Search Results (202)

Oxidative stress-induced mitochondrial dysfunction and apoptosis are critical factors in the pathogenesis of neurodegenerative diseases. This study investigated the synergistic neuroprotective effects of anthocyanin-enriched Morus alba L. extract combined with vitamin C (MAC) against hydrogen peroxide (H₂O₂)-induced oxidative stress in SH-SY5Y neuronal cells. Exposure to H₂O₂ triggered excessive reactive oxygen species (ROS) production and apoptosis, whereas treatment with MAC markedly alleviated these effects. Biochemical analyses revealed that MAC significantly reduced malondialdehyde (MDA) and enhanced the activities of antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px), thereby contributing to improved redox balance. Furthermore, MAC modulated apoptosis-related signaling by upregulating extracellular signal-regulated kinase (ERK), cAMP response element-binding protein (CREB), and the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2), while downregulating the pro-apoptotic protein Bcl-2-associated X (BAX) and cleaved caspase-3. Collectively, these findings demonstrate that MAC acts synergistically as a promising nutraceutical ingredient, supporting the development of functional foods for the prevention or mitigation of oxidative stress-related neurodegenerative disorders. Full article

Glioblastoma multiforme (GBM) is the most aggressive brain tumor with a high recurrence rate and mortality. A major obstacle to the effective treatment of GBM is the blood–brain barrier (BBB), which hinders the transfer of therapeutic cargo to the tumor lesion. Polysorbate-coated drug carriers are known to efficiently cross the BBB via apolipoprotein E (ApoE)-mediated transcytosis. In this study, we developed cancer-targeted nanocarriers using folic acid (FA)-conjugated polysorbate (Tween 80, T80) for safe and efficient chemo-sonodynamic combination therapy against GBM. T80-based nanocarriers effectively co-encapsulated doxorubicin (DOX, chemotherapeutic agent) and oxygen-deficient MnWOx nanoparticles (sonosensitizer). FA-conjugated T80 nanocarriers encapsulating DOX and MnWOx (FA-T-DOX@MnWOx) boosted the cellular uptake of DOX in human glioblastoma U87MG cells. The efficient ability of the T80-based drug carriers to cross the BBB was demonstrated using an in vitro transwell BBB model. In addition, sonosensitizer MnWOx nanoparticles in the T80-based carriers triggered GSH depletion, synergistically enhancing intracellular reactive oxygen species (ROS) generation in U87MG cells upon US irradiation. As a result, FA-T-DOX@MnWOx combined with US triggered significant apoptosis in U87MG cells. This study demonstrated that FA-conjugated, MnWOx-loaded, T80-based nanocarriers capable of crossing the BBB hold significant potential for treating GBM through a combined chemo-sonodynamic therapy. Full article

On acid soils, aluminum (Al³⁺) is typically toxic to plants, though certain species like Pogostemon cablin (patchouli) show growth stimulation. This study reveals that Al functions as a root development stimulant in patchouli under acidic conditions. Treatment with 1.0 mM AlCl₃ for 34 days significantly enhanced root architecture, increasing total root length by 172.12% and root dry weight by 161.75%, without affecting shoot biomass. Structural analysis showed Al accumulation in root tip meristems and lateral root primordia, triggering a 103.77% increase in meristem activity and a 111.9% promotion of cell elongation. Physiological assays showed that Al treatment reduced H₂O₂ and malondialdehyde (MDA) levels by 49.2% and 67.6%, respectively, while boosting glutathione (GSH) content by 187.5%, thereby mitigating oxidative membrane damage mainly through the non-enzymatic antioxidant system. Moreover, Al deprivation impaired lateral root elongation, highlighting its functional importance. Gene expression profiling further indicated that Al regulated pathways related to cell proliferation, cell wall remodeling, and lateral root development. Taken together, our findings uncover a novel mechanism by which Al, traditionally regarded as toxic, acts as a stimulator of root development in patchouli, providing new insights into the molecular networks underlying plant abiotic stress responses. Full article

