Oxidative Stress Effects of Soluble Sulfide on Human Hepatocyte Cell Line LO2

Soluble sulfide is well known for its toxicity and corrosion for hundreds of years. However, recent studies have demonstrated that hydrogen sulfide (H2S)—a novel gasotransmitter—supports a critical role during neuromodulation, cell proliferation, and cardioprotection for organisms. In particular, soluble sulfide plays multifaceted signaling functions in mammals during oxidative stress processes. However, the specific molecular regulation of soluble sulfide during oxidative stress remains unclear. In this study, Na2S was implemented as a soluble sulfide donor to expose LO2 cells. The 3-(4,5-dimethylthiazolyl-2),-2,5-diphenyltetrazolium bromide (MTT) assay, hydroxyl radical assay, superoxide dismutase (SOD) assay, and glutathione peroxidase (GSH-PX) assay were applied to analyze cytotoxicity, hydroxyl radical levels, SOD and GSH-Px activities, respectively. Soluble sulfide at a concentration 0.01–1.0 mM/L resulted in a marked and concentration-dependent reduction of LO2 cell viability. At low concentrations, sulfide solutions increased SOD activity and GSH-Px activity of LO2 after 24 h exposure, exhibiting a clear hormesis-effect and indicating the protective ability of soluble sulfide against oxidative stress. The decline in SOD and GSH-Px and the increase in hydroxyl radical (0.08–1.0 mM/L) suggested that oxidative damage could be a possible mechanism for sulfide-induced cytotoxicity.

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Acrylamide-induced oxidative stress in human erythrocytes

Human & Experimental Toxicology ◽

10.1177/0960327109350664 ◽

2009 ◽

Vol 28 (10) ◽

pp. 611-617 ◽

Cited By ~ 30

Author(s):

Betul Catalgol ◽

Gül Özhan ◽

Buket Alpertunga

Keyword(s):

Oxidative Stress ◽

Reduced Glutathione ◽

Human Erythrocytes ◽

Antioxidant Enzyme Activities ◽

Total Glutathione ◽

Sod Activity ◽

Spectrophotometric Methods ◽

Low Concentrations ◽

Different Doses

Acrylamide (AA), a widely used industrial chemical, is shown to be neurotoxic, mutagenic and carcinogenic. This study was carried out to investigate the effects of different doses of AA on lipid peroxidation (LPO), haemolysis, methaemoglobin (MetHb) and antioxidant system in human erythrocytes in vitro. Erythrocyte solutions were incubated with 0.10, 0.25, 0.50 and 1.00 mM of AA at 37°C for 1 hour. At the end of the incubation, malondialdehyde (MDA), an end product of LPO, was determined by liquid chromatography (LC) while total glutathione, reduced glutathione (GSH) levels, activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzymes and the rates of haemolysis and MetHb were determined by spectrophotometric methods. All of the studied concentrations of AA increased MetHb formation and SOD activity, and induced MDA formation and haemolysis due to the destruction of erythrocyte cell membrane. AA caused a decrease in the activities of GSH-Px, CAT and GSH levels. However, these effects of AA were seen only at higher concentrations than AA intake estimated for populations in many countries. We suggest that LPO process may not be involved in the toxic effects of AA in low concentrations, although the present results showed that the studied concentrations of AA exert deteriorating effects on antioxidant enzyme activities, LPO process and haemolysis.

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Polymorphism of Transferrin Gene Impacts the Mediating Effects of Psychotic Symptoms on the Relationship between Oxidative Stress and Cognition in Patients with Chronic Schizophrenia

Antioxidants ◽

10.3390/antiox11010125 ◽

2022 ◽

Vol 11 (1) ◽

pp. 125

Author(s):

Pinhong Chen ◽

Dongmei Wang ◽

Meihong Xiu ◽

Dachun Chen ◽

Blake Lackey ◽

...

Keyword(s):

