Search Results (309)

Soil contamination with petroleum hydrocarbons is a serious environmental issue, necessitating the development of effective and environmentally friendly remediation methods that align with the principles of sustainable development. This study investigated the impact of selected biosurfactants on the efficiency of the biodegradation of total petroleum hydrocarbons (TPH) and polycyclic aromatic hydrocarbons (PAHs) in contaminated soil. Six biosurfactants—poly-γ-glutamic acid (γ-PGA), rhamnolipid, surfactin, a mixture of γ-PGA, rhamnolipids, and surfactin (PSR), as well as two commercial formulations (JBR 425 and JBR 320)—were evaluated in combination with a bacterial consortium. Biodegradation experiments were conducted under laboratory conditions for a 90-day period. The effectiveness of the tested biosurfactants was assessed using respirometric analysis, the chromatographic determination of the residual hydrocarbon content, and toxicity assays. The results showed that the application of a bacterial consortium enriched with a mixture of biosurfactants PSR (a biosurfactant concentration in the inoculating mixture: 5 g/dm³) was the most effective approach, resulting in an oxygen uptake of 5164.8 mgO₂/dm³ after 90 days, with TPH and PAH degradation rates of 77.3% and 70.32%, respectively. Phytotoxicity values decreased significantly, with TU values ranging from 6.32 to 4.62 (growth inhibition) and 3.77 to 4.13 (germination). Toxicity also decreased in the ostracodtoxkit test (TU = 4.35) and the Microtox SPT test (TU = 4.91). Among the tested biosurfactants, surfactin showed the least improvement in its bioremediation efficiency. Under the same concentration as in the PSR mixture, the oxygen uptake was 3446.7 mgO₂/dm³, with TPH and PAH degradation rates of 60.64% and 52.64%, respectively. In the system inoculated with the bacterial consortium alone (without biosurfactants), the biodegradation efficiency reached 44.35% for TPH and 36.97% for PAHs. The results demonstrate that biosurfactants can significantly enhance the biodegradation of petroleum hydrocarbons in soil, supporting their potential application in sustainable bioremediation strategies. Full article

Nitrogen (N) critically regulates wheat growth and grain quality, yet the molecular mechanisms underlying foliar nitrogen application remain unclear. This study evaluated the effects of foliar nitrogen application (12.25 kg ha⁻¹) on the growth, grain yield, and quality of spring wheat, as well as its molecular mechanisms. The results indicated that N was absorbed within 3 h post-application, with leaf nitrogen concentration peaking at 12 h. The N treatment increased whole-plant dry matter accumulation and grain protein content by 11.34% and 6.8%, respectively. Amino acid content peaked 24 h post-application, increasing by 25.3% compared to the control. RNA-sequencing analysis identified 4559 and 3455 differentially expressed genes at 3 h and 24 h after urea treatment, respectively, these DEGs being primarily involved in nitrogen metabolism, photosynthetic carbon fixation, amino acid biosynthesis, antioxidant systems, and nucleotide biosynthesis. Notably, the plastidic glutamine synthetase gene (GS2) is crucial in the initial phase of urea application (3 h post-treatment). The pronounced downregulation of GS2 initiates a reconfiguration of nitrogen assimilation pathways. This downregulation impedes glutamine synthesis, resulting in a transient accumulation of free ammonia. In response to ammonia toxicity, the leaves promptly activate the GDH (glutamate dehydrogenase) pathway to facilitate the temporary translocation of ammonium. This compensatory mechanism suggests that GS2 downregulation may be a key switch that redirects nitrogen metabolism from the GS/GOGAT cycle to the GDH bypass. Additionally, the upregulation of the purine and pyrimidine metabolic routes channels nitrogen resources towards nucleic acid synthesis, and thereby supporting growth. Amino acids are then transported to the seeds, culminating in enhanced seed protein content. This research elucidates the molecular mechanisms underlying the foliar response to urea application, offering significant insights for further investigation. Full article