Background/Objectives: Obesity increases reactive oxygen species (ROS), thereby triggering oxidative stress. Coriander seeds contain polyphenolic compounds that act as natural antioxidants to reduce oxidative stress. Coriander seed ethanolic extract has been proven to decrease malondialdehyde and increase catalase activity in the liver of high-fat-diet-fed rats. Thus, coriander seeds are thought to protect against obesity-induced oxidative liver damage; however, their molecular mechanism has not been revealed. Nuclear factor erythroid 2-related factor 2 (Nrf2) and Forkhead Box O3 (FOXO3) are transcription factors involved in cellular antioxidant regulation (e.g., superoxide dismutase/SOD, glutathione peroxidase/GPx expression, and reduced glutathione/GSH) that are negatively regulated by Kelch-like ECH-associated Protein 1 (Keap1) and 14-3-3 protein to maintain cellular homeostasis. This study aimed to analyze the regulation of antioxidant expression through in silico and in vivo experiments. Methods: The in silico study assessed the potential of coriander seed ethanolic extract to inhibit Keap1 and 14-3-3 using molecular docking. Then, the drug-likeness, pharmacokinetics, and toxicity of the top three compounds were analyzed. Meanwhile, the in vivo study investigated how the coriander seed ethanolic extract impacted the level of Nrf2, FOXO3, and their downstream effectors (T-SOD, MnSOD, GPx, and GSH). The in vivo study involved five groups of rats with obesity induced by a high-fat diet that were fed with 100 mg/kgBW coriander seed ethanolic extract for 12 weeks. Results: The in silico tests revealed that shionoside b had the highest potential to inhibit Keap1 (ΔG = −8.90 kcal/mol; Ki = 298.01 nM) and 14-3-3 protein (ΔG = −6.85 kcal/mol; Ki = 9.46 µM). The in vivo tests showed that the Nrf2, FOXO3, MnSOD, and GPx mRNA expression was significantly different between the groups (p < 0.05). Meanwhile, T-SOD, MnSOD, GPx, and GSH activity were not significantly different between the groups (p > 0.05). Nrf2 was significantly correlated with FOXO3 as well as the T-SOD, MnSOD, and GPx activity, and FOXO3 was significantly correlated with the T-SOD, MnSOD, GPx, and GSH activity. Conclusions: In obese rats, coriander seeds tend to increase Nrf2 and FOXO3 expression, which is positively correlated with their downstream enzymatic and nonenzymatic antioxidant activity. This is possibly due to the interaction between the coriander seed phytoconstituents and protein inhibitors (Keap1 and 14-3-3), which contribute to the stability and nuclear mobilization of Nrf2 and FOXO3. Full article

The bacterial flagellum plays a crucial role in pathogenesis. However, the mechanism by which the flagellum interferes with host energy metabolism remains unclear. In this study, we confirmed that deletion of the fliC gene resulted in a 30% reduction in the virulence of Pseudomonas plecoglossicida against the large yellow croaker (Larimichthys crocea). Compared to the wild-type strain (WT) infection group, the ΔfliC infection group exhibited a 29.54% decrease in the number of vacuolar degeneration hepatocytes and a 50.83% higher liver glycogen content. Furthermore, infection led to decreased mitochondrial complex V activity, a reduced NAD+/NADH ratio, lower levels of reduced glutathione (GSH), and increased lipid peroxide levels; however, these metabolic perturbations were significantly ameliorated in the ΔfliC group compared to the WT group. Proteomic analysis revealed that the dysregulation of the complement cascade and core carbon metabolic pathways observed in the WT infection group liver was significantly alleviated in the ΔfliC infection group. Additionally, in the ΔfliC infection group, pro-inflammatory genes (such as Tlr5, Tnfα, and Il1β) were downregulated, while lipid metabolism-related genes (such as Acox1, Cpt1a, and Pparα) were upregulated, suggesting the suppression of the Tlr5/NF-κB immune signaling axis and enhanced fatty acid β-oxidation. Collectively, fliC may mediate the disruption of host glucose and lipid metabolism homeostasis through a Tlr5-triggered immunometabolic regulatory axis. In conclusion, this study demonstrates that bacterial flagella modulate host energy metabolism, expanding our understanding of flagellum-mediated pathogenesis. Full article

