Search Results (125)

Soil salinity poses a critical threat to global agricultural productivity, exacerbating food security challenges in arid and semi-arid regions. This review synthesizes current knowledge on the physiological and biochemical impacts of salinity stress in plants, with a focus on the role of gibberellic acid (GA₃) in mitigating these effects. Salinity disrupts ion homeostasis, induces osmotic stress, and generates reactive oxygen species (ROS), leading to reduced chlorophyll content, impaired photosynthesis, and stunted growth across all developmental stages, i.e., from seed germination to flowering. Excess sodium (Na⁺) and chloride (Cl⁻) accumulation disrupts nutrient uptake, destabilizes membranes, and inhibits enzymes critical for carbon fixation, such as Rubisco. GA₃ emerges as a key regulator of salinity resilience, enhancing stress tolerance through various mechanisms like scavenging ROS, stabilizing photosynthetic machinery, modulating stomatal conductance, and promoting osmotic adjustment via osmolyte accumulation (e.g., proline). Plant hormone’s interaction with DELLA proteins and cross-talk with abscisic acid, ethylene, and calcium signaling pathways further fine-tune stress responses. However, gaps persist in understanding GA₃-mediated floral induction under salinity and its precise role in restoring photosynthetic efficiency. While exogenous GA₃ application improves growth parameters, its efficacy depends on the concentration- and species-dependent, with lower doses often proving beneficial and optimum doses potentially inhibitory. Field validation of lab-based findings is critical, given variations in soil chemistry and irrigation practices. Future research must integrate biotechnological tools (CRISPR, transcriptomics) to unravel GA₃ signaling networks, optimize delivery methods, and develop climate-resilient crops. This review underscores the urgency of interdisciplinary approaches to harness GA₃’s potential in sustainable salinity management, ensuring food security and safety in the rapidly salinizing world. Full article

Drought is a major stressor affecting tree physiology and is expected to intensify under climate extremes. Stems, partly due to their photosynthetic capacity, tend to be more drought-resilient than leaves. This study aimed to assess stem photosynthetic and its impact on carbon balance in leafless stems under drought conditions. Severe drought caused a marked decline in stem and root water potential (Ψ) and reduced stem water vapor conductance (g_tw) by about 40%. Despite this, stems retained the capacity for active gas exchange: though with reduced stem CO₂ efflux (ECO₂) and enhanced CO₂ refixation, which increased from about 40% under control conditions to ~55%–60% after drought, accompanied by a twofold increase in intrinsic water use efficiency (iWUE). Chlorophyll a fluorescence and pigment analyses indicated that the integrity of photosystem II (PSII) was preserved under drought, supporting sustained corticular photosynthesis. Concentrations of chloride, malate, and citrate in the xylem sap did not change significantly under drought, indicating a high capacity of stems to maintain homeostasis. Stable isotope analyses revealed drought-induced shifts in δ¹³C, consistent with altered carbon allocation following leaf abscission. These results confirm that stem photosynthesis and CO₂ reassimilation contribute significantly to stem metabolic resilience, mitigating drought-induced carbon losses and helping to preserve plant survival. Full article

Background: In this study, hydroponic experiments were conducted to examine the roles of sulphur (S), calcium (Ca), and nitric oxide (NO) in alleviating salt stress (20 mM NaCl) in tomato (Solanum lycopersicum L.) seedlings. Methods: Analyses included Na⁺/K⁺ contents, inorganic nitrogen (nitrate, nitrite, ammonium), nitrogen- and ammonium-assimilating enzymes (NR, NiR, GS, GOGAT), sulphur-assimilating enzymes (ATPS, OASTL), protein content, ROS (O₂^∙−, H₂O₂), and in vivo NO visualization were conducted. Results: We observed that salt stress increased Na⁺, reduced K⁺, disrupted nitrogen and sulphur metabolism, elevated ROS, and decreased NO, causing oxidative stress and reduced enzymatic activity. Supplementation with potassium sulphate (40 µM), calcium chloride (30 µM), and sodium nitroprusside (SNP; 40 µM) mitigated these effects, enhancing enzymatic activities, restoring Na⁺/K⁺ balance, improving protein content, and lowering ROS. The protective role of NO was confirmed using inhibitors L-NAME (500 µM) and cPTIO (100 µM), which reversed SNP’s benefits and aggravated stress damage. Conclusion: Overall, S, Ca, and NO were found to synergistically improve salt stress tolerance by modulating ion homeostasis, nitrogen and sulphur metabolism, and oxidative balance, offering nutrient- and signal-based strategies to enhance tomato resilience under salinity. Full article

