Glutathione Peroxidase Research Articles

Dietary antioxidants: An overview

The substances which inhibit oxidation are called as antioxidants. They are also known as free radical scavengers. The decrease in concentration of antioxidant is termed as oxidative stress. The presence of antioxidants decreases the risk of inflammation, liver disease, cardiovascular, cataract, nephrotoxicity and neurodegenerative diseases. They are categorized as exogenous and endogenous. Endogenous antioxidants include enzymatic and non-enzymatic. Enzymatic antioxidants are glutathione peroxidase, superoxide dismutase and catalase whereas non-enzymatic are uric acid, metanonin lipoic acid, glutathione and bilirubin. Exogenous are carotenoids, Vitamin E, A, C and flavonoids. Apart from natural antioxidants, synthetic antioxidants such as octyl gallate, butylated hydroxyanisole, propyl gallate, hydroxytoluene and tertbutylhydroquinone are used to enhance flavor, color extending shelf life of the product. This paper discusses on the various role of antioxidants.

Oxidative stress and apoptosis of the spinal cord in a rat model of retinoic acid-induced neural tube defects.

Neural tube defects (NTDs) are severe congenital anomalies that significantly impact the central nervous system, arising from the neural tube's failure to close during early embryogenesis. In this study, we investigated NTDs and associated pathophysiological mechanisms in foetal rats following exposure to all-trans retinoic acid (atRA). Out of 168 embryos from 15 pregnant rats in the experimental group, 78% displayed NTDs with notable spinal deformities, primarily in the lumbar-sacral region, similar to human cases. Body weight and crown-rump length (CRL) measurements indicated significant growth impairment in the NTD group compared to controls, while the atRA-treated group without NTDs showed no notable differences in growth. Immunohistochemistry (IHC) results demonstrated decreased NeuN and PCNA expression in the NTD group's spinal cord. Oxidative stress markers showed markedly reduced superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) activity, alongside increased malondialdehyde (MDA) levels in the NTD group, indicating heightened oxidative stress. Analysis of apoptosis-related proteins revealed elevated Bax and caspase-3 levels, reduced Bcl-2 and lower poly (ADP-ribose) polymerase (PARP) in the NTD group, suggesting a pronounced shift towards proapoptotic pathways, potentially contributing to NTD progression. Our findings indicate that oxidative stress and apoptosis play significant roles in the development of NTDs. Future investigations should aim to pinpoint critical regulatory genes or proteins that might be targeted for therapeutic interventions to alleviate oxidative stress and apoptosis in NTD development.

Antiplasmodial Potentials, Phytocompounds and the Possible Toxic Effects of Administration of Ethylacetate Extract of Spondias mombin Linn.

Malaria, caused by Plasmodium parasites, is a global health concern. Natural products, such as plant extracts, are investigated for new antimalarial agents. Spondias mombin, traditionally used for medicinal purposes, was examined for its effects on parasitemia, haematological parameters, antioxidant activities, liver function biomarkers, and serum electrolytes in Plasmodium berghei-infected mice. Mice received varying doses of the ethylacetate extract. Various dosages of the extract and the prescribed medication dramatically slowed the parasite's growth. The extract significantly improved red blood cell (RBC) and platelet counts, particularly at higher doses. Hemoglobin levels were decreased dose-dependently. Antioxidant analysis showed increased superoxide dismutase (SOD), glutathione peroxidase (GPx), and reduced catalase (CAT) activities and malondialdehyde (MDA) levels, indicating robust antioxidant properties. Liver function tests showed mixed effects, with elevated AST, ALP, and TB levels at some doses, yet decreased ALT at the highest dose, suggesting possible hepatoprotective effects. Serum electrolyte levels remained stable. Seventy-eight (78) bioactive components were identified in the extract by GC-MS analysis. The extract demonstrated substantial antimalarial and antioxidant capacities, with minimal liver stress and stable electrolyte levels, suggesting safety as an adjunct therapy for malaria. Further research is needed to ascertain the specific antimalarial bioactive constituents and their mechanisms of action.