Reactive oxygen species (ROS) function as critical signaling molecules in cancer biology, promoting proliferation, angiogenesis, and metastasis at controlled levels while inducing lethal damage when exceeding the cell’s buffering capacity. To survive under this state of chronic oxidative stress, cancer cells become dependent on a hyperactive antioxidant shield, primarily orchestrated by the Nrf2, glutathione (GSH), and thioredoxin (Trx) systems. These defenses maintain redox homeostasis and sustain oncogenic signaling, notably through the oxidative inactivation of tumor-suppressor phosphatases, such as PTEN, which drives the PI3K/AKT/mTOR pathway. Targeting this addiction to a rewired redox state has emerged as a compelling therapeutic strategy. Pro-oxidant therapies aim to overwhelm cellular defenses, with agents like high-dose vitamin C and arsenic trioxide (ATO) showing significant tumor-selective toxicity. Inhibiting the master regulator Nrf2 with compounds such as Brusatol or ML385 disrupts the core antioxidant response. Disruption of the GSH system by inhibiting cysteine uptake with sulfasalazine or erastin potently induces ferroptosis, a non-apoptotic cell death driven by lipid peroxidation. Furthermore, the thioredoxin system is targeted by the repurposed drug auranofin, which irreversibly inhibits thioredoxin reductase (TrxR). Extensive preclinical data and ongoing clinical trials support the concept that this reliance on redox adaptation is a cancer-selective vulnerability. Moreover, novel therapeutic strategies, including the expanding field of redox-active metal complexes, such as manganese porphyrins, which strategically leverage the differential redox state of normal versus cancer cells through both pro-oxidant and indirect Nrf2-mediated antioxidative mechanisms (triggered by Keap1 oxidation), with several agents currently in advanced clinical trials, have also been discussed. Essentially, pharmacologically tipping the redox balance beyond the threshold of tolerance offers a rational and powerful approach to eliminate malignant cells, defining a novel frontier for targeted cancer therapy. Full article

Lipopolysaccharide (LPS) triggers oxidative damage in sheep hepatocytes, linked to ferroptosis. Ferulic acid (FA) is known for its antioxidative properties, but its protective role against LPS via ferroptosis regulation was unclear. The objective of this research is to explore the protective role of FA in mitigating LPS-induced oxidative stress in sheep hepatocytes. The experimental setup consisted of three groups: a control group, an LPS group treated with 10 µg/mL of LPS, and FA group that received both 10 µg/mL of LPS and 750 µg/mL of FA. We found that FA treatment decreased in contents of MDA and LDH. Metabolomics revealed that LPS affected glycerophospholipid metabolism, unsaturated fatty acids biosynthesis, ferroptosis, and arachidonic acid metabolism mainly by reducing the level of PUFAs and LPC in the hepatocyte supernatant, while FA affected glutathione metabolism by increasing L-cysteine, L-ornithine, L-glutamic acid, and L-glutamine. Moreover, transcriptomics demonstrated that the comparison of LPS and control groups were mainly enriched in arachidonic acid metabolism, glycerophospholipid metabolism, and ferroptosis, the comparison of FA and LPS groups was mainly enriched in glutathione metabolism. The results further confirmed the findings in the metabolomics and transcriptomics analyses, showing that LPS treatment upregulated the mRNA expression of ACSL4, LPCAT3, ALOX15, STEAP3, GPX4, GCLC, and GCL in hepatocytes, while reducing GSH and GR levels. In contrast, FA intervention attenuated LPS-induced iron overload by decreasing Fe²⁺ accumulation and suppressing the mRNA expression of ACSL4, LPCAT3, STEAP3, and ALOX15. Furthermore, FA enhanced the expression of GPX4, GCLC, GCLM, and restored GSH content in LPS-exposed hepatocytes. The above results demonstrated that the protective effect of FA on LPS-induced oxidative damage in the sheep hepatocytes was achieved by activating the GSH-GPX4 pathway and inhibiting lipid metabolism-mediated ferroptosis. Full article

