Showing papers on "Malondialdehyde published in 2022"

Oxidative Stress and Diseases Associated with High-Altitude Exposure

Abstract: Several diseases associated with high-altitude exposure affect unacclimated individuals. These diseases include acute mountain sickness (AMS), high-altitude cerebral edema (HACE), high-altitude pulmonary edema (HAPE), chronic mountain sickness (CMS), and, notably, high-altitude pulmonary hypertension (HAPH), which can eventually lead to right ventricle hypertrophy and heart failure. The development of these pathologies involves different molecules and molecular pathways that might be related to oxidative stress. Studies have shown that acute, intermittent, and chronic exposure to hypobaric hypoxia induce oxidative stress, causing alterations to molecular pathways and cellular components (lipids, proteins, and DNA). Therefore, the aim of this review is to discuss the oxidative molecules and pathways involved in the development of high-altitude diseases. In summary, all high-altitude pathologies are related to oxidative stress, as indicated by increases in the malondialdehyde (MDA) biomarker and decreases in superoxide dismutase (SOD) and glutathione peroxidase (GPx) antioxidant activity. In addition, in CMS, the levels of 8-iso-PGF2α and H2O2 are increased, and evidence strongly indicates an increase in Nox4 activity in HAPH. Therefore, antioxidant treatments seem to be a promising approach to mitigating high-altitude pathologies.

Long-COVID post-viral chronic fatigue and affective symptoms are associated with oxidative damage, lowered antioxidant defenses and inflammation: a proof of concept and mechanism study

Abstract: The immune-inflammatory response during the acute phase of COVID-19, as assessed using peak body temperature (PBT) and peripheral oxygen saturation (SpO2), predicts the severity of chronic fatigue, depression and anxiety symptoms 3–4 months later. The present study was performed to examine the effects of SpO2 and PBT during acute infection on immune, oxidative and nitrosative stress (IO&NS) pathways and neuropsychiatric symptoms of Long COVID. This study assayed SpO2 and PBT during acute COVID-19, and C-reactive protein (CRP), malondialdehyde (MDA), protein carbonyls (PCs), myeloperoxidase (MPO), nitric oxide (NO), zinc, and glutathione peroxidase (Gpx) in 120 Long COVID individuals and 36 controls. Cluster analysis showed that 31.7% of the Long COVID patients had severe abnormalities in SpO2, body temperature, increased oxidative toxicity (OSTOX) and lowered antioxidant defenses (ANTIOX), and increased total Hamilton Depression (HAMD) and Anxiety (HAMA) and Fibromylagia-Fatigue (FF) scores. Around 60% of the variance in the neuropsychiatric symptoms of Long COVID (a factor extracted from HAMD, HAMA and FF scores) was explained by OSTOX/ANTIOX ratio, PBT and SpO2. Increased PBT predicted increased CRP and lowered ANTIOX and zinc levels, while lowered SpO2 predicted lowered Gpx and increased NO production. Lowered SpO2 strongly predicts OSTOX/ANTIOX during Long COVID. In conclusion, the impact of acute COVID-19 on the symptoms of Long COVID is partly mediated by OSTOX/ANTIOX, especially lowered Gpx and zinc, increased MPO and NO production and lipid peroxidation-associated aldehyde formation. The results suggest that post-viral somatic and mental symptoms have a neuroimmune and neuro-oxidative origin.

Deferoxamine Alleviates Osteoarthritis by Inhibiting Chondrocyte Ferroptosis and Activating the Nrf2 Pathway

