Upregulation Of Antioxidant Enzymes Research Articles

Zinc oxide nanoparticle biofortification of lentil seedlings enhances plant growth and zinc bioavailability in rats

This study aimed to evaluate the potential of zinc oxide nanoparticles (ZnO NPs) in the biofortification of lentil seedlings and subsequently improve the Zn status in rats. In the first phase of the study, the effects of various ZnO NPs concentrations (0, 10, 20, 40, 80, and 160 ppm) on the lentil growth, Zn accumulation, and other physiological parameters were investigated. Subsequently, the rats were fed ZnO NP-biofortified lentil seedlings (20 and 160 ppm) to assess their impact on animal health and Zn status. The results highlighted a concentration-dependent response of lentil seedlings to ZnO NPs, with optimal growth observed at 20 ppm, whereas higher concentrations inhibited lentil growth. Pigment and biochemical analyses revealed a complex interplay between chlorophyll, carotenoids, soluble sugars, and proteins with distinct responses to nanoparticle concentrations. Elevated levels of hydrogen peroxide and malondialdehyde of lentil seedlings at high concentrations of ZnO NPs suggest oxidative stress, countered by the upregulation of antioxidant enzymes and increased phenolic compounds. On the other hand. animal studies have showed that ZnO NP-biofortified lentil seedlings enhance serum zinc and magnesium levels in rats without affecting body weight. While serum triglyceride levels of rats decreased in both treatment groups, an elevation in creatinine and a marked increase in aspartate aminotransferase (AST) levels were observed at a higher ZnO NP concentration (160 ppm), indicative of potential kidney and liver stress. Paradoxically, serum iron levels were lower in all groups consuming lentil seedlings than in the control group, suggesting a potential interaction between lentil components and iron metabolism. These findings suggest that ZnO NP-biofortified lentils may be a promising approach to enhance Zn nutrition; however, further investigation is needed to optimize ZnO NPs concentration and assess long-term safety.

Tri-iso-butyl phosphate (TiBP) exposure induces neurotoxicity by triggering oxidative stress accompanied by neurotransmitter system disruptions and apoptosis in zebrafish larvae

The current research sheds light on the biological toxicity of organophosphate flame retardants (OPFRs), yet it overlooks the neurotoxicity and potential molecular mechanisms of tris(1,3-dichloro-2-propyl) phosphate (TiBP), a prominent constituent of the OPFRs. To address this, we utilized zebrafish larvae as a model to investigate TiBP's acute toxicity and neurotoxic effects, along with the associated molecular pathways. Our findings revealed that the 96 h and 120 h LC50 values for TiBP were 56.51 mg/L and 48.85 mg/L, respectively. Gradient exposure based on the 120 h LC50 demonstrated that TiBP induced developmental toxicity, characterized by elevated heart rate, reduced body length, and diminished eye distance. Additionally, a decrease in swimming activity was observed in the light test, along with the inhibition of the neuro crest cell development in Tg (HuC:eGFP) and Tg (sox10: eGFP) zebrafish larvae following TiBP exposure, as well as the alterations of neurogenesis and ACh-related genes. Expression of key neurodevelopment genes, including mbpa, gap43, nestin, ngfra, was significantly downregulated. Furthermore, heightened anxiety-like behaviors in open field and phototaxis tests were observed, concomitant with neurotransmitter imbalances. Specifically, there was an increase in DA levels, a decrease in GABA, and an upregulation of AChE activity. These disruptions were primarily mediated through transcriptional dysregulation of neurotransmitter synthesis, transport, and reception. Upon exposure to TiBP, zebrafish larvae exhibited a concentration-dependent increase in both ROS level and apoptosis. An upregulation of antioxidant enzymes and their transcription levels indicated the presence of oxidative stress in the larvae. The induction of ddit3 was congruent with the observed apoptosis, suggesting that it may be triggered by oxidative stress via the ERs-CHOP pathway. In summary, our study indicates that oxidative stress is a pivotal molecular event in the neurotoxicity induced by TiBP, implicating the disruption of the GABAergic, dopaminergic, and cholinergic systems, as well as triggering apoptosis.

