Polyhydroxyfullerene Binds Cadmium Ions and Alleviates Metal-Induced Oxidative Stress in Saccharomyces cerevisiae

ABSTRACTThe water-soluble polyhydroxyfullerene (PHF) is a functionalized carbon nanomaterial with several industrial and commercial applications. There have been controversial reports on the toxicity and/or antioxidant properties of fullerenes and their derivatives. Conversely, metals have been recognized as toxic mainly due to their ability to induce oxidative stress in living organisms. We investigated the interactive effects of PHF and cadmium ions (Cd) on the model yeastSaccharomyces cerevisiaeby exposing cells to Cd (≤5 mg liter−1) in the absence or presence of PHF (≤500 mg liter−1) at different pHs (5.8 to 6.8). In the absence of Cd, PHF stimulated yeast growth up to 10.4%. Cd inhibited growth up to 79.7%, induced intracellular accumulation of reactive oxygen species (ROS), and promoted plasma membrane disruption in a dose- and pH-dependent manner. The negative effects of Cd on growth were attenuated by the presence of PHF, and maximum growth recovery (53.8%) was obtained at the highest PHF concentration and pH. The coexposure to Cd and PHF decreased ROS accumulation up to 36.7% and membrane disruption up to 30.7% in a dose- and pH-dependent manner. Two mechanisms helped to explain the role of PHF in alleviating Cd toxicity to yeasts: PHF decreased Cd-induced oxidative stress and bound significant amounts of Cd in the extracellular medium, reducing its bioavailability to the cells.

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Isolation, Characterization and Neuroprotective Activity of Folecitin: An In Vivo Study

Life ◽

10.3390/life11080825 ◽

2021 ◽

Vol 11 (8) ◽

pp. 825

Author(s):

Umar Farooq ◽

Taous Khan ◽

Shahid Ali Shah ◽

Md. Sanower Hossain ◽

Yousaf Ali ◽

...

Keyword(s):

Oxidative Stress ◽

Body Weight ◽

Nlrp3 Inflammasome ◽

Interleukin 1 ◽

Antioxidant Properties ◽

Neuroprotective Activity ◽

Bioactive Metabolites ◽

Inflammasome Activation ◽

Dependent Manner ◽

Rat Pups

Neurodegenerative diseases (NDs) extend the global health burden. Consumption of alcohol as well as maternal exposure to ethanol can damage several neuronal functions and cause cognition and behavioral abnormalities. Ethanol induces oxidative stress that is linked to the development of NDs. Treatment options for NDs are yet scarce, and natural product-based treatments could facilitate ND management since plants possess plenty of bioactive metabolites, including flavonoids, which typically demonstrate antioxidant and anti-inflammatory properties. Hypericum oblongifolium is an important traditional medicinal plant used for hepatitis, gastric ulcer, external wounds, and other gastrointestinal disorders. However, it also possesses multiple bioactive compounds and antioxidant properties, but the evaluation of isolated pure compounds for neuroprotective efficacy has not been done yet. Therefore, in the current study, we aim to isolate and characterize the bioactive flavonoid folecitin and evaluate its neuroprotective activity against ethanol-induced oxidative-stress-mediated neurodegeneration in the hippocampus of postnatal day 7 (PND-7) rat pups. A single dose of ethanol (5 g/kg body weight) was intraperitoneally administered after the birth of rat pups on PND-7. This caused oxidative stress accompanied by the activation of phosphorylated-c-Jun N-terminal kinase (p-JNK), nod-like receptor family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein (ASC), and cysteine-aspartic acid protease-1 (caspase-1) proteins to form a complex called the NLRP3-inflammasome, which converts pro-interleukin 1 beta (IL-1B) to activate IL-1B and induce widespread neuroinflammation and neurodegeneration. In contrast, co-administration of folecitin (30 mg/kg body weight) reduced ethanol-induced oxidative stress, inhibited p-JNK, and deactivated the NLRP3-inflammasome complex. Furthermore, folecitin administration reduced neuroinflammatory and neurodegenerative protein markers, including decreased caspase-3, BCL-2-associated X protein (BAX), B cell CLL/lymphoma 2 (BCL-2), and poly (ADP-ribose) polymerase-1 (PARP-1) expression in the immature rat brain. These findings conclude that folecitin is a flavone compound, and it might be a novel, natural and safe agent to curb oxidative stress and its downstream harmful effects, including inflammasome activation, neuroinflammation, and neurodegeneration. Further evaluation in a dose-dependent manner would be worth it in order to find a suitable dose regimen for NDs.