Oxidative Stress ◽

Negative Symptoms ◽

Critical Role ◽

Chronic Schizophrenia ◽

Psychotic Symptoms ◽

Sod Activity ◽

Neuropsychological Status ◽

Transferrin Gene ◽

Tf Gene ◽

The Relationship

A series of studies indicated that iron distribution that partly derives from transferrin-bound iron in the peripheral nervous system in the brain may act in processes such as myelination and brain development. However, the relationship between schizophrenia, its psychotic symptoms, and the transferrin (TF) gene has not been systematically explored. Our study aimed to investigate how a particular polymorphism of the transferrin gene, rs3811655, affects the superoxide dismutase (SOD), malondialdehyde (MDA), psychotic symptoms, cognition, or the mediation model between antioxidant enzymes and cognition via symptoms. A total of 564 patients with chronic schizophrenia and 468 healthy control subjects were recruited. The psychotic symptoms and cognition were assessed by the Positive and Negative Syndrome Scale (PANSS) and the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), respectively. Furthermore, the serum SOD, MDA activity, and transferrin gene polymorphism were measured in patients. Our results demonstrated that patients with the G allele possessed more severe negative symptoms, worse cognitive performance with respect to attention, and higher serum Mn-SOD activity. Additionally, the rs3811655 polymorphism may act as a moderator in the association between Cu/Zn-SOD activity and cognition, as well as psychotic symptoms in patients suffering from schizophrenia. According to this study, the single nucleotide polymorphism (SNP) rs3811655 polymorphism may fail to contribute to the susceptibility of schizophrenia in an individual but is involved in the iron-induced oxidative stress disturbance and cognitive impairment in schizophrenia. This deepens our understanding of the critical role of iron-induced oxidative stress that might underlie the pathophysiology of schizophrenia.

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Effects of oxidative stress on expression of extracellular superoxide dismutase, CuZn-superoxide dismutase and Mn-superoxide dismutase in human dermal fibroblasts

Biochemical Journal ◽

10.1042/bj2980347 ◽

1994 ◽

Vol 298 (2) ◽

pp. 347-352 ◽

Cited By ~ 71

Author(s):

P Strålin ◽

S L Marklund

Keyword(s):

Oxidative Stress ◽

Superoxide Dismutase ◽

Cumene Hydroperoxide ◽

Dermal Fibroblasts ◽

Serum Starvation ◽

Extracellular Superoxide Dismutase ◽

Sod Activity ◽

Low Concentrations ◽

Buthionine Sulphoximine ◽

High Doses

To determine the effect of oxidative stress on expression of extracellular superoxide dismutase (EC-SOD), CuZn-SOD and Mn-SOD, two fibroblast lines were exposed for periods of up to 4 days to a wide concentration range of oxidizing agents: xanthine oxidase plus hypoxanthine, paraquat, pyrogallol, alpha-naphthoflavone, hydroquinone, catechol, Fe2+ ions, Cu2+ ions, buthionine sulphoximine, diethylmaleate, t-butyl hydroperoxide, cumene hydroperoxide, selenite, citiolone and high oxygen partial pressure. The cell lines were cultured both under serum starvation and at a serum concentration that permitted growth. Under no condition was there any evidence of EC-SOD induction. Instead, the agents uniformly, dose-dependently and continuously reduced EC-SOD expression. We interpret the effect to be due to toxicity. Enhancement of the protection against oxidative stress by addition of CuZn-SOD, catalase and low concentrations of selenite did not influence the expression of any of the SOD isoenzymes. Removal of EC-SOD from cell surfaces by heparin also did not influence SOD expression. Mn-SOD was moderately induced by high doses of the first 11 oxidants. Apart from reduction at high toxic doses, there were no significant effects on the CuZn-SOD activity by any of the treatments. Thus EC-SOD, previously shown to be profoundly influenced by inflammatory cytokines, was not induced by its substrate or other oxidants. In a similar fashion, Mn-SOD, previously shown to be greatly induced and depressed by cytokines, was only moderately influenced by oxidants. We suggest that the regulation of these SOD isoenzymes in mammalian tissues primarily occurs in a manner co-ordinated by cytokines, rather than as a response of individual cells to oxidants.

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Effects of two lichen acids isolated from Pseudevernia furfuracea (L.) Zopf in cultured human lymphocytes

Zeitschrift für Naturforschung C ◽

10.1515/znc-2017-0209 ◽

2018 ◽

Vol 73 (7-8) ◽

pp. 303-312 ◽

Cited By ~ 6

Author(s):

Bugrahan Emsen ◽

Basak Togar ◽

Hasan Turkez ◽

Ali Aslan

Keyword(s):

