Exogenous L-carnitine a meliorated burn-induced cellular and mitochondrial injuries of hepatocytes via recovering CPT1 activity

2021 ◽  
Author(s):  
Pengtao Li ◽  
Zhengguo Xia ◽  
Weichang Kong ◽  
Qiong Wang ◽  
Ziyue Zhao ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Membrane Potential ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Membrane Potential ◽  
Differentially Expressed Genes ◽  
Liver Tissue ◽  
Mitochondrial Membrane ◽  
Cellular Fatty Acid ◽  
Burn Patients ◽  
Severe Burn

Abstract Background : Impaired liver fatty acid metabolism and persistent mitochondrial dysfunction are common phenomena and associated with liver failure. Decreased serum L-carnitine, a vitamin involved in fatty-acid and energy metabolisms, has been reported in severe burn patients. The current research aimed to study the effects and mechanism of L-carnitine on mitochondrial damage and other hepatocytic injuries. Methods : Serum carnitine and indicators for hepatocytic injuries including AST, ALT, LDH, TG and OCT in severe burn patients and healthy controls were analyzed. The burn model in rats was established by skin scalding, and the carnitine was administered to the rats. The indicators mentioned above in the serum, and oil red staining, TUNEL staining and TEM observation, mitochondrial membrane potential, and CPT1 activity as well as CPT1 expression of the liver tissue were examined. HepG2 cells, treated with the CPT1 inhibitor etomoxir, were supplied with/without carnitine for 24h. The indicators mentioned above were examined, and apoptotic cells were analyzed by flow cytometry. Transcriptom high throughput sequencing of the rat liver tissues was performed, and differentially expressed genes Fabp4, Acacb, Acsm5 and Pnpla3 were further determined by RT-qPCR. Results : Significantly decreased carnitine and increased AST, ALT, LDH and OCT in the serum were detected in the severe burn patients and the scalded rats. Accumulation of TG, obvious mitochondrial shrinking, altered mitochondrial membrane potential, decreased ketogenesis and declined CPT1 activity were found in the liver tissue of the scalded rats. Administration of carnitine recovered CPT1 activity and improved all the parameters for cellular, fatty acid metabolic and mitochondrial injuries. Inhibition of CPT1 activity with etomoxir in vitro induced similar hepatocytic injuries found in the burn patients and the scalded rats, and supplementation of carnitine restored CPT1 activity and ameliorated these injuries. Differentially expressed genes Fabp4, Acacb, Acsm5 and Pnpla3 in the liver tissue and in the etomoxir-treated hepatocytes were also restored by exogenous carnitine. Conclusion : Exogenous carnitine exerts its protective effect on severe burn-induced cellular, fatty-acid metabolic and mitochondrial dysfunction of the hepatocytes via restore of CPT1 activity.

scholarly journals Exogenous L-carnitine ameliorates burn-induced cellular and mitochondrial injury of hepatocytes by restoring CPT1 activity

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Pengtao Li ◽  
Zhengguo Xia ◽  
Weichang Kong ◽  
Qiong Wang ◽  
Ziyue Zhao ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Membrane Potential ◽  
Fatty Acid Metabolism ◽  
Liver Tissue ◽  
Mitochondrial Membrane ◽  
Acid Metabolism ◽  
Serum Levels ◽  
Burn Patients ◽  
Carnitine Supplementation ◽  
Severe Burn