Dietary antioxidant capacity is inversely associated with F2- isoprostane and body fat percentage in elite soccer referees

Background Dietary antioxidant Capacity (DaC) has been used as a tool for predicting plasma and dietary antioxidant concentrations. However, the DaC association with oxidative stress (OS) and body composition parameters is an unexplored area, mainly in physically active individuals. Given the potential for increased OS in physically active individuals, it becomes crucial to investigate this association. The aim of this study was to analyze the association between DaC, OS biomarkers, and body composition in healthy and physically active individuals. Methods This Cross-sectional study included 20 male soccer referees. Body composition measurements (body mass, fat mass, lean mass, and waist circumference), OS biomarkers (F2-isoprostane, total antioxidant state, total oxidative status, reduced glutathione, oxidized glutathione, superoxide dismutase, glutathione peroxidase (GPx) and catalase), and DaC were evaluated. Linear regression models were used to determine the association between DaC and the dependent variables. The study was approved by the Human Research Ethics Committee of the Federal University of Santa Catarina (UFSC), CAAE 82584318.0.0000.0121, and file no. 2.572.301. Results DaC was inversely associated with F2-isoprostane (p = 0.044), GPx activity (p = 0.048), and body fat percentage (p = 0.025). Conclusions Increased DaC in physically active individuals may bring benefits related to biomarkers of OS, such as decreasing F2-isoprostane and increasing GPx activity. The increase in DaC also showed an improvement in body composition, demonstrated by the lower percentage of body fat in the study subjects.

DNMT aberration-incurred GPX4 suppression prompts osteoblast ferroptosis and osteoporosis

Osteoporosis (OP) is a common and fracture-prone skeletal disease characterized by deteriorated trabecular microstructure and pathologically involving various forms of regulated bone cell death. However, the exact role, cellular nature and regulatory mechanisms of ferroptosis in OP are not fully understood. Here, we reported that OP femurs from ovariectomized (Ovx) mice exhibited pronounced iron deposition, ferroptosis, and transcriptional suppression of a key anti-ferroptotic factor GPX4 (glutathione peroxidase 4). GPX4 suppression was accompanied by hypermethylation of the Gpx4 promoter and an increase in DNA methyltransferases DNMT1/3a/3b and was transcriptionally promoted by repressive KLF5 and the transcriptional corepressors NCoR and SnoN. Conversely, DNMT inhibition with SGI-1027 reversed promoter hypermethylation, GPX4 suppression and ferroptotic osteoporosis. In cultured primary bone cells, ferric ammonium citrate (FAC) mimicking iron loading similarly induced GPX4 suppression and ferroptosis in osteoblasts but not in osteoclasts, which were rescued by siRNA-mediated individual knockdown of DNMT 1/3a/3b. Intriguingly, SGI-1027 alleviated the ferroptotic changes caused by FAC, but not by a GPX4 inactivator RSL3. More importantly, we generated a strain of osteoblast-specific Gpx4 haplo-deficient mice Gpx4Ob+/− that developed spontaneous and more severe ferroptotic OP alterations after Ovx operation, and showed that GPX4 inactivation by RSL3 or semi-knockout in osteoblasts largely abolished the anti-ferroptotic and osteoprotective effects of SGI-1027. Taken together, our data suggest that GPX4 epigenetic suppression caused by DNMT aberration and the resulting osteoblastic ferroptosis contribute significantly to OP pathogenesis, and that the strategies preserving GPX4 by DNMT intervention are potentially effective to treat OP and related bone disorders.

EVALUATION OF GLUTATHIONE PEROXIDASE ACTIVITY, MALONYLALDEHYDE AND SELENIUM LEVELS IN SICKLE CELL ANAEMIA INDIVIDUALS ATTENDING NAUTH, NNEWI IN SOUTH-EASTERN NIGERIA.