Obesity is characterized by low-grade chronic inflammation, similar to the pathophysiology of inflammatory bowel disease (IBD) and colon cancer. IBD, which includes Crohn’s disease and ulcerative colitis, is becoming increasingly common in obese individuals. Our previous research documented that both IBD and obesity involve disrupted NaCl homeostasis in the small intestine. The present study investigated how obesity affects NaCl homeostasis in the distal colon, using the Zucker (Lepr^fa) rat as a genetic model of obesity. The functional and molecular alterations in NaCl homeostasis were evaluated through radioactive uptakes, RT-qPCR, and Western blot studies. We found a significant reduction in Cl absorption via Cl⁻/HCO₃⁻ exchanger, Downregulated in Adenoma (DRA) in the distal colon of obese rats compared to lean controls. This reduction was due to a decrease in the maximum transport capacity (V_max) of DRA, with no change in the affinity of the exchanger for chloride. DRA mRNA and protein levels were also downregulated in obese animals. In contrast, Na absorption via Na⁺/H⁺ exchanger and its expression remained unchanged. These findings are the first to demonstrate that DRA is significantly impaired in the distal colon due to obesity. This suggests that net NaCl absorption in the distal colon is compromised in obesity, potentially increasing the risk for IBD and colon cancer. Full article

Neuronal chloride (Cl⁻) homeostasis is fundamental for brain function, with disruptions increasingly recognized as pathogenic across neurological disorders. This review synthesizes evidence from preclinical models and clinical studies, integrating electrophysiological measurements, molecular analyses, imaging with genetically encoded sensors like ClopHensor, and behavioral assays. Key findings demonstrate that Cl⁻ dysregulation follows distinct patterns: (1) in epilepsy, KCC2 downregulation converts GABAergic inhibition to excitation, promoting seizures; (2) in Alzheimer’s disease (AD) models, pre-symptomatic KCC2 loss in hippocampus is observed, with KCC2 restoration reversing aspects of cognitive decline; (3) in autism spectrum disorders (ASD), developmental delays in GABA polarity shifts feature due to altered NKCC1/KCC2 ratios; and (4) in Huntington’s disease (HD), striatal neuron-specific Cl⁻ imbalances are linked to motor dysfunction. Methodologically, advanced tools—including subcellular Cl⁻ imaging and high-throughput drug screening—have enabled precise dissection of these mechanisms. Therapeutic strategies targeting Cl⁻ transporters (NKCC1 inhibitors like bumetanide, KCC2 enhancers like CLP290) show preclinical promise but require improved central nervous system (CNS) delivery and selectivity. These findings establish Cl⁻ homeostasis as both a biomarker and therapeutic target, necessitating precision medicine approaches to address heterogeneity in neurological disorders. Full article

Mutations in the CFTR genes causing cystic fibrosis (CF) are associated with the presence of thick, viscous mucus and the formation of biofilms in the gastrointestinal tract (GI) that impair intestinal homeostasis, triggering chronic inflammation, epithelial barrier dysfunction, and changes in the composition and activity of the gut microbiota. CFTR protein modulators represent a promising approach to enhancing lower GI function in patients with CF. The aim of the review is to present the complex relationships between the presence of CFTR gene mutations and the gut microbiota dysbiosis in patients with cystic fibrosis. Mutations in the CFTR gene, the molecular basis of cystic fibrosis (CF), disrupt epithelial ion transport and profoundly alter the gastrointestinal environment. Defective chloride and bicarbonate secretion leads to dehydration of the mucosal layer, increased mucus viscosity, and the formation of biofilms that favour microbial persistence, which together promote gut microbiota dysbiosis. This dysbiotic state contributes to impaired epithelial barrier function, chronic intestinal inflammation, and abnormal immune activation, thereby reinforcing disease progression. The interplay between CFTR dysfunction and microbial imbalance appears to be bidirectional, as dysbiosis may further exacerbate epithelial stress and inflammatory signalling. Therapeutic interventions with CFTR protein modulators offer the potential to partially restore epithelial physiology, improve mucus hydration, and foster a microbial milieu more consistent with intestinal homeostasis. The aim of this review is to elucidate the complex relationships between CFTR gene mutations and gut microbiota dysbiosis in patients with cystic fibrosis, with a particular emphasis on the clinical implications of these interactions and their potential to inform novel therapeutic strategies. Full article