Alleviation of cadmium toxicity in soybean (Glycine max L.): Up-regulating antioxidant capacity and enzyme gene expressions and down-regulating cadmium uptake by organic or inorganic selenium

Although much interest has been focused on the role of selenium (Se) in plant nutrition over the last 20 years, the influences of organic selenium (selenomethionine; Se-Met) and inorganic selenium (potassium selenite; Se-K) on the growth and physiological characters of cadmium (Cd)-stressed Glycine max L.) seedlings have not yet been studied. In this study, the impacts of Se-Met or Se-K on the growth, water physiological parameters (gaseous exchange and leaf water content), photosynthetic and antioxidant capacities, and hormonal balance of G. max seedlings grown under 1.0 mM Cd stress were studied. The results showed that 30 μM Se-K up-regulates water physiological parameters, photosynthetic indices, antioxidant systems, enzymatic gene expression, total antioxidant activity (TAA), and hormonal balance. In addition, it down-regulates levels of reactive oxygen species (ROS; superoxide free radicals and hydrogen peroxide), oxidative damage (malondialdehyde content as an indicator of lipid peroxidation and electrolyte leakage), Cd translocation factor, and Cd content of Cd-stressed G. max seedlings. These positive findings were in favor of seedling growth and development under Cd stress. However, 50 μM Se-Met was more efficient than 30 μM Se-K in promoting the above-mentioned parameters of Cd-stressed G. max seedlings. From the current results, we conclude Se-Met could represent a promising strategy to contribute to the development and sustainability of crop production on soils contaminated with Cd at a concentration of up to 1.0 mM. However, further work is warranted to better understand the precise mechanisms of Se-Met action under Cd stress conditions.

Cardioprotective potential of oleuropein, hydroxytyrosol, oleocanthal and their combination: Unravelling complementary effects on acute myocardial infarction and metabolic syndrome

Clinical studies have previously established the role of olive products in cardiovascular disease (CVD) prevention, whilst the identification of the responsible constituents for the beneficial effects is still pending. We sought to assess and compare the cardioprotective potential of oleuropein (OL), hydroxytyrosol (HT), oleocanthal (OC) and oleanolic Acid (OA), regarding Ischemia/Reperfusion Injury (IRI) and CVD risk factors alleviation. The scope of the study was to design a potent and safe combinatorial therapy for high-cardiovascular-risk patients on a bench-to-bedside approach. We evaluated the IRI-limiting potential of 6-weeks treatment with OL, HT, OC or OA at nutritional doses, in healthy and metabolic syndrome (MS)-burdened mice. Three combinatorial regimens were designed and the mixture with preponderant benefits (OL-HT-OC, Combo 2), including infarct sparing and antiglycemic potency, compared to the isolated compounds, was further investigated for its anti-atherosclerotic effects. In vivo experiments revealed that the combination regimen of Combo 2 presented the most favorable effects in limiting infarct size and hyperglycemia, which was selected to be further investigated in the clinical setting in Chronic Coronary Artery Syndrome (CCAS) patients. Cardiac function, inflammation markers and oxidative stress were assessed at baseline and after 4 weeks of treatment with the OL-HT-OC supplement in the clinical study. We found that OL, OC and OA significantly reduced infarct size in vivo compared to Controls. OL exhibited antihyperglycemic properties and OA attenuated hypercholesterolemia. OL-HT-OA, OL-HT-OC and OL-HT-OC-OA combination regimens were cardioprotective, whereas only OL-HT-OC mitigated hyperglycemia. Combo 2 cardioprotection was attributed to apoptosis suppression, enhanced antioxidant effects and upregulation of antioxidant enzymes. Additionally, it reduced atherosclerotic plaque extent in vivo. OL-HT-OC supplement ameliorated cardiac, vascular and endothelial function in the small-scale clinical study. Conclusively, OL-HT-OC combination therapy exerts potent cardioprotective, antihyperglycemic and anti-atherosclerotic properties in vivo, with remarkable and clinically translatable cardiovascular benefits in high-risk patients.