Background: Oxidative stress is an imbalance between the production and clearance of toxic free radicals known as reactive oxygen species (ROS). It is associated with hemolysis, a hallmark of SCD. SCD has long been recognized as an inflammatory condition and oxidative stress play important role in pathophysiology of SCA. Imbalance between production and elimination of reactive oxygen species (ROS) damages cell structures, including lipids, membranes, proteins and nucleic acids resulting in cell death or altered cell function. Aim: The aim of this study was to measure the serum level of Glutathione peroxidase, Malonaldehyde and Selenium in SCA (HbSS) in their steady state, AA (Healthy adult) and AS (sickle cell carriers) Methods: This is a cross- sectional study. A total of one hundred and fifty aged matched participants were recruited for this study.50 SCA subjects with sickle cell anemia (SS). Glutathione peroxidase and Malonyaldehyde were measured using turbidometry and colorimetric methods respectively while Selenium was analysed using Atomic Absorption Spectrophotometry (AAS) Results: The result of analysis of variance (ANOVA) showed that the mean serum level of MDA concentration (2.97±0.29) was higher in the SS group and was statistically significant (p< 0.05). MDA concentration was lower in the AS group. In the post hoc analysis MDA was statistically significant between SS vs AS and AA vs AA. The glutathione peroxidase activity was significantly lower in the SS group (0.85±0.12) compare with the mean values obtained in the AA and AS group. The GPx activity among the three groups was statistically significant while the post hoc analysis among the three groups showed statistical difference and was significant (p < 0.005) The Selenium levels in the SS group is lower compared with the values observed between the AA and AS group. The Se levels in the SS group was statistically lower (5.73±1.34) (p < 0.05) and showed significant difference. The comparison study between AS vs SS and AA vs AA were statistically significant. Conclusion: The decrease in selenium level potentiates low and weakened antioxidant activity and capacity which also is a reflection of low level of glutathione peroxidase observed which is supposed to attack free radicals to prevent oxidative stress. The findings from this study are in tandem with other researches suggesting that the pathophysiology of sickle cell disease is associated with oxidative stress

Molecular insights into the physiological impact of low-frequency noise on sea slug Onchidium reevesii: Activation of p53 signaling and oxidative stress response

To investigate the regulatory role of tumor protein p53 of sea slug (Onchidium reevesii) under oxidative stress conditions, we examined the response mechanisms of O. reevesii to low-frequency noise pollution (1000 Hz) using molecular and cellular biology techniques. We successfully cloned the O. reevesii p53 gene (Orp53) from O. reevesii, obtaining a 3356 bp sequence containing a 2727 bp open reading frame (ORF). Phylogenetic analysis revealed that O. reevesii shares a close evolutionary relationship with other molluscs, including Bulinus truncatus and Elysia marginata. Expression analysis showed that Orp53 is expressed across various tissues, with the highest expression levels in the hepatopancreas. Using RNA interference (RNAi) to silence the Orp53 gene, we found that the mRNA expressions of Orp53 and its downstream apoptosis-related genes, including cytochrome C (Cyt_C), Caspase 9, and Caspase 3, were significantly suppressed until the third day of interference (P < 0.05). Moreover, sip53 treatment resulted in significant reductions in the mRNA expression and protein levels of all studied genes (P < 0.05) compared to the noise-exposed group. In addition, the low-frequency noise exposure decreased central nervous system (CNS) viability while increasing oxidative stress markers, including reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione S-transferase (GST). On the other hand, silencing Orp53 expression via siRNA resulted in significant reductions in CNS cell viability (P < 0.05). Our study establishes a molecular basis for evaluating the consequences of marine noise pollution, confirming that low-frequency noise activates the p53 signaling pathway, oxidative stress, and that p53 can regulate oxidative stress and apoptosis-related genes.

Longikaurin A induces ferroptosis and inhibits glioblastoma progression through DNA methylation - Mediated GPX4 suppression.

Glioblastoma (GBM) is the most common primary intracranial tumor highly resistant to conventional clinical chemotherapy. Recently, the induction of ferroptosis is emerging as a putative strategy to treat various tumors. However, the identification of the effective and applicable tumor ferroptosis-inducing agents remains challenging. In this study, we showed that longikaurin A (LK-A), a natural diterpenoid isolated from the medicinal plant Isodon ternifolius with strong anti-GBM capacities, induced remarkable GBM cell ferroptosis along with suppressing the key anti-ferroptosis factor glutathione peroxidase 4 (GPX4). GPX4 promoter contains conserved CpG islands. The LK-A-induced GPX4 suppression coincided with the inhibition of ten-eleven translocation 2 (TET2), a key DNA demethylation enzyme and an increase in the hypermethylation of the GPX4 promoter. Further, LK-A promoted the GBM ferroptotic alterations and inhibited GBM progression in both subcutaneous and orthotopic xenograft mouse models, whereas GPX4 overexpression largely abrogated its anti-GBM effects both in vitro and in vivo, suggesting that LK-A inductions of the DNA methylation-incurred GPX4 suppression and ferroptosis are crucial for its anti-GBM functions. Together, our study has elaborated an important epigenetic pathway of GBM ferroptosis and uncovered a critical pharmacological property of LK-A for treating GBM patients.