Abstract Background Impaired hepatic fatty acid metabolism and persistent mitochondrial dysfunction are phenomena commonly associated with liver failure. Decreased serum levels of L-carnitine, a amino acid derivative involved in fatty-acid and energy metabolism, have been reported in severe burn patients. The current study aimed to evaluate the effects of L-carnitine supplementation on mitochondrial damage and other hepatocyte injuries following severe burns and the related mechanisms. Methods Serum carnitine and other indicators of hepatocytic injury, including AST, ALT, LDH, TG, and OCT, were analyzed in severe burn patients and healthy controls. A burn model was established on the back skin of rats; thereafter, carnitine was administered, and serum levels of the above indicators were evaluated along with Oil Red O and TUNEL staining, transmission electron microscopy, and assessment of mitochondrial membrane potential and carnitine palmitoyltransferase 1 (CPT1) activity and expression levels in the liver. HepG2 cells pretreated with the CPT1 inhibitor etomoxir were treated with or without carnitine for 24 h. Next, the above indicators were examined, and apoptotic cells were analyzed via flow cytometry. High-throughput sequencing of rat liver tissues identified several differentially expressed genes (Fabp4, Acacb, Acsm5, and Pnpla3) were confirmed using RT-qPCR. Results Substantially decreased serum levels of carnitine and increased levels of AST, ALT, LDH, and OCT were detected in severe burn patients and the burn model rats. Accumulation of TG, evident mitochondrial shrinkage, altered mitochondrial membrane potential, decreased ketogenesis, and reduced CPT1 activity were detected in the liver tissue of the burned rats. Carnitine administration recovered CPT1 activity and improved all indicators related to cellular and fatty acid metabolism and mitochondrial injury. Inhibition of CPT1 activity with etomoxir induced hepatocyte injuries similar to those in burn patients and burned rats; carnitine supplementation restored CPT1 activity and ameliorated these injuries. The expression levels of the differentially expressed genes Fabp4, Acacb, Acsm5, and Pnpla3 in the liver tissue from burned rats and etomoxir-treated hepatocytes were also restored by treatment with exogenous carnitine. Conclusion Exogenous carnitine exerts protective effects against severe burn-induced cellular, fatty-acid metabolism, and mitochondrial dysfunction of hepatocytes by restoring CPT1 activity.

scholarly journals Alpha-Tocotrienol Prevents Oxidative Stress-Mediated Post-Translational Cleavage of Bcl-xL in Primary Hippocampal Neurons

2019 ◽  
Vol 21 (1) ◽  
pp. 220 ◽  
Author(s):  
Han-A Park ◽  
Nelli Mnatsakanyan ◽  
Katheryn Broman ◽  
Abigail U. Davis ◽  
Jordan May ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Hippocampal Neurons ◽  
Mitochondrial Membrane ◽  
Antioxidant Properties ◽  
B Cell Lymphoma ◽  
Atp Depletion ◽  
Primary Hippocampal Neurons

B-cell lymphoma-extra large (Bcl-xL) is an anti-apoptotic member of the Bcl2 family of proteins, which supports neurite outgrowth and neurotransmission by improving mitochondrial function. During excitotoxic stimulation, however, Bcl-xL undergoes post-translational cleavage to ∆N-Bcl-xL, and accumulation of ∆N-Bcl-xL causes mitochondrial dysfunction and neuronal death. In this study, we hypothesized that the generation of reactive oxygen species (ROS) during excitotoxicity leads to formation of ∆N-Bcl-xL. We further proposed that the application of an antioxidant with neuroprotective properties such as α-tocotrienol (TCT) will prevent ∆N-Bcl-xL-induced mitochondrial dysfunction via its antioxidant properties. Primary hippocampal neurons were treated with α-TCT, glutamate, or a combination of both. Glutamate challenge significantly increased cytosolic and mitochondrial ROS and ∆N-Bcl-xL levels. ∆N-Bcl-xL accumulation was accompanied by intracellular ATP depletion, loss of mitochondrial membrane potential, and cell death. α-TCT prevented loss of mitochondrial membrane potential in hippocampal neurons overexpressing ∆N-Bcl-xL, suggesting that ∆N-Bcl-xL caused the loss of mitochondrial function under excitotoxic conditions. Our data suggest that production of ROS is an important cause of ∆N-Bcl-xL formation and that preventing ROS production may be an effective strategy to prevent ∆N-Bcl-xL-mediated mitochondrial dysfunction and thus promote neuronal survival.

scholarly journals Mitochondrial dysfunction in insulin resistance: differential contributions of chronic insulin and saturated fatty acid exposure in muscle cells

