Drought stress induces the excessive accumulation of hydrogen peroxide (H2O2), leading to oxidative damage and reduced crop productivity. This study presents a dual-function nanotechnology-based strategy for monitoring and mitigating drought-induced oxidative stress in cereal crops. Hierarchical CuO nanostructures were grown directly on copper substrates by hydrothermal oxidation, and the influence of growth time on morphology and hydrogen peroxide sensing performance was systematically evaluated. An optimal growth time of 3 h produced CuO nanoflower architectures with high surface area, yielding superior electrocatalytic activity toward H2O2 detection, with a low detection limit of 1.9 µM and high sensitivity of 11.92 mA·mM−1·cm−2. The optimized sensor enabled reliable quantification of H2O2 in oat (Avena sativa) and rye (Secale cereale) under drought stress, revealing species-dependent oxidative responses. In parallel, magnesium oxide (MgO) nanoparticles effectively alleviated drought-induced oxidative damage, reducing H2O2 accumulation by up to 63% in oat and 61% in rye and significantly improving plant growth and chlorophyll content. The integration of CuO-based sensing with MgO nanoparticle-assisted stress mitigation provides a robust framework for plant stress diagnostics and intervention, highlighting the potential of nanotechnology-enabled strategies for crop stress diagnostics and precision agriculture.

Spirulina supplementation regulates inflammation and supports cartilage health in adult sedentary horses following moderate-intensity exercise.

Water extract of Ampelopsis grossedentata improves reproductive performance in laying hens by regulating gut microbiota and PI3K/AKT signaling pathway.

Tunable PEGylated albumin nanocarriers enhance 5-FU cytotoxic selectivity and modulate oxidative and immune stress in colorectal cancer model.

TPPU alleviates hepatic ischemia-reperfusion injury by regulating macrophage polarization.

Molecular crosstalk between herbal phytochemicals and microRNAs in electronic cigarette vapor: Implications for respiratory health.

Life without air: Metabolic responses of the tree frog Boana pulchella under anoxic conditions.

Commercial glyphosate formulations exceed active ingredient toxicity via mitochondrial ROS and transcriptomic disruption.

Multiscale molecular engineering co-modulated dual-mode ratiometric probe for monitoring tumor-associated macrophage repolarization.

Pleurotus ostreatus polysaccharides improve microcystin-LR-induced intestinal damage in tadpoles by regulating the interaction between microbiota and intestine.

A dual-delivery nanotherapeutic strategy using chitosan-epigallocatechin-3-gallate nanoparticles encapsulated in exosomes: A novel approach to combat brain aging.

β-Sitosterol attenuates gentamicin-induced nephrotoxicity via ADAM-17/ACE2/Ang 1-7/MasR Axis modulation in rats.

S-adenosyl-L-methionine reverses ethanol-induced developmental toxicity in FASD model of Danio rerio embryos via dual-modulation of oxidative stress and glutathione homeostasis.

Stroke is an intricate oxidative and inflammatory response resulting from cerebral ischemia followed by reperfusion injury. The complex pathophysiology of stroke poses challenges for treatment. Peroxisome proliferated-activated receptor (PPAR) expression in the rat hippocampus is markedly elevated post cerebral ischemia/reperfusion injury (I/R injury). Hence, Saroglitazar, a dual PPAR-α/γ agonist, was investigated against cerebral I/R injury in rats. Male Sprague Dawley rats were subjected to bilateral common carotid artery occlusion for 30 min and reperfusion for 3 days. During the reperfusion, animals were treated with vehicle or Saroglitazar once a day for 3 days. The behavioral parameters were assessed, and animals were sacrificed to measure oxidative markers (Malondialdehyde, Superoxide dismutase, catalase, and reduced glutathione), inflammatory markers (interleukin-6, tumor necrosis factor-α, nuclear factor kappa-light chain enhancer of activated B cells [NF-κB], and high mobility group box 1 protein [HMGB-1]), infarction, and histopathology changes. Following I/R injury, antioxidant enzymes were reduced, while nitric oxide and inflammatory markers were increased in the disease group. In the rat hippocampus, these changes led to neurobehavioral impairment and cerebral infarction. Saroglitazar improved the levels of antioxidants and reduced inflammation. 2,3,5-triphenyltetrazolium chloride staining and histopathological analysis revealed the neuroprotective effect of Saroglitazar in the hippocampus region. The neuroprotective effects of Saroglitazar were attributed to its activation of both PPAR-α and PPAR-γ. It improved antioxidant levels and inhibited pro-inflammatory cytokines by suppressing the HMGB-1/NF-κB signaling pathway. These findings underscore the potential of Saroglitazar in mitigating cerebral I/R injury.