Induction of GPX4-regulated ferroptotic stress promotes epithelial-to-mesenchymal transition in renal tubule cells induced by PM2.5

Increasing evidence links exposure to fine particulate matter (PM2.5) with an elevated risk of kidney disease. In this study, we investigated the effect of PM2.5 exposure on human proximal tubular epithelial (HK−2) cells and found that it elevated ferroptotic stress markers, including increased iron, reactive oxygen species (ROS), and malondialdehyde (MDA), along with reducing glutathione (GSH) levels. PM2.5 promotes the epithelial-to-mesenchymal transition (EMT) in these cells, which is associated with the loss of epithelial morphology, lowered expression of E-cadherin, and elevated expression of α-smooth muscle actin (α-SMA). Notably, a reduction in PM2.5-induced EMT characteristics was observed using either a ferroptosis-specific inhibitor (Fer-1) or a mitochondrial ROS scavenger (Mito-Tempo). Moreover, Fer-1 effectively counteracted ferroptotic stress and restored glutathione peroxidase 4 (GPX4) expression in PM2.5-exposed cells, which may explain its efficacy in inhibiting EMT induced by PM2.5. In contrast, GPX4 knockdown exacerbated EMT features in PM2.5-treated cells. Further studies showed that GPX4 overexpression alleviated EMT markers in mouse tubular cells following PM2.5 exposure, indicating the role of GPX4 in reducing ferroptotic stress and may prevent tubular injury caused by PM2.5 exposure. Our study highlights that PM2.5 may induce GPX4-regulated ferroptotic stress in tubular cells, potentially triggering the EMT process and contributing to kidney injury.

Evolutionary Insights and Expression Dynamics of the Glutathione Peroxidase (GPX) Gene Family in Water lily (Nymphaea colorata) in Response to Multiple Abiotic Stresses

The glutathione peroxidase (GPX) family in plants contains various isoenzymes, each with distinct subcellular localizations, tissue-specific expression patterns, and responses to environmental stress. In current study, we conducted genome-wide bioinformatics analyses of the GPX gene family in Nymphaea colorata, identifying five putative NcGPX genes dispersed across five of the fourteen chromosomes. Examination of the protein sequences revealed that NcGPXs comprehend three conserved cysteine residues, with predicted in-silico subcellular localizations in chloroplast, extracellular, or cytoplasm. We reported that NcGPX genes protein lengths and molecular weight (MW) ranged from 171-248 amino acids (aa) and 18.798-27.076 kDa, respectively. A comparative neighbor-joining phylogenetic study revealed that GPX genes were clustered into four main groups (Group A– D) from water lily and two closely related plant species, alongside with Arabidopsis thaliana. The universal analysis showed that segmental duplications occurred within the NcGPX gene family. Investigation of gene structure and motifs suggested that most NcGPX genes have relatively conserved exon-intron structures and motif arrangements. Promoter region exploration of NcGPX genes revealed numerous cis-acting regulatory elements associated with development, stress, and hormone responses. The identified 3D protein structures showed that water lily GPXs form conserved dimeric protein signatures. Finally, gene expression and enzymes accumulation of NcGPXs in response to different abiotic stresses, in leaves of N. colorata were analysed using real-time RT-qPCR and spectrophotometry. The results indicate that different members of the GPX gene family are co-ordinately regulated under specific environmental stress conditions, establishing a foundation for studying their gene functions and improving abiotic stress tolerance in water lily genetic breeding.