Surgical trauma triggers oxidative and inflammatory responses that contribute to postoperative complications. Although the antioxidant and anti-inflammatory effects of ketamine have been reported, the impact of anesthesia duration on these mechanisms remains unclear. Forty-two male Wistar rats were randomized into healthy control (HG), ketamine only (KET; 60 mg/kg, i.p.), or laparotomy plus ketamine with 0–4 additional ketamine doses at 20 min intervals (KET + L, KET + L1–L4). At 24 h, levels of MDA, tGSH, SOD, CAT, IL-1β, IL-6, TNF-α, adrenaline and noradrenaline were measured in tail-vein blood. One-way ANOVA with Tukey’s post hoc test was used. Laparotomy under single-dose ketamine increased MDA and pro-inflammatory cytokines and decreased tGSH, SOD, CAT, ADR, and NDR versus HG and KET (all p < 0.001). After laparotomy, repeated ketamine dosing produced graded decreases in MDA and cytokines and increases in tGSH, SOD, CAT, ADR, and NDR toward control levels; effects were most pronounced in KET + L4 (all p < 0.001). Ketamine alone did not differ significantly from HG. In rats, ketamine modulates postoperative biological stress in a duration-dependent manner; prolonging anesthesia reduces oxidative–inflammatory load and restores catecholaminergic tone. These findings strongly support revisiting dose–duration protocols and underscore the need for mechanistic and clinical studies. Full article

Background: Dibutyl phthalate (DBP) is a prevalent environmental pollutant that can accumulate in organisms, becoming amplified after the food cycle and ultimately affecting human health. Recent studies have provided evidence suggesting a potential association between exposure to DBP and cardiovascular diseases (CVDs). Objectives: This study’s objective is to investigate the toxic cardiovascular effects of long-term exposure to DBP, particularly its impact on the heart and blood vessels. To be specific, we hypothesized and verified the potential mechanisms underlying DBP-induced cardiac and vascular injuries, focusing on oxidative stress, pyroptosis, inflammatory responses, and metabolic pathways. Methods: The rats were divided into 5 groups: Control group, DBP-Low group, DBP-Medium group, DBP-High group, and DBP-High + Vitamin E group. The entire experimental period lasted 12 weeks. We conducted examinations on echocardiography, histopathology, oxidative stress biomarkers, pyroptosis-related biomarkers, and inflammatory cytokine biomarkers. Additionally, we carried out serum metabolomics analysis. Result: Our research findings indicate that long-term exposure to DBP can cause significant toxic effects on the cardiovascular system. Specifically, DBP leads to changes in oxidative stress indicators (ROS and an increase in MDA levels, alongside a decrease in GSH levels) and protein levels related to pyroptosis (NLRP3, Caspase-1 and GSDMD levels increase) in cardiac and vascular tissues, triggering oxidative inflammatory responses (IL-1β and IL-18 levels increase), damaging the heart and blood vessels (organizational structure deformation and collagen fiber infiltration) and ultimately affecting their functions (abnormalities in cardiac function and hemodynamics). Additionally, the results of metabolomics studies suggest that metabolic pathways (Biotin metabolism, TCA cycle, Vitamin B6 metabolism, Pantothenate and CoA biosynthesis, and Riboflavin metabolism) and metabolites may also be of great significance. Conclusion: Long-term exposure to DBP can induce cardiovascular toxicity in rats, manifesting as cardiac and vascular damage, as well as alterations in organ function. This process is characterized by oxidative stress, activation of the pyroptosis pathway, inflammatory responses, and modifications to metabolic pathways. Full article

The maintenance of intracellular redox homeostasis depends on the GSH/GSSG pair, which is the primary intracellular redox buffer. However, the NADPH/NADP⁺ pair also plays a vital role in this process. The primary source of NADPH is the pentose phosphate pathway and deficiency in the enzymes responsible for NADPH production in this pathway leads to developing of alternative NADPH supply strategies. The choice of compensation strategy has several consequences for cells physiology. The present study investigates how Saccharomyces cerevisiae yeast strains defective in generating NADPH via the pentose phosphate pathway due to deletion of ZWF1, GND1, or GND2 genes, respond to redox homeostasis disruption caused by allyl alcohol, a metabolic precursor of acrolein. Acrolein is a highly reactive aldehyde that rapidly depletes glutathione and triggers oxidative stress. Therefore, cells respond to acrolein through attempts to increase glutathione synthesis, but also by increasing NADPH production. The response requires coordinated action of glutathione- and NADPH-dependent systems. The high sensitivity of the Δgnd1 strain, which is unable to activate an adequate stress response, is evidence of this. The strategy employed by this strain to maintain redox homeostasis is inadequate and may even exacerbate allyl alcohol toxicity. Full article