In this study, we investigated the potential of a three-mushroom complex extract (GMK) to inhibit neuronal cell death induced by the activation of AMPA and NMDA receptors following glutamate treatment in NGF-differentiated PC12 neuronal cells. GMK significantly mitigated glutamate-induced excitotoxic neuronal apoptosis by reducing the elevated expression of BAX, a critical regulator of apoptosis, and restoring BCL2 levels. These neuroprotective effects were associated with redox regulation, as evidenced by the upregulation of SOD, CAT, and GSH levels, and the downregulation of MDA levels. Mechanistic studies further revealed that GMK effectively scavenged ROS by downregulating NOX1, NOX2, and NOX4, while upregulating NRF1, P62, NRF2, HO1, and NQO1. Additionally, in the same model, GMK treatment increased acetylcholine, choline acetyltransferase, and GABA levels while reducing acetylcholinesterase activity. These effects were also attributed to the regulation of redox balance. Furthermore, we investigated the antioxidant and anti-inflammatory mechanisms of GMK in LPS-stimulated BV2 microglia. GMK inhibited the activation of IκB and MAPK pathways, positively regulated the BCL2/BAX ratio, suppressed TXNIP activity, and upregulated NQO1 and NOX1. In conclusion, GMK improved neuronal excitotoxicity and microglial inflammation through the positive modulation of the redox regulatory system, demonstrating its potential as a natural resource for pharmaceutical applications and functional health foods. Full article

One of the world’s most sustainable solutions is to replace fossil-based polymers with biopolymers. The production of xanthan gum can be optimized using various renewable and cost-effective raw materials, which is a key focus in industrial biotechnology. Xanthan gum is a bioengineered thickening, stabilizing, and emulsifying agent. It has unique properties for use in many industries (food, biotechnology, petrochemicals, agricultural, cosmetics, wastewater treatment) and medical applications. It is tasteless, environmentally safe, non-toxic, and biodegradable. The biotechnological production of xanthan gum depends on several factors: bacterial strain development, culture medium preparation, carbon sources, fermentation parameters and modes, pH, temperature, recovery, purification, and quality control regulations. Bio-innovative strategies have been developed to optimize the production of xanthan gum. A variety of carbon and nitrogen sources, as well as alternative renewable sources, have been used in the production of xanthan gum. The aim of the present study was to optimize the xanthan gum yield using Xanthomonas campestris bacteria and different carbon (D-glucose, D-sorbitol, lactose, sucrose, D-mannitol, D-fructose, erythritol, coconut palm sugar, L-arabinose, unrefined cane sugar), various nitrogen (bacterial peptone, casein peptone, L-glutamic acid, L-arginine, L-methionine, L-tryptophan, malt extract, meat extract, L-phenylalanine, soy peptone) and alternative carbon (orange peels, tangerine peels, lemon peels, avocado peels, melon peels, apple peels, cellulose, xylose, xylitol) sources. The xanthan gum samples were analyzed using antioxidant methods. Our study showed that using L-glutamic acid as the carbon source for 72 h of bacterial fermentation of Xanthomonas campestris resulted in the highest xanthan gum yield: 32.34 g/L. However, using renewable resources, we achieved a very high concentration of xanthan gum in just 24 h of fermentation. According to the reducing power and DPPH methods, the highest antioxidant activities were measured for xanthan gum whose biosynthesis was based on renewable resources. Xanthan gum structures have been verified by FT-IR and ¹H NMR analysis. The sustainable biotechnology study has the advantage of increasing the sustainable production of xanthan gum by using renewable alternative resources compared to other production processes. Xanthan gum continues to be a valuable biopolymer with a wide range of industrial applications while promoting environmentally friendly production practices. Full article