2012 ◽  
Vol 32 (5) ◽  
pp. 465-478 ◽  
Author(s):  
Chenjing Yang ◽  
Cho Cho Aye ◽  
Xiaoxin Li ◽  
Angels Diaz Ramos ◽  
Antonio Zorzano ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Oxygen Consumption ◽  
Fatty Acid ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Saturated Fatty Acid ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Acid Exposure ◽  
High Insulin

Mitochondrial dysfunction has been associated with insulin resistance, obesity and diabetes. Hyperinsulinaemia and hyperlipidaemia are hallmarks of the insulin-resistant state. We sought to determine the contributions of high insulin and saturated fatty acid exposure to mitochondrial function and biogenesis in cultured myocytes. Differentiated C2C12 myotubes were left untreated or exposed to chronic high insulin or high palmitate. Mitochondrial function was determined assessing: oxygen consumption, mitochondrial membrane potential, ATP content and ROS (reactive oxygen species) production. We also determined the expression of several mitochondrial genes. Chronic insulin treatment of myotubes caused insulin resistance with reduced PI3K (phosphoinositide 3-kinase) and ERK (extracellular-signal-regulated kinase) signalling. Insulin treatment increased oxygen consumption but reduced mitochondrial membrane potential and ROS production. ATP cellular levels were maintained through an increased glycolytic rate. The expression of mitochondrial OXPHOS (oxidative phosphorylation) subunits or Mfn-2 (mitofusin 2) were not significantly altered in comparison with untreated cells, whereas expression of PGC-1α (peroxisome-proliferator-activated receptor γ co-activator-1α) and UCPs (uncoupling proteins) were reduced. In contrast, saturated fatty acid exposure caused insulin resistance, reducing PI3K (phosphoinositide 3-kinase) and ERK (extracellular-signal-regulated kinase) activation while increasing activation of stress kinases JNK (c-Jun N-terminal kinase) and p38. Fatty acids reduced oxygen consumption and mitochondrial membrane potential while up-regulating the expression of mitochondrial ETC (electron chain complex) protein subunits and UCP proteins. Mfn-2 expression was not modified by palmitate. Palmitate-treated cells also showed a reduced glycolytic rate. Taken together, our findings indicate that chronic insulin and fatty acid-induced insulin resistance differentially affect mitochondrial function. In both conditions, cells were able to maintain ATP levels despite the loss of membrane potential; however, different protein expression suggests different adaptation mechanisms.

NAD+ deficiency and mitochondrial dysfunction in granulosa cells of women with polycystic ovary syndrome‡

2021 ◽  
Author(s):  
Yujiao Wang ◽  
Qingling Yang ◽  
Huan Wang ◽  
Jing Zhu ◽  
Luping Cong ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Polycystic Ovary Syndrome ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Membrane Potential ◽  
Granulosa Cells ◽  
Mitochondrial Membrane ◽  
Polycystic Ovary ◽  
Tumor Cell Line ◽  
Ovary Syndrome ◽  
Atp Generation

Abstract Polycystic ovary syndrome (PCOS) is a prevalent heterogeneous endocrine disorder characterized by ovulation dysfunction, androgen excess, ovarian polycystic changes, insulin resistance, and infertility. Although underlying mechanisms for PCOS are still unknown, inflammation and mitochondrial dysfunction in granulosa cells (GCs) of PCOS patients have been reported. Here, we found that Nicotinamide Adenine Dinucleotide (NAD+) levels in GCs of PCOS patients was significantly decreased when compared with controls. Also, we found that higher expression of inflammation factors, increased reactive oxygen species (ROS) accumulation, lower adenosine triphosphate (ATP) generation, and decreased mitochondrial membrane potential, as well as abnormal mitochondrial dynamics in GCs of PCOS patients. In addition, the NAD+ levels were decreased after activation of inflammation in human granulosa-like tumor cell line (KGN) treated by Lipopolysaccharide (LPS). However, supplementation of nicotinamide riboside (NR), a NAD+ precursor, could largely restore the NAD+ content, reduce ROS levels and improve mitochondrial function demonstrated by increased mitochondrial membrane potential and ATP generation in LPS-treated KGN cells. Our data suggested that inflammation decreased NAD+ levels in GCs of PCOS patients, while supplementation of NR could restore NAD+ levels and alleviated mitochondrial dysfunction in GCs of PCOS patients.