1α,25-hydroxyvitamin D3 alleviated rotavirus infection induced ferroptosis in IPEC-J2 cells by regulating the ATF3-SLC7A11-GPX4 axis

Rotavirus (RV) mainly infects mature intestinal epithelial cells and impairs intestinal absorption function, which leads to the death of infected cells and eventually fatal diarrhea. Ferroptosis is a novel regulatory cell death pattern, which can be caused by virus infection. 1α,25-hydroxyvitamin D3 (1,25D3) has an anti-RV infection effect and can regulate ferroptosis. However, whether RV infection can induce ferroptosis, and whether 1,25D3 can inhibit RV infection by regulating ferroptosis has not yet been studied. Present study shows that RV infection or erastin treatment induces IPEC-J2 cell death, which results in mitochondrial shrinkage, decreased mitochondrial membrane potential (MMP) and glutathione (GSH) content, increased MMP, intracellular Fe2+, reactive oxygen species (ROS), and malondialdehyde (MDA) contents. Meanwhile, ferrostatin-1 (Fer-1), liproxstatin-1 (Lip-1), and deferoxamine (DFO) treatment can effectively reverse the increase of intracellular Fe2+, ROS and MDA levels induced by RV infection. Moreover, RV infection increases activating transcription factor 3 (ATF3) mRNA and protein expressions, and inhibited SLC7A11 and glutathione peroxidase 4 (GPX4) expressions, which was partially alleviated by siATF3. 1,25D3 treatment significantly eliminates RV induced ferroptosis via ATF3-SLC7A11-GPX4 axis. Therefore, our results reveals that RV infection induces ferroptosis in IPEC-J2 cell and 1,25D3 alleviates RV induced ferroptosis by regulating the ATF3-SLC7A11-GPX4 axis.

Ferroptosis suppressor protein 1 regulated oligodendrocytes ferroptosis rescued by idebenone in spinal cord injury

Ferroptosis has been demonstrated to be involved in the progression of spinal cord injury (SCI). Ferroptosis suppressor protein 1 (FSP1) can inhibit ferroptosis in parallel with Glutathione peroxidase 4 (GPX4). However, the role of FSP1 in the pathogenesis of spinal cord injury is unclear. The protein and gene levels of FSP1 were found to be downregulated during both the acute and subacute stages after SCI. In addition to regulating ferroptosis by mediating CoQ, FSP1 also influences ferroptosis sensitivity by modulating cellular homeostasis and the metal ion response system, as demonstrated by FSP1 knockdown experiments. Furthermore, Idebenone (IDE) was identified as a ferroptosis inhibitor. IDE was shown to inhibit reactive oxygen species (ROS) and restore the expression of GPX4 and xCT, thereby suppressing ferroptosis of oligodendrocytes, even when FSP1 was knocked down. In vivo results indicated that IDE could effectively rescue oligodendrocytes and neurons from ferroptosis, promoting myelination of the injured spinal cord and facilitating tissue repair and functional recovery. This study provides a novel strategy for repairing SCI through the regulation of FSP1 in ferroptosis.

Meta-analysis of dietary supplementation with flavonoids in small ruminants: Growth performance, antioxidant status, nutrient digestibility, ruminal fermentation, and meat quality

This study aimed to evaluate the effects of dietary supplementation with flavonoids on growth performance, antioxidant status, nutrient digestibility, ruminal fermentation, and meat quality of small ruminants through a meta-analytic approach. The data used in the meta-analysis were extracted from 29 scientific articles identified through systematic searches following the PRISMA methodology. Der-Simonian and Laird, random effects models, were used to assess effect sizes using weighted mean differences. Dietary supplementation with flavonoids increased (P < 0.05) dry matter intake, average daily gain, hot carcass weight, hot carcass yield, Longissimus dorsi muscle area, and backfat thickness. In contrast, the feed conversion ratio decreased (P < 0.05) in response to dietary flavonoid supplementation. Dietary supplementation with flavonoids increased (P < 0.001) the serum concentration of superoxide dismutase, catalase, glutathione peroxidase, and total antioxidant capacity but decreased (P < 0.001) the serum concentration of malondialdehyde (MDA). The digestibility of dry matter, organic matter, crude protein, neutral detergent fiber, and acid detergent fiber increased (P < 0.05) in response to dietary flavonoid supplementation. Dietary supplementation with flavonoids decreased (P < 0.001) the ruminal concentration of ammonia nitrogen and increased (P < 0.001) the ruminal concentration of total volatile fatty acids and acetate. Dietary supplementation with flavonoids decreased (P < 0.001) cooking loss, shear force, and MDA in meat. In conclusion, dietary supplementation with flavonoids can be used as a nutritional strategy to improve growth performance, antioxidant status in blood serum, nutrient digestibility, ruminal fermentation, and meat quality in small ruminants.