Transcriptomic and metabolomic analysis of quality deterioration of postharvest okra fruit at different storage temperatures

Okra fruit have short postharvest potential and are susceptible to chilling injury (CI). To increase our understanding of the metabolism of okra fruit we have analyzed the transcriptomic and metabolomic changes of the fruit stored at 4, 10, and 22 ℃ for six days. Compared with 0 d, storage at 22 °C for 6 days, senescence and lignification of fruit were associated with upregulation of genes related to abscisic acid (ABA) synthesis and signal transduction (ZEP, NCED, AAO, PYR/PYL, PP2C), lignin synthesis (HCT, 4CL, CCR, CAD, F5H, COMT), and cellulose synthesis (CesA). Chilling injury of okra at 4 ℃ may be caused by the activation of the α-linolenic acid metabolic pathway and flavonoid synthesis pathway, compromised membrane integrity, and higher reactive oxygen species levels. Storage at 10 ℃ resulted in the downregulation of ABA synthesis, signal transduction, and lignin synthesis genes, inhibition of α-linolenic acid pathway metabolites, and the expression of membrane lipid degradation genes (PLD, PLA, lipase, DGK, LOX). Conversely, there was an upregulation of antioxidant enzymes (APX, AO, POD, Grx, MDHAR) and genes involved in the flavonoid synthesis pathway (C4H, CHS, CHI, F3H, ANS), and with their corresponding metabolites (pinocembrin, butin, epiafzelechin, catechin). These changes were associated with slower fruit senescence, indicating that 10 ℃ better maintained the physiological quality of okra fruit after harvest. Based on these findings, a network model was established to control the postharvest quality of okra fruit under different temperature treatments. This study explored the regulatory mechanism of okra at different temperatures at the molecular level and laid a theoretical foundation for improving the quality of postharvest okra and extending its shelf life.

Structure-anti-inflammatory activity relationship of garlic fructans in mice with dextran sulfate sodium-induced colitis: Impact of chain length

The present study identified the protective effects of garlic oligo/poly-saccharides of different chain lengths against dextran sulfate sodium (DSS)-induced colitis in mice and elucidated the structure-function relationships. The results showed that oral intake of garlic oligo/poly-saccharides decreased disease activity index, reduced colon shortening and spleen enlargement, and ameliorated pathological damage in the mouse colon. The dysregulation of colonic pro/anti-inflammatory cytokines was significantly alleviated, accompanied by up-regulated antioxidant enzymes, blocked TLR4-MyD88-NF-κB signaling pathway, enhanced intestinal barrier integrity, and restored SCFA production. Garlic oligo/poly-saccharides also reversed gut microbiota dysbiosis in colitic mice by expanding beneficial bacteria and suppressing the growth of harmful bacteria. High-molecular-weight polysaccharides exhibited stronger alleviating effects on DSS-induced colitic symptoms in mice than low-molecular-weight oligo/poly-saccharides did, probably due to their greater ability to be fermented in the colon. Taken together, this study demonstrated the anti-inflammatory effects of garlic oligo/poly-saccharides and revealed that high-molecular-weight polysaccharide fractions were more effective in alleviating DSS-induced colitis.

VALD-2 mitigates cisplatin-induced acute kidney injury: Mechanistic insights into oxidative stress modulation and inflammation suppression.

This study explores the compelling antitumor properties of VALD-2, a synthetic Schiff base ligand known for its low toxicity. The focus is on investigating VALD-2's protective role against cisplatin-induced acute kidney injury (AKI) in mice, with a specific emphasis on mitigating oxidative stress and inflammation. The study involves daily intraperitoneal injections of amifostine or VALD-2 over 7 days to establish an AKI model. Subsequently, mice were assigned to normal control, cisplatin group, cisplatin + amifostine group, and cisplatin + VALD-2 10 mg/kg group, cisplatin + VALD-2 20 mg/kg, and cisplatin + VALD-2 40 mg/kg. Kidney injury is assessed through serum blood urea nitrogen (BUN) and creatinine (Cr) activity assays. Levels of inflammatory factors,tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), in kidney tissue of mice were assessed through enzyme-linked immunosorbent assay (ELISA). The protective effect of VALD-2 is further examined through HE staining to observe pathological changes in kidney injury. The ultrastructural changes of renal cells and tubular epithelial cells were observed by electron microscopy under experimental conditions, indicating the effect of VALD-2 on reversing cisplatin-induced renal injury. The study delves into VALD-2's protective mechanisms against cisplatin-induced kidney injury by using western blot analysis to assess the expression levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) in kidney tissues. VALD-2 demonstrates significant improvement in cisplatin-induced AKI, as evidenced by increased BUN and Cr levels. It effectively protects kidney tissue from oxidative damage, enhancing SOD and GSH-Px activities while reducing MDA levels. The study also reveals a decrease in TNF-α and IL-6 levels, supported by ELISA results, and histological findings confirm anti-nephrotoxic effects. Western blot analysis shows an upregulation of antioxidant enzymes (SOD, GSH-Px) and a reduction in MDA production. VALD-2 emerges as a promising mitigator of cisplatin-induced AKI, showcasing its ability to enhance oxidative stress-related protein expression. The findings suggest VALD-2 as a potential therapeutic agent for protecting against cisplatin-induced kidney injury.