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Ginsenoside Rg1 Protects Cardiomyocytes Against Hypoxia/Reoxygenation Injury via Activation of Nrf2/HO-1 Signaling and Inhibition of JNK

Cellular Physiology and Biochemistry ◽

10.1159/000484578 ◽

2017 ◽

Vol 44 (1) ◽

pp. 21-37 ◽

Cited By ~ 39

Author(s):

Qianhui Li ◽

Yin Xiang ◽

Yu Chen ◽

Yong Tang ◽

Yachen Zhang

Keyword(s):

Oxidative Stress ◽

Antioxidant Properties ◽

Heme Oxygenase 1 ◽

Related Factor ◽

Dependent Manner ◽

Ginsenoside Rg1 ◽

H9c2 Cells ◽

Stress Injury ◽

Mitochondrial Membrane Depolarization ◽

Hypoxia Reoxygenation

Background/Aims: Excessive reactive oxygen species (ROS) disturb the physiology of H9c2 cells, which is regarded as a major cause of H9c2 cardiomyocyte apoptosis. Ginsenoside Rg1 is the main active extract of ginseng, which has important antioxidant properties in various cell models. This project investigated the role of ginsenoside Rg1 in hypoxia/reoxygenation (H/R)-induced oxidative stress injury in cultured H9c2 cells to reveal the underlying signaling pathways. Methods: H9c2 cells were pretreated with ginsenoside Rg1 for 12 h before exposure to H/R. In the absence or presence of Nrf2siRNA, HO-1 inhibitor (ZnPP-IX), and inhibitors of the MAPK pathway (SB203580, PD98059, SP600125), H9c2 cells were subjected to H/R with Rg1 treatment. The effects and mechanisms of H/R-induced cardiomyocyte injury were measured. Results: Ginsenoside Rg1 treatment suppressed H/R-induced apoptosis and caspase-3 activation. Ginsenoside Rg1 treatment decreased ROS production and mitochondrial membrane depolarization by elevating the intracellular antioxidant capacity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and reduced glutathione (GSH). Furthermore, ginsenoside Rg1 stimulation appeared to result in nuclear translocation of NF-E2-related factor 2 (Nrf2), along with enhanced expression of the downstream target gene heme oxygenase-1 (HO-1) in a dose-dependent manner. However, ginsenoside Rg1-mediated cardioprotection was abolished by Nrf2-siRNA and HO-1 inhibitor. H/R treatment increased the levels of phosphorylated c-Jun N-terminal kinases (p-JNK), which was dramatically attenuated by ginsenoside Rg1 and SP600125 (a specific JNK inhibitor). Conclusion: These observations indicate that ginsenoside Rg1 activates the Nrf2/HO-1 axis and inhibits the JNK pathway in H9c2 cells to protect against oxidative stress.

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Antioxidant Properties of Fullerene Derivatives Depend on Their Chemical Structure: A Study of Two Fullerene Derivatives on HELFs

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/4398695 ◽

2019 ◽

Vol 2019 ◽

pp. 1-13 ◽

Cited By ~ 8

Author(s):

Vasilina Sergeeva ◽

Olga Kraevaya ◽

Elizaveta Ershova ◽

Larisa Kameneva ◽

Elena Malinovskaya ◽

...

Keyword(s):

Oxidative Stress ◽

Chemical Structure ◽

Antioxidant Properties ◽

Water Soluble ◽

Lung Fibroblasts ◽

Human Embryonic Lung ◽

Fullerene Derivatives ◽

The Past ◽

Wide Range ◽

Short Times

Oxidative stress is a major issue in a wide number of pathologies (neurodegenerative, cardiovascular, immune diseases, and cancer). Because of this, the search for new antioxidants is an important issue. One of the potential antioxidants that has been enthusiastically discussed in the past twenty years is fullerene and its derivatives. Although in aqueous solutions fullerene derivatives have shown to be antioxidants, their properties in this regard within the cells are controversially discussed. We have studied two different water-soluble fullerene C60 and C70 derivatives on human embryonic lung fibroblasts at a wide range of concentrations. Both of them cause a decrease in cellular ROS at short times of incubation (1 hour). Their prolonged action, however, is fundamentally different: derivative GI-761 causes secondary oxidative stress whereas derivative VI-419-P3K keeps ROS levels under control values. To gain a better understanding of this effect, we assessed factors that could play a role in the response of cells to fullerene derivatives. Increased ROS production occurred due to NOX4 upregulation by GI-761. Derivative VI-419-P3K activated the transcription of antioxidant master regulator NRF2 and caused its translocation to the nucleus. This data suggests that the antioxidant effect of fullerene derivatives depends on their chemical structure.