The widespread application of pesticides in agriculture has raised increasing concerns regarding their ecological impact, particularly in aquatic environments. Among these, α-cypermethrin, a highly active isomeric form of cypermethrin, has been extensively used due to its potent insecticidal efficacy and low mammalian toxicity. However, its toxicity to non-target aquatic organisms remains insufficiently understood at the metabolic level. In this study, a targeted metabolomics approach was employed to investigate the biochemical effects of α-cypermethrin in adult zebrafish. Acute toxicity was first determined to establish sublethal exposure concentrations (0.15 µg/L and 1.5 µg/L), followed by a 48 h exposure under a controlled flow-through system. GC-MS/MS-based analysis quantified 395 metabolites, and multivariate statistical models (principal component analysis (PCA) and partial least square-discriminant analysis (PLS-DA)) revealed clear dose-dependent metabolic alterations at two time points. Pathway analysis identified disruptions in glycolysis, glycerolipid metabolism, amino acid turnover, and glutathione pathways. Notably, glutamate depletion and associated reductions in GABA (4-Aminobutanoate) and TCA (Tricarboxylic acid) cycle intermediates suggest oxidative stress-induced metabolic bottlenecks. These results provide mechanistic insights into α-cypermethrin-induced toxicity and demonstrate the utility of metabolite-level biomarkers for environmental monitoring. This study contributes to a systems-level understanding of how sublethal pesticide exposure affects vertebrate metabolism, offering a basis for improved ecological risk assessment and pesticide regulation. Full article

Chinese perch (Siniperca chuatsi), an economically important freshwater fish in China, faces ammonia nitrogen stress under high-density aquaculture. This study investigated chronic ammonia nitrogen exposure effects on juvenile fish (95 ± 5 g) to establish safe concentration. Acute toxicity tests revealed a 96 h-LC₅₀ of 12.91 mg/L ammonia nitrogen, with a safe concentration of 1.29 mg/L ammonia nitrogen (non-ionic ammonia: 0.097 mg/L). In 28-day chronic experiments with ammonia nitrogen levels at 0, 0.61, 1.29, and 2.58 mg/L, ammonia nitrogen induced hepatic oxidative stress, with total superoxide dismutase, catalase, and glutathione peroxidase activities and malondialdehyde content increasing proportionally to ammonia nitrogen concentration initially but declining over time. Concurrently, gill Na⁺-K⁺-ATPase activity was significantly suppressed, while the gene expression of ammonia transporters (rhag, rhbg, and rhcg) exhibited ammonia nitrogen concentration-dependent upregulation, inversely correlated with the exposure duration. Histological gill damage intensified at higher concentrations. Hepatic ammonia detoxification enzymes activities (asparagine synthase, glutamine synthetase, and glutamate dehydrogenase) and glutamine accumulation increased with ammonia nitrogen levels, aligning with gene expression trends, though enzyme activity diminished over time. Serum alanine aminotransferase and aspartate aminotransferase activities and their gene expressions rose with ammonia nitrogen levels, while total protein declined. These findings demonstrate that chronic ammonia nitrogen stress disrupts antioxidant capacity, osmoregulation, and nitrogen metabolism, compelling Chinese perch to mitigate toxicity via glutamine synthesis. To ensure sustainable aquaculture, ammonia nitrogen levels should remain below 1.29 mg/L under adequate dissolved oxygen conditions. Full article

Lead (Pb) is a pervasive neurotoxicant with well-documented detrimental effects on the central nervous system, particularly in vulnerable populations such as children. Despite historical recognition of its toxicity, Pb exposure remains a significant public health concern due to its environmental persistence, historical industrial use, and ongoing applications in modern technologies. This review focuses on the mechanisms by which Pb disrupts glutamatergic signaling, a critical pathway for learning, memory, and synaptic plasticity. Pb’s interference with glutamate receptors (ionotropic NMDA and AMPA, as well as metabotropic receptors), transporters (EAATs, VGLUTs, and SNATs), and metabolic pathways (glutamate–glutamine cycle, TCA cycle, and glutathione synthesis) are detailed. By mimicking divalent cations like Ca²⁺ and Zn²⁺, Pb²⁺ disrupts calcium homeostasis, exacerbates excitotoxicity, and induces oxidative stress, ultimately impairing neuronal communication and synaptic function. These molecular disruptions manifest cognitive deficits, behavioral abnormalities, and increased susceptibility to neurodevelopmental and neurodegenerative disorders. Understanding Pb’s impact on glutamatergic neurotransmission offers critical insights into its neurotoxic profile and highlights the importance of addressing its effects on neural function. Full article