Adolescent treadmill exercise enhances hippocampal brain-derived neurotrophic factor (BDNF) expression and improves cognition in autism-modeled rats

Autism spectrum disorder (ASD) is a prevalent neurodevelopmental disorder characterized by repetitive behaviors and altered communication abilities. Exercise is a low-cost intervention that could improve cognitive function and improve brain plasticity mechanisms. Here, the valproic acid (VPA) model was utilized to induce ASD-like phenotypes in rodents. Animals were exercised on a treadmill and performance was evaluated on a cognitive flexibility task. Biomarkers related to exercise and plasticity regulation were quantified from the prefrontal cortex, hippocampus, and skeletal muscle. Exercised VPA animals had higher levels of hippocampal BDNF compared to sedentary VPA animals and upregulated antioxidant enzyme expression in skeletal muscle. Cognitive improvements were demonstrated in both sexes, but in different domains of cognitive flexibility. This research demonstrates the benefits of exercise and provides evidence that molecular responses to exercise occur in both the central nervous system and in the periphery. These results suggest that improving regulation of BDNF via exercise, even at low intensity, could provide better synaptic regulation and cognitive benefits for individuals with ASD.

ISKNV Triggers AMPK/mTOR-Mediated Autophagy Signaling through Oxidative Stress, Inducing Antioxidant Enzyme Expression and Enhancing Viral Replication in GF-1 Cells.

Infectious spleen and kidney necrosis virus (ISKNV) infections can induce the process of host cellular autophagy but have rarely been identified within the molecular autophagy signaling pathway. In the present study, we demonstrated that ISKNV induces ROS-mediated oxidative stress signals for the induction of 5'AMP-activated protein kinase/mechanistic target of rapamycin kinase (AMPK/mTOR)-mediated autophagy and upregulation of host antioxidant enzymes in fish GF-1 cells. We also examined ISKNV-induced oxidative stress, finding that reactive oxidative species (ROS) increased by 1.5-fold and 2.5-fold from day 2 to day 3, respectively, as assessed by the H2DCFDA assay for tracing hydrogen peroxide (H2O2), which was blocked by NAC treatment in fish GF-1 cells. Furthermore, ISKNV infection was shown to trigger oxidative stress/Nrf2 signaling from day 1 to day 3; this event was then correlated with the upregulation of antioxidant enzymes such as Cu/ZnSOD and MnSOD and was blocked by the antioxidant NAC. Using an MDC assay, TEM analysis and autophagy marker LC3-II/I ratio, we found that ROS stress can regulate autophagosome formation within the induction of autophagy, which was inhibited by NAC treatment in GF-1 cells. Through signal analysis, we found that AMPK/mTOR flux was modulated through inhibition of mTOR and activation of AMPK, indicating phosphorylation levels of mTOR Ser 2448 and AMPK Thr 172 from day 1 to day 3; however, this process was reversed by NAC treatment, which also caused a reduction in virus titer (TCID50%) of up to 1000 times by day 3 in GF-1 cells. Thus, ISKNV-induced oxidative stress signaling is blocked by antioxidant NAC, which can also either suppress mTOR/AMPK autophagic signals or reduce viral replication. These findings may provide the basis for the creation of DNA control and treatment strategies.