Hesperidoside abolishes dichlorvos-mediated neurotoxicity in rats by suppressing oxidative stress, acetylcholinesterase inhibition, and NF-κB-p65/p53/caspase-3-mediated apoptosis

BackgroundIn third-world countries, poisoning due to dichlorvos (DDVP), an organophosphate insecticide, is prevalent due to its widespread usage in household and agriculture, with the brain bearing the brunt of the consequences. Hence, this study assessed the likely beneficial impact of hesperidoside (HESP) on the DDVP-mediated cerebral dysfunction in rat model. MethodRandomization was employed to earmark forty-two rats into seven groups: control, DDVP alone (8 mg.kg⁻¹day⁻¹), DDVP plus HESP (50 and 100 mg.kg⁻¹day⁻¹) and reference drug atropine (0.2 mg.kg⁻¹day⁻¹), and HESP alone (50 and 100 mg.kg⁻¹day⁻¹). ResultsHESP intervention remarkably (p < 0.05) mitigated DDVP-potentiated augmentations in cerebral concentrations of H₂O₂, NO, and malondialdehyde; impaired DDVP-induced decrease in cerebral GSH, GST, SOD, catalase, glutathione peroxidase, and acetylcholinesterase; significantly (p < 0.05) suppressed DDVP-invoked upregulation of mRNA expression of NF-κB-p65, p53, BAX, caspase-3, and TNF-α; and significantly (p < 0.05) revoked DDVP-incited downregulation of interleukin-10. ConclusionHESP chemotherapeutic interventions enhanced cerebral functions in DDVP-treated rats by abrogating oxidative stress, acetylcholinesterase inhibition, and NF-κB-p65/p53/caspases-3 signaling.

Anti-oxidative and immunological role of Cyclocarya paliurus polysaccharide on the liver injury of diabetic rats.

To investigate the effects of Cyclocarya paliurus (C. paliurus) polysaccharide on the liver injury of diabetic rats. Rats were divided into 6 groups, including normal group, model group, control group, low-dose group of C. paliurus polysaccharide treatment, middle-dose group of C. paliurus polysaccharide treatment and high-dose group of C. paliurus polysaccharide treatment. Histological analysis of liver was analyzed using hematoxilin and eosin. Levels of plasma biological parameters and anti-oxidative enzymes were determined by spectrophotometry. Nuclear factor kappa-B-p65 (NF-κB p65), tumor necrosis factor-α (TNF-α), interleukins 6 (IL-6), IL-1β were measured by real-time polymerase chain reaction and enzyme-linked immunosorbent assay. Compared with that of model group, the glucose level of plasma decreased 62.32% (P < 0.01), but glycogen and insulin level increased 1.51 times and 1.27 times in the high-dose group of C. paliurus polysaccharide treatment, respectively. Plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) level decreased 47.47% (P < 0.05), 43.65% (P < 0.05) and 50.51% (P < 0.05) in the high-dose group of C. paliurus polysaccharide treatment, respectively. Superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase level increased 1.16 times (P < 0.01), 71.28% (P < 0.05), 1.29 times (P < 0.01) and 87.46% (P < 0.05) in the high-dose group of C. paliurus polysaccharide treatment, respectively. Enzyme activities of NF-κB, TNF-α, IL-1β and IL-6 were decreased 39.29% (P < 0.05), 51.11% (P < 0.05), 37.42% (P < 0.05) and 36.50% (P < 0.05), respectively. Administration of C. paliurus polysaccharide may play a protecting role for liver injury of diabetic rats through lowering glucose, ALT, AST, ALP level, increasing glycogen and insulin level, enhancing the anti-oxidative ability and down-regulating the inflammatory factors expression.