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Safranal Treatment Improves Hyperglycemia, Hyperlipidemia and Oxidative Stress in Streptozotocin-Induced Diabetic Rats

Journal of Pharmacy & Pharmaceutical Sciences ◽

10.18433/j3zs3q ◽

2013 ◽

Vol 16 (2) ◽

pp. 352 ◽

Cited By ~ 49

Author(s):

Saeed Samarghandian ◽

Abasalt Borji ◽

Mohammad Bagher Delkhosh ◽

Fariborz Samini

Keyword(s):

Oxidative Stress ◽

Blood Glucose ◽

Antioxidant Properties ◽

Diabetic Rats ◽

Dependent Manner ◽

Protective Effects ◽

Total Lipids ◽

Sod Activity ◽

Chemically Induced ◽

Antioxidant Defense Systems

Purpose. Clinical research has confirmed the efficacy of several plant extracts in the modulation of oxidative stress associated with diabetes mellitus. Findings indicate that safranal has antioxidant properties. The aim of the present study was the evaluation of possible protective effects of safranal against oxidative damage in diabetic rats. Methods. In this study, the rats were divided into the following groups of 8 animals each: control, untreated diabetic, three safranal (0.25, 0.50, 0.75 mg/kg/day)-treated diabetic groups. Diabetes was induced by streptozotocin (STZ) in rats. STZ was injected intraperitoneally at a single dose of 60 mg/kg for diabetes induction. Safranal (intraperitoneal injection) was administered 3 days after STZ administration; these injections were continued to the end of the study (4 weeks). At the end of the 4-week period, blood was drawn for biochemical assays. In order to determine the changes of cellular antioxidant defense systems, antioxidant enzymes including glutathione peroxidase (GSHPx), superoxide dismutase (SOD) and catalase (CAT) activities were measured in serum. Moreover we also measured serum nitric oxide (NO) and serum malondialdehyde (MDA) levels, a marker of lipid peroxidation. Results. STZ-induced diabetes caused an elevation (p < 0.001) of blood glucose, MDA, NO, total lipids, triglycerides and cholesterol, with reduction of GSH level and CAT and SOD activities. The results indicated that the significant elevation in the blood glucose, MDA, NO, total lipids, triglycerides, cholesterol and reduction of glutathione level and CAT and SOD activity were ameliorated in the safranal–treated diabetic groups compared with the untreated groups, in a dose dependent manner (p < 0.05, p<0.01, p < 0.001). Conclusion. These results suggest that safranal has antioxidant properties and improves chemically-induced diabetes and its complications by modulation of oxidative stress. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

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Carvedilol Attenuates the Progression of Hepatic Fibrosis Induced by Bile Duct Ligation

BioMed Research International ◽

10.1155/2017/4612769 ◽

2017 ◽

Vol 2017 ◽

pp. 1-10 ◽

Cited By ~ 8

Author(s):

Xiaopeng Tian ◽

Chunhong Zhao ◽

Jinbo Guo ◽

Shurui Xie ◽

Fengrong Yin ◽

...

Keyword(s):

Oxidative Stress ◽

Bile Duct ◽

Hepatic Fibrosis ◽

Transforming Growth Factor ◽

Bile Duct Ligation ◽

Antioxidant Properties ◽

Dependent Manner ◽

Sod Activity ◽

Duct Ligation ◽

Clinical Benefits

Background.The sympathetic nervous system (SNS) is responsible for hepatic stellate cells (HSCs) activation and the accumulation of collagen that occurs in hepatic fibrogenesis. Carvedilol has been widely used for the complication of hepatic cirrhosis in the clinic. Furthermore, it has powerful antioxidant properties. We assessed the potential antifibrotic effects of carvedilol and the underlying mechanisms that may further enhance its clinical benefits.Methods.Using a bile duct ligation rat model of hepatic fibrosis, we studied the effects of carvedilol on the fibrosis, collagen deposition, and oxidative stress based on histology, immunohistochemistry, western blot, and RT-PCR analyses.Results.Carvedilol attenuated liver fibrosis, as evidenced by reduced hydroxyproline content and the accumulation of collagen, downregulated TIMP-1 and TIMP-2, and upregulated MMP-13. MMP-2 was an exception, which was decreased after carvedilol treatment for 2 weeks and upregulated after carvedilol treatment for 4 weeks. Carvedilol reduced the activation of HSCs, decreased the induction of collagen, transforming growth factor-β1, and MDA content, and strengthened the SOD activity. The antifibrotic effects were augmented as dosages increased.Conclusions.The study indicates that carvedilol attenuated hepatic fibrosis in a dose-dependent manner. It can decrease collagen accumulation and HSCs activation by the amelioration of oxidative stress.