scholarly journals Mitochondrial dysfunction in antiphospholipid syndrome: implications in the pathogenesis of the disease and effects of coenzyme Q10 treatment

Blood ◽  
2012 ◽  
Vol 119 (24) ◽  
pp. 5859-5870 ◽  
Author(s):  
Carlos Perez-Sanchez ◽  
Patricia Ruiz-Limon ◽  
Maria Angeles Aguirre ◽  
Maria Laura Bertolaccini ◽  
Munther A. Khamashta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Membrane Potential ◽  
Antiphospholipid Syndrome ◽  
Coenzyme Q10 ◽  
Mitochondrial Membrane ◽  
Antiphospholipid Antibody ◽  
Antibody Treatment

Abstract The exact mechanisms underlying the role of oxidative stress in the pathogenesis and the prothrombotic or proinflammatory status of antiphospholipid syndrome (APS) remain unknown. Here, we investigate the role of oxidative stress and mitochondrial dysfunction in the proatherothrombotic status of APS patients induced by IgG-antiphospholipid antibodies and the beneficial effects of supplementing cells with coenzyme Q10 (CoQ10). A significant increase in relevant prothrombotic and inflammatory parameters in 43 APS patients was found compared with 38 healthy donors. Increased peroxide production, nuclear abundance of Nrf2, antioxidant enzymatic activity, decreased intracellular glutathione, and altered mitochondrial membrane potential were found in monocytes and neutrophils from APS patients. Accelerated atherosclerosis in APS patients was found associated with their inflammatory or oxidative status. CoQ10 preincubation of healthy monocytes before IgG-antiphospholipid antibody treatment decreased oxidative stress, the percentage of cells with altered mitochondrial membrane potential, and the induced expression of tissue factor, VEGF, and Flt1. In addition, CoQ10 significantly improved the ultrastructural preservation of mitochondria and prevented IgG-APS–induced fission mediated by Drp-1 and Fis-1 proteins. In conclusion, the oxidative perturbation in APS patient leukocytes, which is directly related to an inflammatory and pro-atherothrombotic status, relies on alterations in mitochondrial dynamics and metabolism that may be prevented, reverted, or both by treatment with CoQ10.

scholarly journals Structurally optimised BODIPY derivatives for imaging of mitochondrial dysfunction in cancer and heart cells

2016 ◽  
Vol 52 (44) ◽  
pp. 7114-7117 ◽  
Author(s):  
Shubhanchi Nigam ◽  
Benjamin P. Burke ◽  
Laura H. Davies ◽  
Juozas Domarkas ◽  
Jennifer F. Wallis ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Dysfunction ◽  
Optical Imaging ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Imaging Agents ◽  
Heart Cells

BODIPY based optical imaging agents with mitochondrial membrane potential dependent uptake are described.

scholarly journals Development of a No-Wash Assay for Mitochondrial Membrane Potential Using the Styryl Dye DASPEI

2010 ◽  
Vol 15 (9) ◽  
pp. 1071-1081 ◽  
Author(s):  
Kristian H. R. Jensen ◽  
Jens C. Rekling
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Membrane Potential ◽  
Cho Cells ◽  
Mitochondrial Membrane ◽  
Large Scale ◽  
Chinese Hamster ◽  
Amyloid Β ◽  
Drug Target Discovery ◽  
Cellular Models