Abstract: Objective: Osteoarthritis (OA) is a common disease with a complex pathology including mechanical load, inflammation, and metabolic factors. Chondrocyte ferroptosis contributes to OA progression. Because iron deposition is a major pathological event in ferroptosis, deferoxamine (DFO), an effective iron chelator, has been used to inhibit ferroptosis in various degenerative disease models. Nevertheless, its OA treatment efficacy remains unknown. We aimed to determine whether DFO alleviates chondrocyte ferroptosis and its effect on OA and to explore its possible mechanism. Methods: Interleukin-1β (IL-1β) was used to simulate inflammation, and chondrocyte ferroptosis was induced by erastin, a classic ferroptosis inducer. A surgical destabilized medial meniscus mouse model was also applied to simulate OA in vivo, and erastin was injected into the articular cavity to induce mouse knee chondrocyte ferroptosis. We determined the effects of DFO on ferroptosis and injury-related events: chondrocyte inflammation, extracellular matrix degradation, oxidative stress, and articular cartilage degradation. Results: IL-1β increased the levels of ROS, lipid ROS, and the lipid peroxidation end product malondialdehyde (MDA) and altered ferroptosis-related protein expression in chondrocytes. Moreover, ferrostatin-1 (Fer-1), a classic ferroptosis inhibitor, rescued the IL-1β–induced decrease in collagen type II (collagen II) expression and increase in matrix metalloproteinase 13 (MMP13) expression. Erastin promoted MMP13 expression in chondrocytes but inhibited collagen II expression. DFO alleviated IL-1β– and erastin-induced cytotoxicity in chondrocytes, abrogated ROS and lipid ROS accumulation and the increase in MDA, improved OA-like changes in chondrocytes, and promoted nuclear factor E2–related factor 2 (Nrf2) antioxidant system activation. Finally, intra-articular injection of DFO enhanced collagen II expression in OA model mice, inhibited erastin-induced articular chondrocyte death, and delayed articular cartilage degradation and OA progression. Conclusion: Our research confirms that ferroptosis occurs in chondrocytes under inflammatory conditions, and inhibition of chondrocyte ferroptosis can alleviate chondrocyte destruction. Erastin-induced chondrocyte ferroptosis can stimulate increased MMP13 expression and decreased collagen II expression in chondrocytes. DFO can suppress chondrocyte ferroptosis and promote activation of the Nrf2 antioxidant system, which is essential for protecting chondrocytes. In addition, ferroptosis inhibition by DFO injection into the articular cavity may be a new OA treatment.

Platycodin D regulates high glucose-induced ferroptosis of HK-2 cells through glutathione peroxidase 4 (GPX4)

Abstract: ABSTRACT Diabetic nephropathy (DN) is associated with inflammation. Platycodin D (PD) demonstrates anti-inflammatory activity. However, whether PD affects DN remains to be explored. Here, we aimed to discuss the role of PD in DN and its underlying mechanisms. High glucose (HG)-induced HK-2 cells were treated with PD, and cell viability was assessed using the Thiazolyl Blue Tetrazolium Bromide (MTT) assay. Ferroptosis-related factors such as lactate dehydrogenase (LDH) activity, lipid reactive oxygen species (ROS), iron (Fe2+) level, GSH level, and malondialdehyde (MDA) level were evaluated. Cell death was evaluated using the TUNEL assay. GPX4 expression was evaluated using Quantitative Real-time PCR (qRT-PCR) and Western blotting analysis. The results indicated that HG increased LDH activity, lipid ROS production, Fe2+ levels, and MDA levels and decreased GSH levels, suggesting that the HG condition induced ferroptosis. PD treatment inhibited ferroptosis in HG-induced cells, downregulated ACSL4 and TFR1 expression, and upregulated FTH-1 and SLC7A11 expression. PD reversed the effects of HG condition on cell death. Moreover, GPX4 expression was downregulated in HG-stimulated cells. Furthermore, we substantiated that PD suppressed ferroptosis by modulating GPX4 expression. In conclusion, PD inhibited ferroptosis in HG-induced HK-2 cells by upregulating GPX4 expression, suggesting that PD may be an effective drug for the clinical treatment of DN. Graphical abstract

Physiological and Qualitative Response of Cucurbita pepo L. to Salicylic Acid under Controlled Water Stress Conditions

Abstract: Limited water stress is one of the most important environmental stresses that affect the growth, quantity and quality of agronomic crops. This study was undertaken to investigate the effect of foliar applied salicylic acid (SA) on physiological responses, antioxidant enzymes and qualitative traits of Cucurbita pepo L. Plants exposed to water-stressed conditions in two years of field studies. Irrigation regimes at three soil matric potential levels (−0.3, −1.2 and −1.8 MPa) and SA at four levels (0.0, 0.5, 1.0 and 1.5 mg/L) were considered as main plot and sub-plots, respectively. The soil matric potential values (MPa) was measured just before irrigation. Results showed that under water stressed conditions alone, the amounts of malondialdehyde (MDA), hydrogen peroxide (H2O2) and ion leakage were higher compared with control treatment. However, spraying of SA under both water stress and non-stress conditions reduced the values of the above parameters. Water stress increased CAT, APX and GR enzymes activity. However foliar application of SA led to the decrease of CAT, APX and GR under all soil matric potential levels. The amount of carbohydrates and fatty acids increased with the intensity of water stress and SA modulated this response. By increasing SA concentration both in optimum and stress conditions, saturated fatty acids content decreased. According to our data, the SA application is an effective approach to improve pumpkin growth under water stress conditions.

Lactobacillus plantarum DP189 Reduces α-SYN Aggravation in MPTP-Induced Parkinson's Disease Mice via Regulating Oxidative Damage, Inflammation, and Gut Microbiota Disorder.