Sulfate availability critically influences plant growth, yet the role of small RNAs, particularly microRNAs (miRNAs), in regulating responses to sulfate deficiency remains poorly understood. Here, we conducted a temporal analysis of sulfate deficiency-responsive miRNAs in the roots and leaves of Solanum lycopersicum (tomato), using an updated miRNA annotation in the SL4.0 genome. We found 40 differentially expressed miRNAs, including 2 novel, tomato-specific miRNAs. Tomato miRNAs showed an important time- and organ-specific regulation, similar to the described response of the mRNA transcriptome. Integration with transcriptomic data and Degradome-seq analysis highlighted both canonical and non-canonical targets for sulfate-responsive miRNAs. miR395, the most extensively studied miRNA, was found to control not only its conserved targets involved in sulfate transport and assimilation, but also genes involved in redox homeostasis, photosynthesis and chloride transport. Notably, most targets were repressed in leaves, suggesting miRNA-mediated downregulation of energy-intensive processes, while root targets were predominantly upregulated, including genes related to protein remodeling and antioxidant defense. Comparative analysis with Arabidopsis thaliana revealed a broader functional repertoire in tomato, suggesting species-specific adaptations to sulfate deficiency. Overall, our results underscore the critical role of miRNAs in fine-tuning organ-specific metabolic reprogramming during nutrient stress, expanding the current understanding of the regulatory landscape underlying sulfate deficiency in plants. Full article

Kupffer cells (KCs) play a pivotal role in the progression of metabolic-associated steatohepatitis (MASH). This study evaluated the impact of short-term KC depletion induced by gadolinium chloride (GdCl₃) in a rat model of MASH. The intervention with GdCl₃ effectively reduced KC markers CD68 and Clec4f, together with pro-inflammatory cytokines (IL-1β, TNFα, NOS2), without affecting anti-inflammatory markers (IL-10, MRC1). Histologically, GdCl₃ reduced hepatocyte ballooning and NAS despite persistent steatosis. KC depletion was associated with decreased oxidative stress markers (TBARS, 3-nitrotyrosine) and antioxidant enzyme activity (SOD, catalase). Additionally, markers of endoplasmic reticulum stress (ATF4, GRP78, CHOP, P58^IPK) and apoptosis (BAX/BCL2 ratio, cleaved caspase-3) were diminished. Despite these improvements, GdCl₃ had no effect on lipid or glucose metabolism in the liver, associated with persistent elevation of PTP1B expression induced by SRD intake. KC depletion, however, increased FGF21 expression. GdCl₃ treatment improved systemic insulin sensitivity and reduced fasting glucose and NEFA serum levels. In white adipose tissue, the treatment decreased adipocyte size, restored insulin signaling, and inhibited lipolysis (ATGL expression) without altering macrophage infiltration (IBA) or thermogenic protein levels (UCP1) in SRD rats. These findings suggest that KC depletion modulates liver-to-adipose tissue crosstalk, potentially through FGF21 signaling, contributing to improved systemic metabolic homeostasis of SRD animals. Full article

Olive oil, a cornerstone of the Mediterranean diet, contains a saponifiable lipid fraction rich in oleic acid, and a non-saponifiable fraction composed of minor bioactive constituents such as squalene, vitamin E, oleuropein aglycone, hydroxytyrosol, oleocanthal, and oleacein, among other phenolic and triterpenic compounds. These components are well-documented for their cardiovascular, anti-inflammatory, antioxidant, and neuroprotective activities. This review explores the physiological relevance of olive oil lipids and their derivatives on cellular membranes and ion transport systems, by combining biochemical and electrophysiological insights. We discuss how oleic acid and its metabolites influence membrane lipid composition, modulate fluidity, and reorganize lipid rafts—key elements for the proper localization and function of ion channels. Additionally, we examine evidence showing that several olive oil components regulate ion channels such as TRP, potassium, calcium, and chloride channels, as well as other transporters, thereby influencing ionic homeostasis, oxidative balance, and signal transduction in excitable and non-excitable cells. By combining these findings, we propose a conceptual framework in which olive oil lipids and their derivatives act as multimodal regulators of bioelectrical signaling. By modulating cell membrane dynamics, these functional molecules help maintain cellular communication and homeostasis. This integrative view not only strengthens our understanding of olive oil’s health-promoting effects but also opens new avenues for targeting ion-regulatory mechanisms in metabolic, cardiovascular, and neurological diseases. Full article