Mitochondrial dysfunction is a hallmark of several diseases and may also result from drugs with unwanted side effects on mitochondrial biochemistry. The mitochondrial membrane potential is a good indicator of mitochondrial function. Here, the authors have developed a no-wash mitochondrial membrane potential assay using 2-(4-(dimethylamino)styryl)-N-ethylpyridinium iodide (DASPEI), a rarely used mitochondrial potentiometric probe, in a 96-well format using a fluorescent plate reader. The assay was validated using 2 protonophores (CCCP, DNP), which are known uncouplers, and the neuroleptic thioridazine, which is a suspected mitochondrial toxicant. CCCP and DNP have short-term depolarizing effects, and thioridazine has long-term hyperpolarizing effects on the mitochondrial membrane potential of Chinese hamster ovary (CHO) cells. The assay also detected changes of the mitochondrial membrane potential in CHO cells exposed to cobalt (mimicking hypoxia) and in PC12 cells exposed to amyloid β, demonstrating that the assay can be used in cellular models of hypoxia and Alzheimer’s disease. The assay needs no washing steps, has a Z′ value >0.5, can be used on standard fluorometers, has good post liquid-handling stability, and thus is suitable for large-scale screening efforts. In summary, the DASPEI assay is simple and rapid and may be of use in toxicological testing, drug target discovery, and mechanistic models of diseases involving mitochondrial dysfunction.

scholarly journals Association between Fatty Acid Composition, Cryotolerance and Fertility Competence of Progressively Motile Bovine Spermatozoa

Animals ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 2948
Author(s):  
Tanya Kogan ◽  
Dana Grossman Dahan ◽  
Ronit Laor ◽  
Nurit Argov-Argaman ◽  
Yoel Zeron ◽  
...  
Keyword(s):  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Acid Composition ◽  
Mitochondrial Membrane ◽  
Structural Characteristics ◽  
Conception Rate ◽  
Omega 3 ◽  
Rate Analysis

An association between progressive motility (PM) and spermatozoa fertility competence has been suggested. However, the mechanism that underlies PM is not clear enough. We examined physiological characteristics and fatty acid composition of fresh spermatozoa with high and low PM. Additional analysis of fatty acid composition and structural characteristics was performed on spermatozoa samples with high and low progressively motile spermatozoa’s survival (PMSS), i.e., the ratio between the proportion of progressively motile spermatozoa after and before cryopreservation. Finally, a fertility field trial was conducted to examine the association between the number of PM spermatozoa within the insemination straw post thawing and conception rate. Analysis of fresh spermatozoa revealed a higher omega-6 to omega-3 ratio in ejaculates with low PM relative to those with high PM (p < 0.01). The proportion of polyunsaturated fatty acids was higher in low-PMSS fresh samples (p < 0.05) relative to their high-PMSS counterparts. Fresh samples with high-PMSS expressed a higher mitochondrial membrane potential (p < 0.05) and a higher proportion of viable cells that expressed reactive oxygen species (ROS; p < 0.05). Post-thawing evaluation revealed a reduced proportion of progressively motile sperm, with a prominent effect in samples with high PM relative to low PM, defined before freezing (p < 0.01). No differences in spermatozoa mitochondrial membrane potential or ROS level were found post-thawing. A fertility study revealed a positive correlation between the number of progressively motile spermatozoa within a standard insemination straw and conception rate (p < 0.05). Considering these, the bull PMSS is suggested to be taken into account at the time of straw preparation.

scholarly journals Exposure to Plasma From Non-alcoholic Fatty Liver Disease Patients Affects Hepatocyte Viability, Generates Mitochondrial Dysfunction, and Modulates Pathways Involved in Fat Accumulation and Inflammation