Persistent bacterial infections and oxidative stress-induced inflammatory responses present significant challenges to wound healing. Conventional wound care approaches frequently prioritize bacterial eradication while overlooking the critical need to modulate inflammation. To address this limitation, we have innovatively developed carrier-free nano-aggregates through the co-precipitation of natural polyphenols (resveratrol and piceatannol) and a porphyrin-based photosensitizer, which function as antibacterial and anti-inflammatory agents, respectively. Significantly, rather than forming a simple mixture, the two components co-assemble via microstructure regulation into a highly ordered architecture exhibiting characteristic J-aggregate features. Specifically, the piceatannol-based aggregates (designated T4PIC NPs) achieved an exceptional photothermal conversion efficiency (PCE) of 51.1% under 730nm irradiation, accompanied by an 86nm spectral redshift, surpassing most previously reported porphyrin-based nanoparticles. These properties enable highly effective sterilization even at low doses. Notably, the natural polyphenols not only enhance phototherapeutic efficacy but also, owing to their multi-hydroxyl structures, effectively scavenge reactive oxygen species and modulate inflammatory responses, thereby accelerating wound healing. This study establishes a straightforward strategy for delivering natural polyphenolic drugs while concurrently constructing highly efficient porphyrin-based photothermal formulations, demonstrating unique advantages for advanced wound management.

Cervical carcinoma continues to be one of the leading causes of cancer-related mortality among women worldwide, disproportionately striking developing regions, including India. High-risk persistent HPV infection has long been recognized as the central etiological factor in cervical carcinogenesis; however, not all infected women end up with malignancy, indicating the role of viral genomic variation and host genetic susceptibility. High-risk HPV variants, primarily comprising lineage clusters of HPV16 and HPV18, exhibit differential oncogenic potential due to mutations in the E6/E7 oncogenes and the LCR, which is responsible for viral persistence, the efficiency of p53/pRb degradation, immune evasion, and epithelial cell transformation. Genetic polymorphisms in the host regulate the natural history of infection and cervical cancer risk. Variants of HLA class I/II alleles influence antigen presentation and Single nucleotide polymorphism in immune regulatory cytokine genes (IL-10, TNF-α, IFN-γ), TP53 codon 72 (Arg/Pro), DNA repair and metabolic genes (XRCC1, MTHFR), and detoxification gene null genotypes (GSTM1, GSTT1) modulate viral persistence, oxidative DNA damage response, and oncogenic progression. Advancements such as next-generation sequencing and immunogenetics, which identify the relationship between HPV variants and host immune genes that modulate disease susceptibility, vaccine responsiveness, and progression patterns across various genetic backgrounds. This review systematically integrates molecular mechanisms of HPV variant-induced oncogenesis and host genetic susceptibility with emphasis on population-based variability in addition to evidence culled from meta-analyses and GWAS data for immune regulation, DNA repair, as well as host single nucleotide polymorphisms in different populations and its implications for personalized prevention measures, screening, and vaccine response.

This study aims to investigate the radioprotective effects of melatonin (MEL) against oxidative damage that may be caused by flattening filter (FF) and flattening filter-free (FFF) beam in the cerebrum and cerebellum of rat using various genetic markers. Forty female Wistar albino rats were randomly assigned to five groups. The control group received no intervention. The FF group received a single 16 Gy fraction at 600 MU/min. The FF+MEL group received the same FF protocol, preceded by melatonin (50 mg/kg, intraperitoneal) administered 15 min before irradiation. The FFF group received a single dose of 16 Gy at 2,400 MU/min. The FFF+MEL group received the same FFF protocol with melatonin administered as above. After treatment, cerebrum and cerebellum tissues were harvested, and mRNA expression levels of BDNF, CREB, BAX, BCL2 and IL6 were measured. Both FF and FFF radiotherapy treatments significantly increased BDNF, CREB, IL6, and BAX gene expression in cerebrum and cerebellum tissues, while decreasing BCL2 levels (P < 0.05). Melatonin treatment increased BDNF and CREB expression, significantly attenuated radiation-induced increases in IL6 and BAX, and partially reversed the decrease in BCL2 (P < 0.05). The increase in the BAX/BCL2 ratio after radiotherapy was significantly attenuated by melatonin treatment. Overall, FFF irradiation induced a stronger oxidative, inflammatory, and pro-apoptotic response than FF, whereas melatonin exhibited potent neuroprotective and anti-apoptotic effects. In conclusion, MEL demonstrates potential as a protective agent for healthy tissues during irradiations, owing to its antiapoptotic, anti-inflammatory, and neurotrophic properties.