Oxidative Stress ◽

Lactate Dehydrogenase ◽

Cytotoxic Effect ◽

Human Lymphocytes ◽

Pseudevernia Furfuracea ◽

Low Concentrations ◽

Diphenyltetrazolium Bromide ◽

Total Antioxidant ◽

Total Oxidative Stress

Abstract The present study aims at assessing the efficacies of olivetoric acid (OA) and physodic acid (PA) isolated from Pseudevernia furfuracea (L.) Zopf (Parmeliaceae) in human lymphocytes (HLs) in vitro. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assays were performed to establish cytotoxicity in HLs. Besides, oxidative stress and genotoxicity were monitored by estimating the changes of total oxidative stress (TOS) and 8-hydroxy-2′-deoxyguanosine (8-OH-dG) levels, respectively, in HLs. At the same time, OA- and PA-induced total antioxidant capacity (TAC) levels in HLs were determined. Although especially low concentrations of OA (IC50=109.94 mg/L) and PA (IC50=665.49 mg/L) did not show cytotoxic effect at high levels in HLs, it was revealed that cytotoxicity was significantly (p<0.05) associated with oxidative stress and genotoxicity via correlation analysis. While TOS level in HLs did not statistically (p>0.05) increase in the presence of all treatments (0.5–100 mg/L) of PA, TAC level was increased by PA applications in certain concentrations (0.5–10 mg/L). Overall, the obtained data indicate that OA and especially PA as lichen compounds that do not cause oxidative stress can be a new resource of therapeutics as recognized in the present study with their high antioxidant features.

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Intermedin protects against renal ischemia-reperfusion injury by inhibition of oxidative stress

AJP Renal Physiology ◽

10.1152/ajprenal.00054.2012 ◽

2013 ◽

Vol 304 (1) ◽

pp. F112-F119 ◽

Cited By ~ 42

Author(s):

Xi Qiao ◽

Rong-Shan Li ◽

Hong Li ◽

Guo-Zhen Zhu ◽

Xiao-Guang Huang ◽

...

Keyword(s):

Oxidative Stress ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Left Kidney ◽

Critical Role ◽

Renal Ischemia ◽

Kidney Cells ◽

Sod Activity ◽

Renal Ischemia Reperfusion Injury

Reactive oxygen species (ROS) play a critical role in renal ischemia-reperfusion injury (IRI). Intermedin (IMD) reportedly protected against myocardial IRI via its antioxidant effects; however, its protective role in renal IRI has not been investigated. We overexpressed IMD in rat kidneys and examined how the kidneys respond to renal IRI. Eukaryotic expression plasmid encoding the rat IMD gene or control empty vector was transfected into the left kidney using an ultrasound-microbubble-mediated delivery system. This method yielded high expression of IMD in kidney cells. Renal IRI was induced by clamping the left renal artery followed by reperfusion. In response to IRI, overexpression of IMD in the kidney significantly improved renal function and pathology compared with the kidney transfected with control plasmid. We investigated the mechanisms by which IMD protects against renal IRI. We examined renal superoxide dismutase (SOD) activity and malondialdehyde (MDA) content and found SOD activity was significantly increased, while MDA level was markedly decreased in kidneys transfected with IMD, suggesting ROS production and oxidative stress were reduced by IMD overexpression. We also measured myeloperoxidase (MPO) activity, tubular cell apoptosis, and the expression of intercellular adhesion molecule-1 (ICAM-1), P-selectin, and endothelin-1 (ET-1) in the kidney. Renal MPO activity and the expression of ICAM-1, P-selectin, and ET-1 stimulated by IRI were significantly inhibited by IMD overexpression. Moreover, IMD overexpression prevented kidney cells from apoptosis caused by IRI. Our results demonstrate that overexpression of IMD in the kidney protects against renal IRI, apparently by reducing oxidative stress, consequently suppressing inflammation and vasoconstrictor production and apoptosis.

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LncRNA SNHG12 Improves Cerebral Ischemic-reperfusion Injury by Activating SIRT1/FOXO3a Pathway through I nhibition of Autophagy and Oxidative Stress

Current Neurovascular Research ◽

10.2174/1567202617666200727142019 ◽

2020 ◽

Vol 17 (4) ◽

pp. 394-401

Author(s):

Yuanhua Wu ◽

Yuan Huang ◽

Jing Cai ◽

Donglan Zhang ◽

Shixi Liu ◽

...

Keyword(s):