2021 ◽  
Vol 8 ◽  
Author(s):  
Elena Grossini ◽  
Divya Praveen Garhwal ◽  
Giuseppe Calamita ◽  
Raffaele Romito ◽  
Cristina Rigamonti ◽  
...  
Keyword(s):  
Liver Disease ◽  
Membrane Potential ◽  
Fatty Liver ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Membrane Potential ◽  
Nlrp3 Inflammasome ◽  
Fatty Liver Disease ◽  
Mitochondrial Membrane ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Changes of lipidic storage, oxidative stress and mitochondrial dysfunction may be involved in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Although the knowledge of intracellular pathways has vastly expanded in recent years, the role and mechanisms of circulating triggering factor(s) are debated. Thus, we tested the hypothesis that factors circulating in the blood of NAFLD patients may influence processes underlying the disease. Huh7.5 cells/primary human hepatocytes were exposed to plasma from 12 NAFLD patients and 12 healthy subjects and specific assays were performed to examine viability, H2O2 and mitochondrial reactive oxygen species (ROS) release, mitochondrial membrane potential and triglycerides content. The involvement of NLRP3 inflammasome and of signaling related to peroxisome-proliferator-activating-ligand-receptor-γ (PPARγ), sterol-regulatory-element-binding-protein-1c (SREBP-1c), nuclear-factor-kappa-light-chain-enhancer of activated B cells (NF-kB), and NADPH oxidase 2 (NOX2) was evaluated by repeating the experiments in the presence of NLRP3 inflammasome blocker, MCC950, and through Western blot. The results obtained shown that plasma of NAFLD patients was able to reduce cell viability and mitochondrial membrane potential by about 48 and 24% (p &lt; 0.05), and to increase H2O2, mitochondrial ROS, and triglycerides content by about 42, 19, and 16% (p &lt; 0.05), respectively. An increased expression of SREBP-1c, PPARγ, NF-kB and NOX2 of about 51, 121, 63, and 46%, respectively, was observed (p &lt; 0.05), as well. Those effects were reduced by the use of MCC950. Thus, in hepatocytes, exposure to plasma from NAFLD patients induces a NAFLD-like phenotype by interference with NLRP3-inflammasome pathways and the activation of intracellular signaling related to SREBP-1c, PPARγ, NF-kB and NOX2.

scholarly journals Egr2 upregulation induced mitochondrial iron overload implicating in sevoflurane-induced cognitive deficits in developing mice

2020 ◽  
Author(s):  
Piao Zhang ◽  
Yeru Chen ◽  
Shuxia Zhang ◽  
Man Fang ◽  
Xianyi Lin ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Cognitive Function ◽  
Mitochondrial Dysfunction ◽  
Prussian Blue ◽  
Mitochondrial Membrane Potential ◽  
Cognitive Deficits ◽  
Mitochondrial Membrane ◽  
Bioinformatics Analysis ◽  
Blue Staining ◽  
Behavioral Tests

Abstract Background Sevoflurane inhalation initiated cognitive deficits implicated in mitochondrial dysfunction and synaptogenesis impairment. Bioinformatics analysis indicated that Egr2 may play a crucial role in maintaining cognitive function. Therefore, we attempted to clarify the potential mechanism regarding Egr2 expression and cognitive deficits induced by sevoflurane administration.Methods Animals received sevoflurane anesthesia, and the behavioral tests including Morris water maze, novel object recognition test and trace fear conditioning were performed. Then, the immunofluorescent staining was employed to detect the effect of sevoflurane inhalation in hippocampal neurons. Meanwhile, bioinformatics analysis was implemented, and the level of lipid peroxidation, mitochondrial membrane potential, morphology and membrane permeability, and cytoplasm calcium levels were investigated after Egr2 interference by using JC-1 probe, MitoTracker staining, Mitochondrial permeability transition pore (mPTP) assay, and Fluo calcium indicators, respectively. Additionally, Prussian blue staining was used to evaluate the iron content.Results The behavioral tests indicated that the cognitive function was significantly attenuated after sevoflurane administration. The Golgi-Cox staining displayed that the dendritic length, density and nodes were significantly reduced following sevoflurane inhalation. The bioinformatics analysis showed that sevoflurane administration results in the Egr2 expression upregulation. Additionally, the results suggested that sevoflurane administration elevated the cytoplasm calcium levels, reduced the mitochondrial membrane potential and triggered the opening of mPTP. Prussian blue staining showed that the iron deposition was apparently increased. However, Egr2 level downregulation partly reversed these above changes. Moreover, the behavioral performance was effectively improved after deferiprone (DFP) administration.Conclusion These findings demonstrated that sevoflurane administration elicited mitochondrial dysfunction and iron dyshomeostasis, and eventually resulted in cognitive impairments, whereas suppressing Egr2 expression partly improved this pathological process.

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