Abstract: This study aimed to evaluate the attenuating effect of Lactobacillus plantarum DP189 on α-synuclein (α-SYN) aggregates in the substantia nigra (SN) of Parkinson's disease (PD) mice via 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced. Our results indicated that L. plantarum DP189 increased the levels of superoxide dismutase (SOD), glutathione peroxide (GSH-Px), and interleukin-10 (IL-10) and decreased the levels of malondialdehyde (MDA), reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). Moreover, L. plantarum DP189 reduced the α-SYN accumulation in SN. Mechanistically, L. plantarum DP189 activated the expression of nuclear factor erythroid 2-related factor (Nrf2)/ARE and PGC-1α pathways and suppressed the NLRP3 inflammasome. Furthermore, fecal analysis showed that L. plantarum DP189 reshaped the gut microbiota in PD mice by reducing the number of pathogenic bacteria (Proteobacteria and Actinobacteria) and increased the abundance of probiotics (Lactobacillus and Prevotella). Our results suggested that L. plantarum DP189 could delay the neurodegeneration caused by the accumulation of α-SYN in the SN of PD mice via suppressing oxidative stress, repressing proinflammatory response, and modulating gut microbiota.

Maresin1 Protect Against Ferroptosis-Induced Liver Injury Through ROS Inhibition and Nrf2/HO-1/GPX4 Activation

Abstract: Drugs, viruses, and chemical poisons stimulating live in a short period of time can cause acute liver injury (ALI). ALI can further develop into serious liver diseases such as cirrhosis and liver cancer. Therefore, how to effectively prevent and treat ALI has become the focus of research. Numerous studies have reported Maresin1 (MaR1) has anti-inflammatory effect and protective functions on organs. In the present study, we used d-galactosamine/lipopolysaccharide (D-GalN/LPS) to establish an ALI model, explored the mechanism of liver cells death caused by D-GalN/LPS, and determined the effect of MaR1 on D-GalN/LPS-induced ALI. In vivo experiments, we found that MaR1 and ferrostatin-1 significantly alleviated D-GalN/LPS-induced ALI, reduced serum alanine transaminase and aspartate transaminase levels, and improved the survival rate of mice. Meanwhile, MaR1 inhibited hepatocyte death, inhibited tissue reactive oxygen species (ROS) expression, reduced malondialdehyde (MDA), reduced glutathione (GSH), GSH/oxidized glutathione (GSSG), and iron content induced by D-GalN/LPS in mice. In addition, MaR1 inhibited ferroptosis-induced liver injury through inhibiting the release of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and IL-6. Subsequently, western blot showed that MaR1 improved the expression of nuclear factor E2-related factor 2(Nrf2)/heme oxygenase-1 (HO-1)/glutathione peroxidase 4 (GPX4). In vitro experiments, we found that MaR1 inhibited LPS-induced and erastin-induced cell viability reduction. Meanwhile, we found that MaR1 increased the MDA and GSH levels in cells. Western blot showed that MaR1 increased the expression level of Nrf2/HO-1/GPX4. Next, the Nrf2 was knocked down in HepG2 cells, and the results showed that the protective effect of MaR1 significantly decreased. Finally, flow cytometry revealed that MaR1 inhibited ROS production and apoptosis. Overall, our study showed MaR1 inhibited ferroptosis-induced liver injury by inhibiting ROS production and Nrf2/HO-1/GPX4 activation.

Novel Antioxidant Collagen Peptides of Siberian Sturgeon (Acipenser baerii) Cartilages: The Preparation, Characterization, and Cytoprotection of H2O2-Damaged Human Umbilical Vein Endothelial Cells (HUVECs)

Abstract: For making full use of aquatic by-products to produce high value-added products, Siberian sturgeon (Acipenser baerii) cartilages were degreased, mineralized, and separately hydrolyzed by five kinds of proteases. The collagen hydrolysate (SCH) generated by Alcalase showed the strongest 2,2-diphenyl-1-picrylhydrazyl radical (DPPH·) and hydroxide radical (HO·) scavenging activity. Subsequently, thirteen antioxidant peptides (SCP1-SCP3) were isolated from SCH, and they were identified as GPTGED, GEPGEQ, GPEGPAG, VPPQD, GLEDHA, GDRGAEG, PRGFRGPV, GEYGFE, GFIGFNG, PSVSLT, IELFPGLP, LRGEAGL, and RGEPGL with molecular weights of 574.55, 615.60, 583.60, 554.60, 640.64, 660.64, 885.04, 700.70, 710.79, 602.67, 942.12, 714.82, and 627.70 Da, respectively. GEYGFE, PSVSLT, and IELFPGLP showed the highest scavenging activity on DPPH· (EC50: 1.27, 1.05, and 1.38 mg/mL, respectively) and HO· (EC50: 1.16, 0.97, and 1.63 mg/mL, respectively), inhibiting capability of lipid peroxidation, and protective functions on H2O2-damaged plasmid DNA. More importantly, GEYGFE, PSVSLT, and IELFPGLP displayed significant cytoprotection on HUVECs against H2O2 injury by regulating the endogenous antioxidant enzymes of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) to decrease the contents of reactive oxygen species (ROS) and malondialdehyde (MDA). Therefore, the research provided better technical assistance for a higher-value utilization of Siberian sturgeon cartilages and the thirteen isolated peptides—especially GEYGFE, PSVSLT, and IELFPGLP—which may serve as antioxidant additives for generating health-prone products to treat chronic diseases caused by oxidative stress.