Lipopolysaccharide (LPS), an essential structural molecule in the outer membrane of Gram-negative bacteria, is recognized as a principal trigger of inflammatory responses and oxidative stress. Thus, the control and clearance of LPS is essential to inhibit LPS-induced excessive inflammation, oxidative stress, and liver injury. In recent years, some native bioactive peptides, such as human β-defensin 126 (DEFB126) and thymopentin (TP5), have been reported to have inhibitory effects against LPS-induced inflammation and oxidative stress. However, the cytotoxicity, weak stability, and poor biological activity have hindered their practical application and clinical development. The development of novel hybrid peptides is a promising approach for overcoming these problems. In this study, we designed a novel hybrid peptide [DTP, DEFB126 (1-39)-TP5] that combines the active center of DEFB126 and full-length thymopentin (TP5). Compared to the parental peptides, DTP has a longer half-life, lower cytotoxicity, and greater anti-inflammatory and antioxidant activity. The anti-inflammatory and antioxidant effects of DTP were demonstrated in a murine LPS-induced sepsis model, which showed that DTP successfully inhibited the indicators associated with LPS-induced liver injury; decreased the contents of TNF-α, IL-6, and IL-1β; increased the level of glutathione (GSH); and improved the activities of catalase (CAT) and superoxide dismutase (SOD). Furthermore, our study revealed that the anti-inflammatory and antioxidant activities of DTP were associated with LPS neutralization, blockade of LPS binding to the Toll-like receptor 4/myeloid differentiation factor 2 (TLR4/MD-2) complex, reduction in reactive oxygen species content, and inhibition of the activation of the nuclear factor kappa-B (NF-кB) signaling pathway. These results elucidate the structural and functional properties of the peptide DTP, reveal its underlying molecular mechanisms, and shed light on its potential as a multifunctional agent for applications in agriculture, food technology, and clinical therapeutics. Full article

Follicular development is recognized as a highly complex biological process regulated by multiple factors. Thyroid hormone (TH) is considered one of the key regulators of female reproduction, and its dysregulation can significantly impair follicular development. Epigallocatechin gallate (EGCG), the main active component of green tea, possesses strong antioxidant properties. Numerous studies have demonstrated that EGCG positively influences reproductive function in both humans and animals. However, whether EGCG directly affects follicular development under conditions of TH dysregulation remains poorly understood. The primary objective of this study was to investigate the impact of hyperthyroidism on ovarian development, examine whether EGCG could mitigate the adverse effects of TH dysregulation, and elucidate the underlying molecular mechanisms. In the T₄-induced hyperthyroidism rat model, ovarian tissues were serially sectioned for Hematoxylin-Eosin (HE) and Masson’s trichrome staining to assess morphological changes, and follicle numbers were quantified at each developmental stage. Granulosa cell (GC) viability, proliferation, and apoptosis induced by T₃ were evaluated using CCK8, EdU, and TUNEL assays, respectively. Antioxidant enzyme activity was measured, and the expression levels of related proteins were analyzed via Western blotting. Results showed that hyperthyroidism altered ovarian structure, significantly increasing the number of atretic follicles. Levels of antioxidant enzymes, including Superoxide Dismutase (SOD), Glutathione Peroxidase (GSH-PX), and Catalase (CAT), were markedly decreased, whereas the lipid peroxidation product malondialdehyde (MDA) was significantly elevated. Furthermore, all ERS-related proteins, phosphorylated Eukaryotic Initiation Factor 2 Alpha (p-eIF2α), Activating Transcription Factor 4 (ATF4), C/EBP homologous protein (CHOP), and Caspase-3, were upregulated, accompanied by decreased glucose-regulated protein 78 (GRP78) expression. Treatment with EGCG alleviated these detrimental effects of hyperthyroidism. At the cellular level, high concentrations of T₃ reduced GC viability and proliferation while increasing apoptosis. Reactive oxygen species levels were elevated, and GRP78 expression was decreased. Notably, all T₃-induced effects were reversed by EGCG treatment. In summary, this study demonstrates that hyperthyroidism induces oxidative stress in GCs, which triggers endoplasmic reticulum stress via the eIF2α/ATF4 pathway and leads to apoptosis. EGCG mitigates apoptosis by enhancing antioxidant capacity, thereby preserving ovarian function. These findings establish EGCG as a protective agent for maintaining ovarian health and fertility. Full article