Oxidative Stress ◽

Molecular Mechanisms ◽

Ischemia Reperfusion ◽

Critical Role ◽

Cell Activity ◽

Ht22 Cells ◽

Cerebral Ischemic ◽

Cerebral Ischemic Reperfusion ◽

And Oxidative Stress

Background: Ischemia/reperfusion (I/R) injury involves complex biological processes and molecular mechanisms such as autophagy. Oxidative stress plays a critical role in the pathogenesis of I/R injury. LncRNAs are the regulatory factor of cerebral I/R injury. Methods: This study constructs cerebral I/R model to investigate role of autophagy and oxidative stress in cerebral I/R injury and the underline regulatory mechanism of SIRT1/ FOXO3a pathway. In this study, lncRNA SNHG12 and FOXO3a expression was up-regulated and SIRT1 expression was down-regulated in HT22 cells of I/R model. Results: Overexpression of lncRNA SNHG12 significantly increased the cell viability and inhibited cerebral ischemicreperfusion injury induced by I/Rthrough inhibition of autophagy. In addition, the transfected p-SIRT1 significantly suppressed the release of LDH and SOD compared with cells co-transfected with SIRT1 and FOXO3a group and cells induced by I/R and transfected with p-SNHG12 group and overexpression of cells co-transfected with SIRT1 and FOXO3 further decreased the I/R induced release of ROS and MDA. Conclusion: In conclusion, lncRNA SNHG12 increased cell activity and inhibited oxidative stress through inhibition of SIRT1/FOXO3a signaling-mediated autophagy in HT22 cells of I/R model. This study might provide new potential therapeutic targets for further investigating the mechanisms in cerebral I/R injury and provide.

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Interleukin-6 and Malondialdehyde in Women with Preterm Birth

Current Immunology Reviews ◽

10.2174/1573395515666191026140006 ◽

2019 ◽

Vol 15 (2) ◽

pp. 207-212

Author(s):

Vinita Verma ◽

Hina Oza ◽

Riddhi Thaker ◽

Sunil Kumar

Keyword(s):

Oxidative Stress ◽

Preterm Birth ◽

Interleukin 6 ◽

Critical Role ◽

Serum Levels ◽

Maternal Serum ◽

Full Term ◽

Mortality And Morbidity ◽

Term Birth ◽

Weak Negative Correlation

Background: Preterm Birth (PTB) is one of the main causes of neonatal death and infant mortality and morbidity. The pro-inflammatory cytokine interleukin-6 (IL-6) is a major proinflammatory mediator of the host response to infection and malondialdehyde (MDA) is a marker of oxidative stress. Objective : To evaluate potential associations between IL-6 and MDA levels in women with preterm birth. Method: A total of 150 women (66 with full-term and 84 with PTB) were enrolled in this case-control study. Predesigned performas were filled through questionnaire interviews to collect data on personal, demographic, occupational, lifestyle and reproductive history. Blood samples were collected within 36 hours of delivery. Serum concentrations of IL-6 and MDA were determined in mothers with full-term and preterm birth. Results: The mean age was marginally higher; whereas BMI was slightly lower in cases (PTB) as compared to controls (full-term) subjects. Serum IL-6 and MDA levels were significantly higher in subjects with PTB than full-term birth. The data were further analyzed with respect to underweight, normal and overweight/obese BMI. In all the BMI categories, the levels of IL-6 and MDA were higher in PTB cases. Among the PTB categories, the levels of IL-6 and MDA were highest in moderate to late preterm birth. A significant positive correlation was found between IL-6 and MDA levels. There was a weak negative correlation between either IL-6 or MDA and the number of gestational weeks. Conclusion : Elevated maternal serum levels of Interleukin-6 and Malondialdehyde in preterm as compared to full-term birth might suggest that inflammation and oxidative stress play a critical role in PTB.

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Analysis of Global Oxidative Status Using Multimarker Scores Reveals a Specific Association Between Renal Dysfunction and Diuretic Therapy in Older Adults

The Journals of Gerontology Series A ◽

10.1093/gerona/glab012 ◽

2021 ◽

Author(s):

Elena Rodríguez-Sánchez ◽

José Alberto Navarro-García ◽

Jennifer Aceves-Ripoll ◽

Laura González-Lafuente ◽

Nerea Corbacho-Alonso ◽

...

Keyword(s):

Oxidative Stress ◽

Older Adults ◽

Renal Function ◽

Oxidative Status ◽

Protein Carbonyls ◽

Multivariate Linear Regression Analysis ◽

Older Population ◽

Sod Activity ◽

Pronounced Increase ◽

Diuretic Treatment

Abstract Aging and chronic kidney disease (CKD) are important interrelated cardiovascular risk (CVR) factors linked to oxidative stress, but this relationship has not been well studied in older adults. We assessed the global oxidative status in an older population with normal to severely impaired renal function. We determined the oxidative status of 93 older adults (mean age 85 years) using multimarker scores. OxyScore was computed as index of systemic oxidative damage by analyzing carbonyl groups, oxidized low-density lipoprotein, 8-hydroxy-2′-deoxyguanosine, and xanthine oxidase activity. AntioxyScore was computed as index of antioxidant defense by analyzing catalase and superoxide dismutase (SOD) activity and total antioxidant capacity. OxyScore and AntioxyScore were higher in subjects with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 than in peers with eGFR >60 mL/min/1.73 m2, with protein carbonyls, catalase, and SOD activity as major drivers. Older adults with a recent cardiovascular event had similar OxyScore and AntioxyScore as peers with eGFR >60 mL/min/1.73 m2. Multivariate linear regression analysis revealed that both indices were associated with decreased eGFR independently of traditional CVR factors. Interestingly, AntioxyScore was also associated with diuretic treatment, and a more pronounced increase was seen in subjects receiving combination therapy. The associations of AntioxyScore with diuretic treatment and eGFR were mutually independent. In conclusion, eGFR is the major contributor to the imbalance in oxidative stress in this older population. Given the association between oxidative stress, CKD, and CVR, the inclusion of renal function parameters in CVR estimators for older populations, such as the SCORE-OP, might improve their modest performance.