Arsenic, a potent metalloid contaminant of drinking water, is known for its ability to act as an initiator and modulator of disease in a variety of human tissues. Upon ingestion, arsenic is bio-transformed in the liver into a variety of metabolites, including arsenite. Arsenite permeates the blood–brain barrier (BBB), inducing oxidative stress that can be detrimental to brain neurons. As the primary glial cell at the BBB interface, astrocytes play a pivotal role in detoxifying xenobiotics such as arsenite via the production of the tripeptide antioxidant γ-glutamylcysteine, or glutathione (GSH). In this study, we assessed the mRNA levels of key components of the GSH synthetic pathway in astrocytes exposed to arsenite compared to vehicle controls. These components included xCT [substrate-specific light chain of the substrate importing transporter, system x_c⁻ (Sx_c⁻)], glutamate-cysteine ligase [both catalytic (GCL_C) and modifying (GCL_M) subunits], and glutathione synthetase (GS). Additionally, we analyzed protein levels of some components by Western blotting and evaluated functional activity of Sx_c⁻ using a fluorescence-based cystine uptake assay. Finally, we utilized a luminescence-based glutathione assay to determine the intracellular and extracellular GSH content in arsenite-treated cells. Arsenite significantly increased xCT, GCL_C, GCL_M, and GS mRNA levels, an effect blocked by the transcriptional inhibitor actinomycin D (ActD). A corresponding increase in Sx_c⁻ activity was also observed in the arsenite treatment groups, along with significant increases in GCL_C and GCL_M protein expression. However, no increase in GS protein expression was detected. Finally, arsenite treatment significantly increased extracellular GSH levels, an effect which was also prevented by the inclusion of ActD. Overall, our study provides evidence that arsenite transcriptionally regulates several cellular processes necessary for GSH synthesis in primary cortical astrocyte cultures, thereby contributing to a better understanding of how this environmental toxicant influences antioxidant defenses in the brain. However, these results should be interpreted with caution regarding their applicability to vivo systems. Full article

As one kind of renewable aromatic polymer, lignin is severely underused due to its chemical recalcitrance. Lignin can endure demethylation modification to improve its activation by releasing more active functional groups. However, the process suffers from expensive, corrosive, and toxic issues by employing halogen-containing reagents, which has become an obstacle to industrial applications. Herein, a series of dicarboxylic acid-based protic ionic liquids (DAPILs) systems composed of ethanolamine and dibasic organic acids (e.g., aspartic acid (Asp), glutamic acid (Glu), succinic acid (SA), and glutaric acid (GA)) with 1~2:1 stoichiometric ratio, have been finely designed for the demethylation of industrial lignin. With [EOA][GA] treatment, the polyphenol content in lignin was favorably increased beyond 1.58 times. The structural tailoring and variation were fully characterized by 2D HSQC and ¹H NMR. The analysis results indicated that, with the increase of phenolic hydroxyl content in lignin, the β-O-4′ bond was broken and the content of structural units (S, G) and the S/G ratio of lignin decreased accordingly. After the treatment, the used IL and tailored lignin can be recovered over 95%. This novel, halogen-free and environmentally friendly lignin-cutting strategy not only opens avenues for high-value utilization of lignin but also expands the field of application of dicarboxylic acid-based protic ionic liquids. Full article