Comparison of infant bone marrow- and umbilical cord-derived mesenchymal stem cells in multilineage differentiation

We compared infant bone marrow-derived mesenchymal stem cells (infant BMSCs) with umbilical cord-derived mesenchymal stem cells (UCSCs) by assessing multilineage differentiation. Proliferation was gauged through changes in cell numbers and doubling time. Senescence-related genes (p16, p21, and p53), senescence-associated β-galactosidase (SA-β-gal), and γH2AX immunofluorescence determined senescence presence. Superoxide dismutases (SODs) and genes related to various differentiations were analyzed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Differentiation was confirmed through histochemical, immunohistochemical, and immunofluorescence staining. Infant BMSCs surpassed UCSCs in proliferation. Infant BMSCs exhibited lower senescence-related gene expression at late passages, upregulated antioxidant enzymes during early passages, and reduced SA-β-gal staining. Chondrogenic gene expression (SOX9, COL2, and COL10) was enhanced in infant BMSCs, along with improved immunohistochemical staining. Infant BMSCs showed higher expression of osteogenic (ALP and OCN) and adipogenic (PPARγ and LPL) genes, confirmed by histochemical staining. However, UCSCs had higher expression of tenogenic genes (MMP3, SCX, DCN, and TNC). Hepatogenic differentiation potential was similar, with no significant difference in hepatogenic gene expression (ALB and TAT). Compared to UCSCs, infant BMSCs demonstrated superior proliferation, reduced senescence, increased antioxidant capacity, and enhanced differentiation potential toward chondrogenic, osteogenic, and adipogenic lineages.

Rhodotorula mucilaginosa A8, a potential helper strain in a vitamin C microbial fermentation process.

In the vitamin C microbial fermentation system, oxidative stress limits the growth and 2-keto-l-gulonic acid (2-KLG, the precursor of vitamin C) production of Ketogulonicigenium vulgare. Most Bacillus strains, as helper strains, have been reported to release key biomolecules to reduce oxidative stress and promote the growth and 2-KLG production of K. vulgare. To understand the specific mechanism by which the helper strain and K. vulgare interact to reduce oxidative stress, a novel helper strain, Rhodotorula mucilaginosa A8, was used to construct a consortium in the co-culture fermentation system. Based on the activities of the antioxidant enzymes and quantitative polymerase chain reaction (qPCR) analysis, R. mucilaginosa A8 could reduce oxidative stress and increase 2-KLG production in K. vulgare by upregulating antioxidant enzyme activities and related gene-expression levels. In addition, the carotenoids of R. mucilaginosa promoted 2-KLG production in K. vulgare. Coculture of R. mucilaginosa with K. vulgare increased the yield of carotenoids. This study suggested that helper strains with the ability to reduce oxidative stress in K. vulgare would likely act as potential helper strains for facilitating 2-KLG biosynthesis. This work could provide a theoretical basis for the search for potential helper strains for vitamin C microbial fermentation and for the construction of synthetic microbial communities to produce valuable products.

Integrated Mechanism of Immune Response Modulation by Arctium Lappa L. Fructans Based on Microbiome and Metabolomics Technologies.

Arctium lappa L. is widely consumed for its various biological effects, and polysaccharides are its main functional components. The present study aimed to evaluate the immunoregulatory effects of the main polysaccharides from burdock (ALP-1) and reveal the underlying mechanisms. ALP-1 consisted of fructose and glucose (14.57:1) and had a molecular weight of 2757 Da, with typical characteristics of (1 → 2)-linked linear fructans. Oral intake of ALP-1 significantly increased the number of colonic goblet cells, serum immunoglobulin A and immunoglobulin G levels, and fecal secretory immunoglobulin A content as well as up-regulated antioxidant enzymes and increased short chain fatty acid production. In addition, ALP-1 administration regulated pro/anti-inflammatory cytokines (i.e., interleukin (IL)-1β, IL-6, tumor necrosis factor-α, interferon-γ, and IL-10), intestinal microbiota structure, and the spatial information on key metabolites. Some gut-microbiota-mediated metabolic processes were also significantly altered. These results indicated that ALP-1 could exert beneficial effects on immune responses and intestinal health in healthy mice.

Protective effects of the bioactive peptide from maggots against skin flap ischemia‒reperfusion injury in rats