The purpose of this work was to determine endothelial, microvascular, skeletal muscle oxidative capacity (SMOC) and cardiorespiratory responses to an acute bout of continuous single leg cycling (SLC) and double leg cycling (DLC). Ten recreationally active men and women volunteered to participate in this investigation and reported to the laboratory on four separate occasions. Visits 1 and 2 consisted of a DLC and SLC test, while visits 3 and 4 were the experimental visits. Participants performed 30min of continuous DLC and SLC at 60% of their DLC . Before, 1 and 2h post-exercise, measures of vascular (i.e., flow mediated dilation (FMD), reactive hyperaemia, microvascular responsiveness) and SMOC were performed. SLC resulted in significantly greater limb specific power (83±23 vs. 51±12W; P<0.001) and carbohydrate oxidation (151±40 vs. 126±30kcal; P=0.017) compared to DLC. There was a significant reduction in % FMD following SLC (baseline: 9.4±3.2%; 1h: 6.9±3.4%; P=0.009), while there was no change following DLC. Both SLC and DLC resulted in a significant increase in SMOC (P<0.001) and a significant decrease in microvascular responsiveness (P<0.001). In conclusion, the reduction in FMD following SLC, likely brought on by greater peripheral and oxidative stress, which are key stimuli for long-term positive adaptations, may be more beneficial at improving peripheral adaptations compared to DLC. This may be particularly advantageous for those with exercise intolerance, as SLC leads to greater peripheral stress for a similar central stress.

Ionising radiation-induced lung injury is a major complication of thoracic radiotherapy, primarily driven by oxidative stress and inflammation. The current study evaluates and compares the protective effects of sulforaphane (SFN) and curcumin (CUR) pretreatment against radiation-induced oxidative damage and inflammation in rat lung tissue. Female Wistar rats were pretreated in vivo with SFN (2 mg/kg b.w./day) or CUR (4.13 mg/kg b.w./day) for 28 days per os. Isolated lung tissues were exposed ex vivo to γ-radiation (absorbed dose: 2 Gy). Oxidative stress markers-malondialdehyde (MDA), ischemia-modified albumin (IMA), total sulfhydryl (SH) groups, reduced glutathione (GSH), and superoxide dismutase (SOD)-and inflammatory markers-tumour necrosis factor alpha (TNF-α), prostaglandin-endoperoxide synthase 2 (PTGS2/COX-2), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β)-were measured to evaluate irradiation and protective effects. Radiation significantly increased MDA, TNF-α, PTGS2/COX-2, and IL-6 levels while decreasing SH groups. Pretreatment with SFN or CUR attenuated these changes. CUR showed a more pronounced effect on oxidative stress-related parameters, whereas SFN more strongly influenced inflammatory markers. These findings suggest that SFN and CUR differentially modulate radiation-induced oxidative and inflammatory responses in lung tissue under the applied experimental conditions and warrant further investigation of their potential as protective agents in radiotherapy.

Aortic diseases, including thoracic and abdominal aneurysms as well as aortic dissections, represent life-threatening vascular disorders characterized by progressive wall degeneration and inflammation. Increasing evidence indicates that oxidative stress is a central driver of aortic pathology through the induction of DNA damage in vascular smooth muscle cells and endothelial cells. Oxidative DNA lesions activate the DNA damage response (DDR), a highly coordinated network of damage sensors, signaling kinases, and repair effectors that determines cell fate decisions such as DNA repair, apoptosis, or cellular senescence. In aortic tissue, persistent or dysregulated DDR signaling contributes to chronic inflammation, extracellular matrix degradation, and loss of vascular integrity. Key molecular regulators, including base excision repair enzymes OGG1 and APE1, as well as DDR mediators such as ATM, ATR, p53, PARP, and NOTCH1, integrate oxidative stress signals with pro-inflammatory and pro-degenerative pathways. Aberrant activation of these mechanisms promotes vascular smooth muscle cell VSMC phenotypic switching from contractile to synthetic phenotype, endothelial dysfunction, and senescence-associated secretory responses, thereby accelerating aortic wall weakening and aneurysm progression. This review highlights the mechanistic links between oxidative stress-induced DNA damage, DDR pathway activation, and vascular remodeling in aortopathies. A deeper understanding of these molecular interactions may uncover novel biomarkers and therapeutic targets aimed at limiting inflammation, preserving genomic stability, and preventing catastrophic aortic events. This work represents a narrative review and therefore has inherent limitations in terms of systematic literature search and selection.