6-PPD quinone (6-PPDQ) is widely distributed in environments. In Caenorhabditis elegans, we first examined the effects of 6-PPDQ on glutamate synthesis and receptor function by analyzing glutamate content, related gene expression, and phenotypes after RNAi of these genes. Moreover, we performed glutamate treatment after 6-PPDQ exposure to determine the potential pharmacological effects of glutamate against 6-PPDQ toxicity. After exposure, the glutamate content was reduced by 0.1–10 μg/L 6-PPDQ, which was due to decreased expression of W07E1.1, glna-1/2/3, and alh-6 governing glutamate synthesis from α-ketoglutarate, glutamine, and proline. RNAi of W07E1.1, glna-1/2/3, and alh-6 decreased glutamate content in 6-PPDQ-exposed nematodes, and caused susceptibility to 6-PPDQ toxicity. Among glutamate transporter genes, glt-1 expression was decreased by 0.1–10 μg/L 6-PPDQ. Moreover, 0.1–10 μg/L 6-PPDQ decreased glutamate receptor genes (glr-1, glr-2, and glr-4), and their expression was decreased by RNAi of W07E1.1, glna-1/2/3, alh-6, and glt-1. RNAi of these receptor genes resulted in susceptibility to 6-PPDQ toxicity, and daf-7, jnk-1, and dbl-1 were identified as targets of neuronal glr-1, glr-2, and glr-4. Furthermore, 5 mM glutamate suppressed 6-PPDQ toxicity and increased expression of glr-1, glr-2, and glr-4. Our results demonstrated the risk of 6-PPDQ exposure in disrupting glutamate synthesis and affecting function of glutamate receptors, which was related to 6-PPDQ toxicity induction. Full article

As the average age of the population increases, memory impairment has become an increasingly prevalent issue. This study investigates the effects of 14 days of oral birch sap administration on memory functions in healthy rats using the Morris water maze (MWM) test and explores the underlying mechanisms. A compositional analysis revealed that birch soap is rich in polysaccharides, specifically a low-molecular weight polysaccharide (MW 1.29 kDa), and exhibits no hepatotoxicity or renal toxicity at the tested dose. The results from the MWM test demonstrated that the time and distance required to reach the platform were significantly shorter in the birch sap-treated group compared to the control group, suggesting that birch sap supports memory preservation. Moreover, rats treated with birch sap showed improved cerebral blood flow compared to the control rats. Additionally, in hippocampal nerve terminals (synaptosomes), rats treated with birch sap exhibited a significant increase in evoked glutamate release, as well as elevated levels of presynaptic proteins, including vesicular glutamate transporter 1 (VGluT1), synaptophysin, synaptobrevin, synaptotagmin, syntaxin, synapsin I, and the 25 kDa synaptosome-associated protein (SNAP-25). Transmission electron microscopy also revealed a notable increase in the number of synaptic vesicles in hippocampal synaptosomes of the birch-sap-treated rats. These findings suggest that birch sap enhances hippocampal presynaptic glutamatergic functions and cerebral blood flow, contributing to its memory-preserving effects in rats. Full article

The pathogenesis of Parkinson’s disease (PD) consists of the apoptosis of dopaminergic neurons in the substantia nigra pars compacta (SNpc) due to oxidative stress. The present study aimed to evaluate the potential antioxidant activity of whey protein isolate (WPI) in PD models, using neurotoxin-exposed SH-SY5Y cells differentiated into dopaminergic-like neurons. Our research shows that WPI’s high glutamic acid, aspartic acid, and leucine contribute to its antioxidant and neuroprotective effects, with glutamic acid crucial for glutathione synthesis. In vitro studies found that WPI, at concentrations of 5–1000 µg/mL, is non-toxic to differentiated SH-SY5Y cells. Notably, the lowest con-centration of WPI (5 µg/mL) significantly decreased intracellular reactive oxygen species (ROS) levels in these cells following a 24 h co-treatment with 1-methyl-4-phenylpyridinium (MPP⁺). The antioxidant effects of WPI were also confirmed by the increased expression of HO1 and GPx antioxidant enzymes, which are Nrf2 pathway target genes and were evaluated by real-time PCR. Furthermore, Nrf2 nuclear translocation in the differentiated SH-SY5Y cells was also increased when the cells were exposed to 5 µg/mL of WPI with MPP⁺. These results together suggest that WPI has antioxidant effects on dopaminergic-like neurons in a Parkinson’s disease model. Full article