Ischemia‒reperfusion (I/R) injury is a frequently observed complication after flap surgery, and it affects skin flap survival and patient prognosis. Currently, there are no proven safe and effective treatment options to treat skin flap I/R injury. Herein, the potential efficacies of the bioactive peptide from maggots (BPM), as well as its underlying mechanisms, were explored in a rat model of skin flap I/R injury and LPS- or H2O2-elicited RAW 264.7 cells. We demonstrated that BPM significantly ameliorated the area of flap survival, and histological changes in skin tissue in vivo. Furthermore, BPM could markedly restore or enhance Nrf2 and HO-1 levels, and suppress the expression of pro-inflammatory cytokines, including TLR4, p-IκB, NFκB p65, p-p65, IL-6, and TNF-α in I/R-injured skin flaps. In addition, BPM treatment exhibited excellent biocompatibility with an adequate safety profile, while it exhibited superior ROS-scavenging ability and the upregulation of antioxidant enzymes in vitro. Mechanistically, the above benefits related to BPM involved the activation of Nrf2/HO-1 and suppression of TLR4/NF-κB pathway. Taken together, this study may provide a scientific basis for the potential therapeutic effect of BPM in the prevention of skin flap I/R injury and other related diseases.

Stress response and phytoextraction potential of two Noccaea caerulescens populations in multicontaminated soil

AbstractMulticontamination of soils by various organic and inorganic pollutants is considered as an obstacle for the development of hyperaccumulator plants and phytoextraction of metals. The aim of this study was to investigate the effect of polycyclic aromatic hydrocarbons (PAHs) in combination with trace elements on the antioxidant response and phytoextraction efficiency of two populations of the hyperaccumulator Noccaea caerulescens from either a metalliferous (Ganges) or a nonmetalliferous (Chavignée) site. Plants were grown for 17 days in soil containing moderate concentrations of trace elements and under the effect of phenanthrene (PHE), a PAH stress model. In general, exposure to PHE resulted in a reduction of growth parameters, together with the upregulation of antioxidant enzymes and compounds and limitations in nutrient uptake and heavy metal extraction in N. caerulescens. Variations were observed in the extent of enzymatic activities and the amount of metals extracted between the two populations studied. Plants from Chavignée exhibited a slightly more tolerant response to PHE stress than those from Ganges. The presence of PHE in the soil proved highly toxic to N. caerulescens, resulting in low numbers of survivors. Nevertheless, the differences observed between the two populations with regard to growth, metal extraction, and antioxidant defense responses suggest that the difference in defense capacity may ensure different tolerance. This difference may be linked to adaptations acquired by each population according to the soil type from which it originates. However, these results need to be confirmed by further experiments.

Galectin-8-like isoform X1 mediates antibacterial, antiviral, and antioxidant responses in red-lip mullet (Planiliza haematocheilus) through positive modulation of pro-inflammatory cytokine, chemokine, and enzymatic antioxidant activity

Galectin 8 belongs to the tandem repeat subclass of the galectin superfamily. It possesses two homologous carbohydrate recognition domains linked by a short peptide and preferentially binds to β-galactoside-containing glycol-conjugates in a calcium-independent manner. This study identified Galectin-8-like isoform X1 (PhGal8X1) from red-lip mullet (Planiliza haematocheilus) and investigated its role in regulating fish immunity. The open reading frame of PhGal8X1 was 918bp, encoding a soluble protein of 305 amino acids. The protein had a theoretical isoelectric (pI) point of 7.7 and an estimated molecular weight of 34.078 kDa. PhGal8X1 was expressed in various tissues of the fish, with prominent levels in the brain, stomach, and intestine. PhGal8X1 expression was significantly (p < 0.05) induced in the blood and spleen upon challenge with different immune stimuli, including polyinosinic:polycytidylic acid, lipopolysaccharide, and Lactococcus garvieae. The recombinant PhGal8X1 protein demonstrated agglutination activity towards various bacterial pathogens at a minimum effective concentration of 50 μg/mL or 100 μg/mL. Subcellular localization observations revealed that PhGal8X1 was primarily localized in the cytoplasm. PhGal8X1 overexpression in fathead minnow cells significantly (p < 0.05) inhibited viral hemorrhagic septicemia virus (VHSV) replication. The expression levels of four proinflammatory cytokines and two chemokines were significantly (p < 0.05) upregulated in PhGal8X1 overexpressing cells in response to VHSV infection. Furthermore, overexpression of PhGal8X1 exhibited protective effects against oxidative stress induced by H2O2 through the upregulation of antioxidant enzymes. Taken together, these findings provide compelling evidence that PhGal8X1 plays a crucial role in enhancing innate immunity and promoting cell survival through effective regulation of antibacterial, antiviral, and antioxidant defense mechanisms in red-lip mullet.

