In this study, we explored the impacts of DBDPE-MPs on neurotoxic biomarkers, tissue damage, and transcriptomics of Eisenia fetida by simulating different exposure patterns of 10 mg kg−1 DBDPE and 10 mg kg−1 DBDPE-MPs (PLA, PP, and PE). Results showed that the activities of acetylcholinesterase, Na+/K+-ATPase, Ca2+/Mg2+-ATPase, carboxylate enzyme, and the contents of calcium and glutamate were significantly stimulated. DBDPE-MP co-exposure caused more severe damage to the epidermis, muscles, and tissues. Transcriptomic analysis revealed that differentially expressed genes (DEGs) of DBDPE-MPs were mainly related to inflammation, the immune system, digestive system, endocrine system, and metabolism. DBDPE and PP-MPs had similar influences on immunity and metabolism. However, DBDPE-PLA and DBDPE-PE further affected the endocrine system and signaling pathways. Specific DEGs showed that detoxification systems in the case of MPs were significantly upregulated. The study indicated that MPs exacerbated DBDPE toxicity in the nervous system, epidermis, and gene regulation of E. fetida, helping to assess the ecological risks of e-wastes and microplastics in soil.

5-Methyltetrahydrofolate Alleviates Memory Impairment in a Rat Model of Alzheimer's Disease Induced by D-Galactose and Aluminum Chloride.

The effects of 5-methyltetrahydrofolate (5-MTHF) on a rat model of Alzheimer's disease (AD) induced by D-galactose (D-gal) and aluminum chloride (AlCl3) were investigated. Wistar rats were given an i.p. injection of 60 mg/kg D-gal and 10 mg/kg AlCl3 to induce AD and three doses of 1 mg/kg, 5 mg/kg or 10 mg/kg 5-MTHF by oral gavage. A positive control group was treated with 1 mg/kg donepezil by gavage. Morris water maze performance showed that 5 and 10 mg/kg 5-MTHF significantly decreased escape latency and increased the number of platform crossings and time spent in the target quadrant for AD rats. The administration of 10 mg/kg 5-MTHF decreased the brain content of amyloid β-protein 1-42 (Aβ1-42) and phosphorylated Tau protein (p-Tau) and decreased acetylcholinesterase and nitric oxide synthase activities. Superoxide dismutase activity, vascular endothelial growth factor level and glutamate concentration were increased, and malondialdehyde, endothelin-1, interleukin-6, tumor necrosis factor-alpha and nitric oxide decreased. The administration of 10 mg/kg 5-MTHF also increased the expression of disintegrin and metallopeptidase domain 10 mRNA and decreased the expression of β-site amyloid precursor protein cleavage enzyme 1 mRNA. In summary, 5-MTHF alleviates memory impairment in a D-gal- and AlCl3-exposed rat model of AD. The inhibition of Aβ1-42 and p-Tau release, reduced oxidative stress, the regulation of amyloid precursor protein processing and the release of excitatory amino acids and cytokines may be responsible.

Molecular Characterization and Dietary Regulation of Glutaminase 1 (gls1) in Triploid Crucian Carp (Carassius auratus)

Kidney-type glutaminase, encoded by the gls1 gene, plays a critical role in glutamate production and improvement of meat flavor. In this study, a gls1 gene encoding 595 amino acids was cloned from triploid crucian carp (Carassius auratus) (TCC) and showed a high similarity with the gls1 gene found in Cyprinus carpio, Sinocyclocheilus rhinocerous and Puntigrus tetrazona. Comparing the abundance of gls1 in different tissues, we found its expression level in the brain and liver were significantly higher than that in heart, gut, kidney, spleen and muscle. gls1 expression in the brain reached the highest value. In addition, the expression levels of gls1 also appeared different in diurnal variation, with the highest expression seen at 9:00, while it was low at 3:00, 6:00, 15:00 and 24:00. Furthermore, dietary regulation of gls1 expression was investigated in our study. In each feeding trial, each diet was randomly assigned to triplicate tanks. Fish were fed one of the tested diets up to satiation twice daily. The results showed that gls1 expression increased in 32% protein group and decreased in 35–41% protein group. The results of different protein source experiments showed that the expression of gls1 gene in the mixed protein group (the control group) was significantly higher than that in the fish meal and soybean meal groups. Glutamate treatment revealed that appropriate concentrations (0.10 mg/mL in vivo and 2.00% in vitro) of glutamate remarkably improved the expression of gls1. Besides, diets supplemented with 0.80–1.60% lysine-glutamate dipeptide exhibited a down regulatory impact on gls1 expression. In conclusion, this study demonstrated that the expression of gls1 in TCC was increased by 32% protein diet, mixed protein source diet and diet with 2.00% glutamate concentration, while decreased by 0.80–1.60% lysine-glutamate dipeptide. The findings of this study provide a reference for the regulation of gls1 and have a potential application in the optimization of dietary formula in aquaculture.

Decreased xCT activity in patients associated with Helicobacter pylori infection.

Objective: In animals, Helicobacter pylori (Hp)-induced gastric injury is accompanied by a decrease in the activity of the cysteine/glutamate transporter (xCT), which regulates extracellular glutamate levels. However, the impact of xCT activity in patients with Hp infection remains unclear. This study aims to investigate variations of xCT activity in the gastric mucosa of patients with Hp infection and to provide a clinical basis for identifying targets related to Hp infection. Methods: Our study included a total of 67 patients with gastritis, which consisted of 44 Hp-negative and 23 Hp-positive peptic ulcer cases. The inclusion criteria used to select patients were as follows: gastric histology was determined with a gastroscope, antral biopsies were taken for urease tests, and pathology and culture were performed for analysis of Hp-colonization. The clinical characteristics of the patients were obtained, the expressions of microRNAs and xCT protein were detected using immune histochemical analysis, and the concentration of glutamate in their gastric secretion was determined. Results: The findings revealed that xCT expression was significantly lower in Hp-positive patients as compared to Hp-negative individuals, which was accompanied by a decrease in glutamate concentration in gastric juice. We also discovered a high expression of microRNAs that have been shown to negatively regulate xCT expression, in Hp-positive patients. Conclusion: Reduced xCT activity in patients may play an important role in gastric ulcers caused by Hp infection. Our findings suggest that the microRNA/xCT pathway could be a potential treatment target for Hp-infection-related ulcers.