Application of hydrogen-rich water maintains red pitaya fruit quality through regulation of ROS and energy metabolism

Hydrogen-rich water (HRW) treatment has been shown to enhance the shelf life of fruit and vegetables. This study aimed to investigate the effects of HRW on improving the quality of red pitaya and its underlying regulatory mechanisms. The results revealed that applying HRW at a 70% concentration reduced decay and weight loss rates, slowed the respiratory rate, and delayed the decline in titratable acidity and total soluble solids. Additionally, HRW treatment mitigated the increase in superoxide anion production and hydrogen peroxide levels, while enhancing antioxidant enzyme activities and gene expression, including those of peroxidase, superoxide dismutase, glutathione peroxidase, catalase, ascorbate peroxidase, monodehydroascorbate reductase, and glutathione reductase. Non-enzymatic antioxidant compounds such as ascorbate and glutathione also increased. Moreover, RT-qPCR analysis showed that HRW treatment upregulated HcMYB6 and downregulated HcR2R3MYB. Dual-luciferase reporter assays indicated that HcMYB6 activated the expression of HcSOD and HcCAT, whereas HcR2R3MYB repressed their expression. These findings suggest that HcMYB6 and HcR2R3MYB may be involved in reactive oxygen species metabolism, with HcMYB6 being induced and HcR2R3MYB inhibited by HRW treatment. Furthermore, HRW treatment led to increased adenosine triphosphate and adenosine diphosphate levels, a decrease in adenosine monophosphate content, and elevated gene expression and activity of Ca2⁺-ATPase, succinate hydrogenase, H⁺-ATPase, and cytochrome C. Collectively, these results demonstrate that HRW treatment effectively reduces oxidative damage and improves energy status, thereby preserving the quality of red pitaya fruit.

Effect of lipoic acid on cisplatin-induced cardiotoxicity and inflammation in cardiomyocytes

Aims: Cisplatin (CPL) is a potent chemotherapeutic agent widely used to treat various cancers. However, CPL causes toxicity in various tissues, including the heart. Lipoic acid (LPA) is a thiol compound with antioxidant, anti-inflammatory, and antiapoptotic properties. Although LPA has been reported to have protective effects in various cardiac diseases, the mechanisms underlying its cardio-protective effects have not been elucidated. This study aimed to establish a CPL-induced cardiotoxicity model in the H9c2 cardiomyocyte cell line, to understand the mechanisms underlying this cardiotoxicity, and to investigate the effect of LPA on cardiotoxicity. Methods: H9c2 cardiomyocyte cells as control (CNT), CPL (40 µm), and LPA-1 (300 µm LPA, and 40 µm CPL), LPA-2 (500 µm LPA, and 40 µm CPL) in combination along with CIS were used. In the analyses made, glutathione (GSH) and glutathione peroxidase (GSHPx) enzyme activity, lipid peroxidation [malondialdehyde, (MDA)] levels, inflammation markers interleukin (IL) -1ß, IL-6, and tumor necrosis factor (TNF) -? levels, total oxidant/antioxidant (TOS and TAS) status levels, reactive oxygen species (ROS) and caspase activity (Casp 3 and 9) in the cells were determined. Results: CIS treatment caused cardiomyocyte cell toxicity and increased Casp 3, Casp 9, ROS, IL-1ß, IL-6, TNF-?, TOS, and MDA levels while decreasing GSHPx, GSH, and TAS levels. Increased inflammation and impaired oxidant/antioxidant balance in cardiomyocyte cells after CPL treatment were regulated by LPA treatment. Conclusion: LPA treatment was found to have a protective effect against CPL-induced cardiotoxicity in cardiomyocyte cells.

Transgenerational Impacts of Oxidative Damage Induced by Prenatal Ethanol Exposure on Spatial Learning/Memory and BDNF in the Hippocampus of Male Rats