Impact of LKB1 status on radiation outcome in patients with stage III non-small-cell lung cancer

Preclinical studies suggest that loss of LKB1 expression renders cancer cells less responsive to radiation partly through NRF2-mediated upregulation of antioxidant enzymes protecting against radiation-induced DNA damage. Here we investigated the association of an alteration in this pathway with radio-resistance in lung cancer patients. Patients with locally advanced non-small cell lung cancer (LA-NSCLC) who were treated with chemoradiotherapy (CRT) and analyzed for LKB1 expression using semiquantitative immunohistochemistry. Clinical characteristics and expression of LKB1 were analyzed for association with radiotherapy outcomes. We analyzed 74 available tumor specimens from 178 patients. After a median follow-up of 40.7 months, 2-year cumulative incidence of locoregional recurrence (LRR) in patients who had LKB1Low expression was significantly higher than those with LKB1High expression (68.8% vs. 31.3%, P = 0.0001). LKB1Low expression was found significantly associated with a higher incidence of distant metastases (DM) (P = 0.0008), shorter disease-free survival (DFS) (P = 0.006), and worse overall survival (OS) (P = 0.02) compared to LKB1High expression. Moreover, patients with LKB1Low expression showed a significantly higher 2-year cumulative incidence of LRR (77.6% vs. 21%; P = 0.02), higher DM recurrence (P = 0.002), and shorter OS (P < 0.0001) compared with the EGFR-mutant group. For all patients with LKB1Low who had LRR, these recurrences occurred within the field of radiation, in contrast to those with LKB1High expression having both in-field, marginal, and out-of-field failures. LKB1 expression may serve as a potential biomarker for poor outcomes after receiving radiation in LA-NSCLC patients. Further studies to confirm the association and application are warranted.

Upregulation of antioxidant enzymes contribute to the elevated tolerance of Juncus acutus offspring from metal contaminated environments

Long-term environmental exposure to metals e.g. zinc (Zn), may allow saltmarsh halophytes to develop metal tolerance to improve the chance of survival of their progeny in future metal-contaminated scenarios. Juncus acutus seeds were collected from mature parents (F0) inhabiting a legacy Zn-contaminated location (Cockle Creek) and an uncontaminated reference location (Swansea) of Lake Macquarie, NSW, Australia. Seeds (J. acutus) were exposed to Zn (0.00 mM (control), 0.01 mM (effective concentration, EC10) and 0.74 mM (EC50)) and resultant germinants (F1) were allowed to grow until 15 days. Seedling growth parameters i.e. biomass, root length and 1st leaf length, and seedling biochemical responses i.e. superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) antioxidant enzyme activity and lipid peroxidation products, malondialdehyde (MDA), were examined in order to assess if enzymes may be implicated in conferring tolerance to the offspring of metal-exposed parents. Control locations exhibited significantly greater declines in biomass and root length with Zn dose compared to seed from contaminated locations, suggesting F1 offspring from contaminated parents were conferred tolerance to Zn. Furthermore, significant upregulation of CAT and GPx enzymes were evident in the seedlings derived from parents of contaminated locations. These are the antioxidative enzymes responsible for minimizing metal-induced oxidative stress, and may, in part, be responsible for increasing seedling fitness and observed tolerance.

Metagenomic and biochemical analyses reveal the potential of silicon to alleviate arsenic toxicity in rice (Oryza sativa L.)

Arsenic (As) pollution in agricultural systems poses a serious threat to crop productivity and food safety. Silicon (Si) has been reported to mitigate toxic effects of heavy metals in plants. However, the mechanisms behind Si-mediated alleviation of As toxicity in rice (Oryza sativa L.) remain poorly understood. Here, we performed metagenomic and biochemical analyses to investigate the potential of Si in alleviating As toxicity to rice plants. As exposure reduced plant growth, chlorophyll contents, antioxidant enzyme levels and soil enzymes activity, while increasing reactive oxygen species (ROS) activity and inducing alterations in the rhizosphere microbiome of rice seedlings. Silicon amendments enhanced rice growth (24%), chlorophyll a (25%), and chlorophyll b (26.7%), indicating enhanced photosynthetic capacity. Si amendments also led to the upregulation of antioxidant enzymes viz., superoxide dismutase (15.4%), and peroxidase (15.6%), resulting in reduced ROS activity and oxidative stress compared to the As-treated control. Furthermore, Si treatment reduced uptake and translocation of As in rice plants, as evidenced by the analysis of elemental contents. Microscopic examination of leaf and root ultrastructure showed that Si mitigated As-induced cellular damage and maintained normal morphology. Metagenomic analysis of the rice rhizosphere microbiome revealed that Si application modulated composition and diversity of microbial communities e.g., Proteobacteria, Actinobacteria, and Firmicutes. Additionally, Si amendments upregulated the relative expression levels of OsGSH, OsPCs, OsNIP1;1 and OsNIP3;3 genes, while the expression levels of the OsLis1 and OsLis2 genes were significantly downregulated compared with As-treated rice plants. Overall, these findings contribute to our understanding of Si-mediated plant resilience to As stress and offer potential strategies for sustainable agriculture in As-contaminated regions.