Background: Oral antiseptic formulations are widely used as adjuncts in oral hygiene to reduce pathogenic microorganisms and prevent oral diseases. While these agents are effective in controlling biofilm, their broader effects may disrupt the oral microbiota’s balance, potentially contributing to systemic health implications. The complex relationship between antiseptic use, microbial composition, and systemic outcomes remains insufficiently mapped. Objective: This scoping review aimed to explore and map the current evidence regarding the impact of antiseptic formulations on oral microbiota composition and to examine their potential associations with systemic diseases. Methods: A comprehensive literature search was performed using PubMed, Scopus, and Web of Science up to June 2025. Studies were included if they investigated antiseptic formulations commonly used in oral healthcare—such as chlorhexidine, essential oils, and cetylpyridinium chloride—and reported effects on oral microbiota and/or systemic health. Eligible study types included human clinical trials, observational studies, in vitro, and animal studies. Two reviewers independently screened and selected studies, with disagreements resolved by consensus. Data extraction focused on study design, antiseptic agents, microbial outcomes, and systemic implications. A total of 12 studies were included and charted. Results: The included studies demonstrated that oral antiseptics effectively reduce pathogenic microorganisms and improve clinical outcomes in oral diseases such as gingivitis and periodontitis. However, several studies also reported alterations in commensal microbial communities, suggesting a potential for dysbiosis. Some studies indicated possible links between antiseptic-induced microbial changes and systemic conditions, including cardiovascular and respiratory diseases. Conclusions: The evidence highlights a dual effect of antiseptic formulations: while beneficial in controlling oral pathogens, they may disrupt microbial homeostasis with possible systemic consequences. Further research is needed to evaluate long-term effects and develop targeted, microbiota-preserving oral hygiene strategies. Full article

Parabens—specifically methylparaben (MeP), ethylparaben (EtP), propylparaben (PrP), and butylparaben (BuP)—are widely used substances in everyday life, particularly as preservatives in pharmaceutical and food products. However, these compounds are not effectively removed by conventional water and wastewater treatment processes, potentially causing disruptions to human homeostasis and the endocrine system. This study conducted a transport and dimensional analysis through simulation of the adsorption process for these parabens, using zinc chloride-activated carbon derived from spent coffee grounds (ACZnCl₂) as the adsorbent, implemented via Aspen Properties^® and Aspen Adsorption^®. Simulations were performed for two inlet concentrations (50 mg/L and 100 mg/L) and two adsorption column heights (3 m and 4 m), considering a volumetric flow rate representative of a medium-sized city with approximately 100,000 inhabitants. The results showed that both density and surface tension of the parabens varied linearly with increasing temperature, and viscosity exhibited a marked reduction above 30 °C. Among the tested conditions, the configuration with 50 mg∙L⁻¹ inlet concentration and a 4 m column height demonstrated the highest adsorption capacity and better performance under adsorption–desorption equilibrium. These findings indicate that the implementation of adsorption beds on an industrial scale in water and wastewater treatment systems is both environmentally and socially viable. Full article

Barium chloride (BaCl₂), a known environmental pollutant, induces organ-specific oxidative stress through disruption of redox homeostasis. This study evaluated the protective effects and safety profile of sodium copper chlorophyllin (SCC) and ascorbic acid (ASC) against BaCl₂-induced oxidative damage in the liver and brain of mice using a two-phase experimental protocol. Animals received either SCC (40 mg/kg), ASC (160 mg/kg), or their combination for 14 days prior to BaCl₂ exposure (150 mg/L in drinking water for 7 days), allowing evaluation of both preventive and therapeutic effects. Toxicological and behavioral assessments confirmed the absence of systemic toxicity or neurobehavioral alterations following supplementation. Body weight, liver and kidney indices, and biochemical markers (Aspartate Aminotransferase (ASAT), Alanine Aminotransferase (ALAT), creatinine) remained within physiological ranges, and no anxiogenic or locomotor effects were observed. In the brain, BaCl₂ exposure significantly increased SOD (+49%), CAT (+66%), GPx (+24%), and GSH (+26%) compared to controls, reflecting a robust compensatory antioxidant response. Although lipid peroxidation (MDA) showed a non-significant increase, SCC, ASC, and their combination reduced MDA levels by 42%, 37%, and 55%, respectively. These treatments normalized antioxidant enzyme activities and GSH, indicating an effective neuroprotective effect. In contrast, the liver exhibited a different oxidative profile. BaCl₂ exposure increased MDA levels by 80% and GSH by 34%, with no activation of SOD, CAT, or GPx. Histological analysis revealed extensive hepatocellular necrosis, vacuolization, and inflammatory infiltration. SCC significantly reduced hepatic MDA by 39% and preserved tissue architecture, while ASC alone or combined with SCC exacerbated inflammation and depleted hepatic GSH by 71% and 78%, respectively, relative to BaCl₂-exposed controls. Collectively, these results highlight a differential, organ-specific response to BaCl₂-induced oxidative stress and the therapeutic potential of SCC and ASC. SCC emerged as a safer and more effective agent, particularly in hepatic protection, while both antioxidants demonstrated neuroprotective effects when used individually or in combination. Full article