Alcohol consumption during pregnancy harms fetal development, leading to various physical and behavioral issues. This study investigates how prenatal ethanol exposure triggers oxidative stress (OS) and affects neurotrophic factors (NTFs), particularly brain-derived growth factor (BDNF) gene expression in the hippocampus, influencing learning and memory decline across two generations of male offspring from ethanol-exposed female rats. A rat model of fetal alcohol spectrum disorder (FASD) was initially generated to reflect on the deficits in the first generation, and then those transmitted via the male germline to the unexposed male ones. The pregnant rats were thus divided into four groups, namely, the control group (CTRL) receiving only distilled water (DW), and three groups being exposed to ethanol (20 %, 4.5 g/kg) by oral gavage, during the first 10-day gestation (FG), the second 10-day gestation (SG), and the entire gestation (EG) periods. Subsequent Morris water maze (MWM) tests on male offspring revealed spatial learning deficits during the second and entire gestational periods in both generations. Analysis of antioxidant enzyme activity including glutathione peroxidase (GPx), superoxide dismutase (SOD), and malondialdehyde (MDA), and BDNF gene expression in the hippocampus further highlighted the impacts of prenatal ethanol exposure. The study results demonstrated that prenatal ethanol exposure caused spatial learning/memory deficits during the SG and EG, altered antioxidant enzyme activity, and reduced BDNF gene expression in both generations. The findings underscore the role of OS in developmental and behavioral issues in FASD rat models and suggest that lasting transgenerational effects in the second generation may stem from alcohol-induced changes.

Drought-mediated oxidative stress and its scavenging differ between citrus hybrids with medium and late fruit maturation

Drought stress is a major environmental factor limiting citrus productivity. Still, differences in drought sensitivity between citrus hybrids of different maturation periods have so far not been reported. Here, we selected a medium-maturing (Fertile orange: FO (Citrus reticulata cv. Fertile orange) and a late-maturing citrus hybrid (Newhall Navel orange: NO (Citrus sinensis Osbeck cv. Newhall) and determined the physiological and biochemical traits of leaves, roots, wood and bark. Our results showed that drought significantly decreased net photosynthetic rate (Pn), stomatal conductance (Gs) and transpiration rate (Tr) of citrus leaves. Oxidative stress upon drought was indicated by enhanced foliar malondialdehyde (MDA) and hydrogen peroxide contents, as well as a stimulation of the anti-oxidative system. This stimulation included the contents of dehydroascorbic acid (DHA), glutathione (GSH) and oxidized glutathione (GSSG) in leaves, roots, wood and bark, as well as activities of antioxidative enzymes of glutathione reductase (GR), dehydroascorbate reductase (DHAR), superoxide dismutase (SOD) and peroxidase (POD). The late maturing NO hybrid not only showed better general physiological performance as indicated by increased Pn in leaves, but also higher biochemical ROS scavenging and osmotic capacity as indicated by increased ascorbic acids (ASA), DHA, and proline contents, as well as activities of enzymes of SOD, POD, ASA/DHA and GSH/GSSG ratios in the investigated tissues compared to the FO hybrid under drought and control conditions. Analysis of molecular mechanisms of signaling, regulatory and functional genes expression are suggested for future studies to elucidate the complex interplay of molecular, biochemical and physiological responses of citrus hybrids to drought.

Integrated analysis of physiology, antioxidant activity and transcriptomic of Lactobacillus plantarum 120 in response to acid stress

This research examined the effects of acid stress on the physiological and antioxidant activity of Lactobacillus plantarum 120 (Lp-120) and explored its underlying mechanisms. The results revealed that the survival rates of the strain significantly decreased as the pH decreased from 5.5 to 4.5. Meanwhile, the ATP concentrations of the strain decreased from 0.51 to 0.12, and the reactive oxygen species levels rose 1.26-fold with a decrease in pH. However, as the pH decreased, the free radical (DPPH, O2−, and OH−) scavenging activity, reducing power, superoxide dismutase, glutathione peroxidase activities, and the total antioxidant capacities of Lp-120 all increased (P<0.05). Among them, the DPPH scavenging power and superoxide radical scavenging power reached the highest value of 35.5% and 30.74% respectively at pH 4.5, and the hydroxyl radical scavenging power reached the highest value of 53.2% at pH 5.0, which indicated that appropriate acid stress could improve the antioxidant activities of the strain. Transcriptomics data showed that the expression levels of genes (ndh, trxA, etc.) were upregulated (0.39-10.54-fold) under acid stress, which related to the “NADH oxidase/ NADH peroxidase” system, glutaredoxin system and thioredoxin system. Taken altogether, this study brought valuable insights for enhancing the antioxidant activities of Lp-120 and provided valuable information on the application of Lactobacillus plantarum as antioxidant starter cultures in fermented foods.