Proline-mediated redox regulation in wheat for mitigating nickel-induced stress and soil decontamination

Nickel (Ni) is known as a plant micronutrient and serves as a component of many significant enzymes, however, it can be extremely toxic to plants when present in excess concentration. Scientists are looking for natural compounds that can influence the development processes of plants. Therefore, it was decided to use proline as a protective agent against Ni toxicity. Proline (Pro) is a popularly known osmoprotectant to regulate the biomass and developmental processes of plants under a variety of environmental stresses, but its role in the modulation of Ni-induced toxicity in wheat is very little explored. This investigation indicated the role of exogenously applied proline (10 mM) on two wheat varieties (V1 = Punjab-11, V2 = Ghazi-11) exposed to Ni (100 mg/kg) stress. Proline mediated a positive rejoinder on morphological, photosynthetic indices, antioxidant enzymes, oxidative stress markers, ion uptake were analyzed with and without Ni stress. Proline alone and in combination with Ni improved the growth, photosynthetic performance, and antioxidant capacity of wheat plants. However, Ni application alone exhibited strong oxidative damage through increased H2O2 (V1 = 28.96, V2 = 55.20) accumulation, lipid peroxidation (V1 = 26.09, V2 = 38.26%), and reduced translocation of macronutrients from root to shoot. Application of Pro to Ni-stressed wheat plants enhanced actions of catalase (CAT), peroxidase (POD), superoxide dismutase (SOD), and total soluble protein (TSP) contents by 45.70, 44.06, 43.40, and 25.11% in V1, and 39.32, 46.46, 42.22, 55.29% in V2, compared to control plants. The upregulation of antioxidant enzymes, proline accumulation, and uptake of essential mineral ions has maintained the equilibrium of Ni in both wheat cultivars, indicating Ni detoxification. This trial insight into an awareness that foliar application of proline can be utilized as a potent biochemical method in mitigating Ni-induced stress and might serve as a strong remedial technique for the decontamination of polluted soil particularly with metals.

Green Synthesis of Cerium Oxide Nanoparticles, Characterization, and Their Neuroprotective Effect on Hydrogen Peroxide-Induced Oxidative Injury in Human Neuroblastoma (SH-SY5Y) Cell Line.

Cerium oxide nanoparticles (CeO2NPs) have a broad scale of applications in the biomedical field due to their excellent physicochemical and catalytic properties. The present study aims to synthesize the CeO2NPs from Centella asiatica (C. asiatica) leaf extract, which has been used in Indian traditional medicine for its neuroprotective properties. The CeO2NPs were characterized by ultraviolet-visible, X-ray diffraction, Fourier transform infrared, Raman spectroscopy, scanning electron microscopy- energy dispersive X-ray spectroscopy, and high-resolution transmission electron microscopy. The antioxidant property was evaluated by 2,2-di (4-tert-octyl phenyl)-1-picrylhydrazyl and OH radical assays. The neuroprotective potential was assessed against the oxidative stress (OS) induced by H2O2 in the human neuroblastoma (SH-SY5Y) cell line. CeO2NPs exhibited significant DPPH and OH radical scavenging activity. Our results revealed that CeO2NPs significantly increased H2O2-induced cell viability, decreased lactate dehydrogenase, protein carbonyls, reactive oxygen species generation, apoptosis, and upregulated antioxidant enzyme activity. Our findings suggest that the CeO2NPs protect the SH-SY5Y cells from OS and apoptosis, which could potentially counter OS-related neurodegenerative disorders.