Silicon Fertigation Regimes Attenuates Cadmium Toxicity and Phytoremediation Potential in Two Maize (Zea mays L.) Cultivars by Minimizing Its Uptake and Oxidative Stress

Abstract: Silicon (Si) is an important plant-derived metabolite that is significantly involved in maintaining the stability of a plant’s metabiological, structural and physiological characteristics under the abiotic stressed environment. We conducted the present study using maize (Zea mays L.) cultivars (Sadaf and EV-20) grown in sand artificially contaminated with cadmium (500 µM) in Hoagland’s nutrient solution to investigate its efficiency. Results from the present study evidenced that the toxic concentration of Cd in sand significantly reduced shoot length, root length, shoot fresh weight, root fresh weight, shoot dry weight and root dry weight by 88, 94, 89, 86 99 and 99%, respectively, in Sadaf while decreasing by 98, 97, 93, 99, 84 and 91%, respectively, in EV-20. Similarly, Cd toxicity decreased total chlorophyll and carotenoid content in both varieties of Z. mays. Moreover, the activities of various antioxidants (superoxidase dismutase, peroxidase and catalase) increased under the toxic concentration of Cd in sand which was manifested by the presence of membrane permeability, malondialdehyde (MDA), and hydrogen peroxide (H2O2). Results additionally showed that the toxic effect of Cd was more severe in EV-20 compared with Sadaf under the same conditions of environmental stresses. In addition, the increased concentration of Cd in sand induced a significantly increased Cd accumulation in the roots (141 and 169 mg kg−1 in Sadaf and EV-20, respectively), and shoots (101 and 141 mg kg−1 in Sadaf and EV-20, respectively), while; EV-20 accumulated higher amounts of Cd than Sadaf, with the values for both bioaccumulation factor (BAF) and translocation factor (TF) among all treatments being less than 1. The subsequent negative results of Cd injury can be overcome by the foliar application of Si which not only increased plant growth and biomass, but also decreased oxidative damage induced by the higher concentrations of MDA and H2O2 under a Cd-stressed environment. Moreover, external application of Si decreased the concentration of Cd in the roots and shoots of plants, therefore suggesting that the application of Si can ameliorate Cd toxicity in Z. mays cultivars and results in improved plant growth and composition under Cd stress by minimizing oxidative damage to membrane-bound organelles.

Ellagic Acid Alleviates Oxidative Stress by Mediating Nrf2 Signaling Pathways and Protects against Paraquat-Induced Intestinal Injury in Piglets

Abstract: The gastrointestinal tract is a key source of superoxide so as to be one of the most vulnerable to oxidative stress damage. Ellagic acid (EA), a polyphenol displays widely biological activities owing to its strong antioxidant properties. Here, we investigated the protective benefits of EA on oxidative stress and intestinal barrier injury in paraquet (PQ)-challenged piglets. A total of 40 weaned piglets were randomly divided into five groups: Control, PQ, 0.005% EA-PQ, 0.01% EA-PQ, and 0.02% EA-PQ. Piglets were intraperitoneally injected with 4 mg/kg (BW) PQ or saline on d-18, and sacrificed on d-21 of experiment. EA treatments eliminated growth-check induced by PQ and increased serum superoxide dismutase (SOD) activity but decreased serum malondialdehyde (MDA) level as compared to PQ group. EA supplementation promoted Nrf2 nuclear translocation and enhanced heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO1) protein abundances of small intestinal mucosa. Additionally, EA improved PQ-induced crypt deepening, goblet cells loss, and villi morphological damage. Consistently, EA increased tight junction protein expression as was evident from the decreased serum diamine oxidase (DAO) levels. EA could ameliorate the PQ-induced oxidative stress and intestinal damage through mediating Nrf2 signaling pathway. Intake of EA-rich food might prevent oxidative stress-mediated gut diseases.