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MicroRNAs and Oxidative Stress: An Intriguing Crosstalk to Be Exploited in the Management of Type 2 Diabetes

Antioxidants ◽

10.3390/antiox10050802 ◽

2021 ◽

Vol 10 (5) ◽

pp. 802

Author(s):

Teresa Vezza ◽

Aranzazu M. de Marañón ◽

Francisco Canet ◽

Pedro Díaz-Pozo ◽

Miguel Marti ◽

...

Keyword(s):

Oxidative Stress ◽

Type 2 Diabetes ◽

Signaling Pathways ◽

Current Knowledge ◽

Critical Role ◽

Cell Dysfunction ◽

Non Coding Rnas ◽

And Oxidative Stress ◽

Molecular Crosstalk

Type 2 diabetes is a chronic disease widespread throughout the world, with significant human, social, and economic costs. Its multifactorial etiology leads to persistent hyperglycemia, impaired carbohydrate and fat metabolism, chronic inflammation, and defects in insulin secretion or insulin action, or both. Emerging evidence reveals that oxidative stress has a critical role in the development of type 2 diabetes. Overproduction of reactive oxygen species can promote an imbalance between the production and neutralization of antioxidant defence systems, thus favoring lipid accumulation, cellular stress, and the activation of cytosolic signaling pathways, and inducing β-cell dysfunction, insulin resistance, and tissue inflammation. Over the last few years, microRNAs (miRNAs) have attracted growing attention as important mediators of diverse aspects of oxidative stress. These small endogenous non-coding RNAs of 19–24 nucleotides act as negative regulators of gene expression, including the modulation of redox signaling pathways. The present review aims to provide an overview of the current knowledge concerning the molecular crosstalk that takes place between oxidative stress and microRNAs in the physiopathology of type 2 diabetes, with a special emphasis on its potential as a therapeutic target.

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10-gingerol induces oxidative stress through HTR1A in cumulus cells: in-vitro and in-silico studies

Journal of Complementary and Integrative Medicine ◽

10.1515/jcim-2019-0042 ◽

2020 ◽

Vol 0 (0) ◽

Author(s):

Kiptiyah Kiptiyah ◽

Widodo Widodo ◽

Gatot Ciptadi ◽

Aulanni’am Aulanni’Am ◽

Mohammad A. Widodo ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Culture ◽

Superoxide Dismutase ◽

In Silico ◽

Cumulus Cell ◽

Cumulus Cells ◽

Sod Activity ◽

In Silico Studies ◽

Incubation Periods

AbstractBackgroundWe investigated whether 10-gingerol is able to induce oxidative stress in cumulus cells.MethodsFor the in-vitro research, we used a cumulus cell culture in M199, containing 10-gingerol in various concentrations (0, 12, 16, and 20 µM), and detected oxidative stress through superoxide dismutase (SOD) activity and malondialdehyde (MDA) concentrations, with incubation periods of 24, 48, 72, and 96 h. The obtained results were confirmed by in-silico studies.ResultsThe in-vitro data revealed that SOD activity and MDA concentration increased with increasing incubation periods: SOD activity at 0 µM (1.39 ± 0.24i), 12 µM (16.42 ± 0.35ab), 16 µM (17.28 ± 0.55ab), 20 µM (17.81 ± 0.12a), with a contribution of 71.1%. MDA concentration at 0 µM (17.82 ± 1.39 l), 12 µM (72.99 ± 0.31c), 16 µM (79.77 ± 4.19b), 20 µM (85.07 ± 2.57a), with a contribution of 73.1%. Based on this, the in-silico data uncovered that 10˗gingerol induces oxidative stress in cumulus cells by inhibiting HTR1A functions and inactivating GSK3B and AKT˗1.Conclusions10-gingerol induces oxidative stress in cumulus cells through enhancing SOD activity and MDA concentration by inhibiting HTR1A functions and inactivating GSK3B and AKT˗1.

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