Burn injuries are among the most difficult skin lesions to manage, as they trigger intense inflammatory responses and oxidative stress, which often impair angiogenesis, delay epithelialization, and increase the risk of chronic non-healing wounds. Hydrolates of Satureja montana L. and Origanum vulgare L., rich in antioxidant and anti-inflammatory compounds, offer a promising natural alternative for wound management. This study investigated their effects on local redox and inflammatory status in full-thickness burn wounds. Male rabbits (n = 5 per group) received full-thickness burns and were assigned to control, untreated, conventional treatment (Levomekol liniment, boric acid, and Betadine-soaked gauze dressings), Satureja montana L. hydrolate, and Origanum vulgare L. hydrolate groups. Skin samples were collected on days 3, 7, and 14. ELISA was used to quantify redox (MDA, SOD, GSH) and inflammation (TNF-α, IL-1, IL-10) markers. Histochemical (H and E, Masson’s trichrome) and immunohistochemical (CD-45) analyses, plus the Greenhalgh score, were used to assess wound healing. Burn injuries significantly altered the redox status in all treated and untreated groups. The hydrolates reduced MDA and restored SOD/GSH levels, with Satureja montana L. showing the most pronounced effects. Satureja montana L. hydrolate modulated pro- and counter-inflammatory cytokines (decreasing IL-1/TNF-α, upregulating IL-10). An assessment of local cellular immunity showed the most prominent decrease in CD45+ cell counts in groups treated with Satureja montana L. and Origanum vulgare L. hydrolates. This study provides promising evidence that Satureja montana L. and Origanum vulgare L. hydrolates offer promise as topical therapies for burn wounds by modulating ROS production and local inflammatory status and by improving wound healing, with Satureja montana L. hydrolate exhibiting the most pronounced therapeutic effect. Full article

Sepsis is a complex condition characterized by an uncontrolled inflammatory response to infection, which can trigger multi-organ dysfunction and is associated with high mortality rates. In this context, oxidative stress plays a key role in the progression of tissue damage. Reduced glutathione (GSH), the primary non-enzymatic intracellular antioxidant, serves as a fundamental pillar in redox defense, acting as a key modulator of immune response, endothelial barrier integrity, and mitochondrial metabolism. This review explores the multifaceted role of GSH in the pathophysiology of sepsis, with emphasis on its biphasic effect on both innate and adaptive immunity, as well as its involvement in vascular alterations and mitochondrial dysfunction. The molecular mechanisms of GSH depletion during sepsis are analyzed, including excessive consumption by reactive species, disruption of its synthesis, and its intracellular compartmentalization. Additionally, the available clinical evidence in humans regarding the functional consequences of GSH loss is reviewed, particularly concerning organ failure—understood more as a bioenergetic and functional disruption than a structural one—and mortality, highlighting the methodological limitations and heterogeneity of the reported findings. Altogether, this analysis intends to provide a comprehensive view of the role of glutathione in redox dysregulation and the pathophysiological mechanisms underlying sepsis. Furthermore, it seeks to consolidate current pathophysiological and clinical knowledge to emphasize the potential role of glutathione as a prognostic marker and possible target for future therapeutic strategies in addressing this complex condition. Full article

Biothiols, including cysteine (Cys), homocysteine (Hcy), and glutathione (GSH), are crucial for physiological regulation and their imbalance poses severe health risks. Herein, we developed a pH-responsive liquid crystal (LC)-based sensing platform for detection of biothiols by doping 4-n-pentylbiphenyl-4-carboxylic acid (PBA) into 4-n-pentyl-4-cyanobiphenyl (5CB). Urease catalyzed urea hydrolysis to produce OH⁻, triggering the deprotonation of PBA, thereby inducing a vertical alignment of LC molecules at the interface corresponding to dark optical appearances. Heavy metal ions (e.g., Hg²⁺) could inhibit urease activity, under which condition LC presents bright optical images and LC molecules maintain a state of tilted arrangement. However, biothiols competitively bind to Hg²⁺, the activity of urease is maintained which enables the occurrence of urea hydrolysis. This case triggers LC molecules to align in a vertical orientation, resulting in bright optical images. This pH-driven reorientation of LCs provides a visual readout (bright-to-dark transition) correlated with biothiol concentration. The detection limits of Cys/Hcy and GSH for the PBA-doped LC platform are 0.1 μM and 0.5 μM, respectively. Overall, this study provides a simple, label-free and low-cost strategy that has a broad application prospect for the detection of biothiols. Full article