The excessive intake of monosodium glutamate (MSG) increases its cellular levels in different organs and induces organ toxicity. The current study aims to investigate the metabolic changes and possible causes of hepatic, renal, and cardiac toxicity induced by MSG overconsumption. Thirty adult male rats were randomly allocated into five groups: control, MSG0.8, MSG1, MSG2, and MSG3, which were orally treated with a daily oral dose of saline, 0.8, 1, 2, and 3 g MSG/kg BW, respectively, for eight weeks. The hepatic, renal, and cardiac biochemical markers; lipid profile; glucose; electrolytes; iNOS; α-KGD; oxidative stress; and inflammatory markers were investigated. The histopathological examination of hepatic and renal tissues was also performed. The results revealed MSG-induced hepato-renal and cardiac toxicity, as indicated by the changes in the biochemical markers and tissue architecture of these organs. The toxicity is observed in the form of dyslipidemia, oxidative stress (increased MDA and NO and decreased GSH, SOD, CAT, and GST), and inflammatory responses (increased TNF-α and IL-6). The histopathological changes in liver and kidney architecture confirmed the obtained results. In conclusion, the MSG-induced hepatic, renal, and cardiac toxicity was dose-dependent, and awareness should be raised about the side effects of the overconsumption of MSG. Full article

Octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine (HMX) is a globally recognized energetic material that widely used in industrial, mining, and military fields. Like hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX) and other nitramine compounds, HMX has also been reported to exhibit neurotoxicity. However, the molecular mechanisms underlying the toxic effects of HMX remain poorly understood. Therefore, this study aims to investigate the neurotoxicity induced by HMX by adopting PC12 cells. The results show that HMX treatment decreased cell viability and upregulated the intracellular free calcium ions (Ca²⁺) in PC12 cells. Furthermore, HMX caused aggravated oxidative stress in PC12 cells, as evidenced by the upregulations of reactive oxygen species (ROS) and malondialdehyde (MDA). Intracellular biochemical assays demonstrated that HMX induced loss of mitochondrial membrane potential in PC12 cells. Notably, altered expression of brain-derived neurotrophic factor (BDNF) and ionotropic glutamate receptors (iGluRs), as well as an abnormal transcription profile, were also observed in PC12 cells treated by HMX. These findings suggest that HMX exerts toxic effects on PC12 cells, involved in oxidative stress, and disturbances in Ca²⁺ and BDNF, accompanied by aberrant iGluRs. Overall, the present study helps us better understand the health hazards associated with HMX and provides valuable insights for developing the health protection standards related to HMX exposure. Full article

Background/Objectives: Alzheimer’s disease (AD) is the most common type of dementia, characterized by complex processes such as neuro-inflammation, oxidative damage, synaptic loss, and neuronal death. Carotenoids are among the potential therapeutic molecules that have attracted attention due to their neuroprotective properties, but their efficacy is limited mainly by their capacity to cross the blood–brain barrier (BBB). Results: The results showed that T. chuii extracts could protect neuronal cells from neurotoxic damage, especially against L-glutamate and H₂O₂. Moreover, the BBB permeability and the intestinal transport analyses revealed that fucoxanthinol, crocoxanthin, diatoxanthin, neoxanthin, violaxanthin, and prasinoxanthin have diverse permeabilities depending on the incubation time and the cell model used. Fucoxanthinol was the carotenoid with the highest and similar permeability in HBMEC cells (4.41%, 5.13%, and 18.94% at 2, 4, and 24 h, respectively) and Caco-2 cells (7.01%, 8.63%, and 18.36% at the same times), while crocoxanthin, diatoxanthin, and neoxanthin showed different kinetics. Methods: The neuroprotective potential of two extracts obtained from Tetraselmis chuii microalga were evaluated against Aβ1-42-, L-glutamate-, and H₂O₂-induced toxicities in SH-SY5Y cells. In addition, the BBB permeability and the intestinal transepithelial transport of the main carotenoids present in the extracts were evaluated and compared using two cell culture models, HBMEC and Caco-2 cells. For that aim, the transport of the bioactive molecules across the barriers was evaluated using UHPLC-q-TOF-MS after 2, 4, and 24 h of incubation. Conclusions: These findings indicate that T. chuii is a promising natural source of bioactive compounds to develop functional foods against neurodegenerative diseases. Full article