The transition from conchocelis to conchosporangia in Pyropia haitanensis represents a pivotal stage in its life cycle. As a commercially vital red alga, P. haitanensis plays a dominant role in global nori production. The transition governing its sporulation efficiency is pivotal for aquaculture success, yet the underlying regulatory mechanisms, especially their integration with metabolic cues such as polyamines, remain poorly understood. This study uncovered a critical role for the polyamine spermine (SPM) in promoting conchosporangial formation, mediated through the signaling activity of superoxide anions (O₂·⁻). Treatment with SPM markedly elevated O₂·⁻ levels, an effect that was effectively inhibited by the NADPH oxidase inhibitor diphenyliodonium chloride (DPI), underscoring the role of O₂·⁻ as a key signaling molecule. Transcriptomic analysis revealed that SPM enhanced photosynthesis, carbon assimilation, and respiratory metabolism, while simultaneously activating antioxidant enzymes, such as superoxide dismutase (SOD), ascorbate peroxidase (APX), and catalase (CAT), to regulate hydrogen peroxide (H₂O₂) levels and maintain redox homeostasis. Furthermore, SPM upregulated genes associated with photosynthetic carbon fixation and the C₂ oxidative photorespiration pathway, supplying the energy and metabolic resources necessary for this developmental transition. These findings suggested that SPM orchestrated O₂·⁻ signaling, photosynthetic activity, and antioxidant defenses to facilitate the transition from conchocelis to conchosporangia in P. haitanensis. Full article

Chloride, long considered a passive extracellular anion, has emerged as a key determinant in the pathophysiology and management of heart failure (HF) and cardiorenal syndrome. In contrast to sodium, which primarily reflects water balance and vasopressin activity, chloride exerts broader effects on neurohormonal activation, acid–base regulation, renal tubular function, and diuretic responsiveness. Its interaction with With-no-Lysine (WNK) kinases and chloride-sensitive transporters underscores its pivotal role in electrolyte and volume homeostasis. Hypochloremia, frequently observed in HF patients treated with loop diuretics, is independently associated with adverse outcomes, diuretic resistance, and arrhythmic risk. Conversely, hyperchloremia—often iatrogenic—may contribute to renal vasoconstriction and hyperchloremic metabolic acidosis. Experimental data also implicate chloride dysregulation in myocardial electrical disturbances and an increased risk of sudden cardiac death. Despite mounting evidence of its clinical importance, serum chloride remains underappreciated in contemporary risk assessment models and treatment algorithms. This review synthesizes emerging evidence on chloride’s role in HF, explores its diagnostic and therapeutic implications, and advocates for its integration into individualized care strategies. Future studies should aim to prospectively validate these associations, evaluate chloride-guided therapeutic interventions, and assess whether incorporating chloride into prognostic models can improve risk stratification and outcomes in patients with heart failure and cardiorenal syndrome. Full article

The GABA_A receptors, through a short-term interaction with a mediator, induce hyperpolarization of the membrane potential (V_m) via the passive influx of chloride ions (Cl⁻) into neurons. The massive (or intense) activation of the GABA_ARs by the agonist could potentially lead to depolarization/excitation of the V_m. Although the ionic mechanisms of GABA_A-mediated depolarization remain incompletely understood, a combination of the outward chloride current and the inward bicarbonate current and the resulting pH shift are the main reasons for this event. The GABA_A responses are determined by the ionic gradients—neuronal pH/bicarbonate homeostasis is maintained by carbonic anhydrase and electroneutral/electrogenic bicarbonate transporters and the chloride level is maintained by secondary active cation–chloride cotransporters. Massive activation can also induce the rundown effect of the receptor function. This rundown effect partly involves phosphorylation, Ca²⁺ and the processes of receptor desensitization. In addition, by various methods (including fluorescence and optical genetic methods), it has been shown that massive activation of GABA_ARs during pathophysiological activity is also associated with an increase in [Cl⁻]_i and a decline in the pH and ATP levels in neurons. Although the relationship between the neuronal changes induced by massive activation of GABAergic signaling and the risk of developing neurodegenerative disease has been extensively studied, the molecular determinants of this process remain somewhat mysterious. The aim of this review is to summarize the data on the relationship between the massive activation of inhibitory signaling and the ionic changes in neurons. The potential role of receptor dysfunction during massive activation and the resulting ionic and metabolic disruption in neurons during the manifestation of network/seizure activity will be considered. Full article