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Oxidative Stress Reducing Osteogenesis Reversed by Curcumin via NF-κB Signaling and Had a Role in Anti-Osteoporosis

10.21203/rs.3.rs-362019/v1 ◽

2021 ◽

Author(s):

Xu JiaQiang ◽

Ran Gao ◽

Wen Liang ◽

ChangJian Wu ◽

FangLing Li ◽

...

Keyword(s):

Oxidative Stress ◽

Signaling Pathway ◽

Cell Model ◽

Antioxidant Properties ◽

Calcium Content ◽

Dependent Manner ◽

Osteoporosis Prevention ◽

High Concentration ◽

Mineral Density

Abstract Objective: Curcumin has good anti-inflammatory and antioxidant properties, and whether it can resist osteoporosis through oxidative stress pathway in a dose-dependent manner.Method: we used an oxidative stress cell model by culture cells with hydrogen peroxide (H2O2), cells were osteogenic differentiation after treated with H2O2，different concentration curcumin were added during differentiation, then measured the early and late osteogenic index, and detected the potential signaling pathway involved. In addition, we employed rat OVX model treated with curcumin to confirm the protection of the anti-oxidant.Result: Low concentrations of curcumin (1-10μM) promoted the proliferation of MC3T3-E1 cells, improved alkaline phosphatase (ALP) activity, elevated calcium content against oxidative stress induced by H2O2, but high concentration (20 μM) failed, moreover, curcumin diminished supernatant receptor activator of nuclear factor kappa-B ligand (RANKL) and IL-6 expression, inhibited the intracellular ROS triggered by H2O2, Notably, curcumin exerted protection by blocking the NF-κB signaling pathway. The curcumin administered for 12 weeks partially reversed the raito of blood malondialdehyde (MDA) and glutathione (GSH) activity in ovariectomized (OVX) rat in vivo. It also increased the bone mineral density (BMD) and improved the micro-architecture of trabecular bones. Conclusion: curcumin exerted protection on osteoporosis, the effect linked to a reduction of oxidative stress and bone resorbing cytokine, This study suggests that curcumin might be a candidate for osteoporosis prevention and the low concentration exerted obviously protection.

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Allicin Attenuated Advanced Oxidation Protein Product-Induced Oxidative Stress and Mitochondrial Apoptosis in Human Nucleus Pulposus Cells

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/6685043 ◽

2020 ◽

Vol 2020 ◽

pp. 1-17

Author(s):

Qian Xiang ◽

Zhangrong Cheng ◽

Juntan Wang ◽

Xiaobo Feng ◽

Wenbin Hua ◽

...

Keyword(s):

Oxidative Stress ◽

Nucleus Pulposus ◽

Mapk Pathway ◽

Antioxidant Properties ◽

Advanced Oxidation ◽

Dependent Manner ◽

Lipid Peroxidation Product ◽

Nucleus Pulposus Cells ◽

Promising Therapeutic Approach ◽

Induced Apoptosis

Intervertebral disc degeneration (IDD) is one of the most common chronic degenerative musculoskeletal disorders. Oxidative stress-induced apoptosis of the nucleus pulposus (NP) cells plays a key role during IDD progression. Advanced oxidation protein products (AOPP), novel biomarkers of oxidative stress, have been reported to function in various diseases due to their potential for disrupting the redox balance. The current study is aimed at investigating the function of AOPP in the oxidative stress-induced apoptosis of human NP cells and the alleviative effects of allicin during this process which was known for its antioxidant properties. AOPP were demonstrated to hamper the viability and proliferation of NP cells in a time- and concentration-dependent manner and cause cell apoptosis markedly. High levels of reactive oxygen species (ROS) and lipid peroxidation product malondialdehyde (MDA) were detected in NP cells after AOPP stimulation, which resulted in depolarized mitochondrial transmembrane potential (MTP). Correspondingly, higher levels of AOPP were discovered in the human degenerative intervertebral discs (IVD). It was also found that allicin could protect NP cells against AOPP-mediated oxidative stress and mitochondrial dysfunction via suppressing the p38-MAPK pathway. These results disclosed a significant role of AOPP in the oxidative stress-induced apoptosis of NP cells, which could be involved in the primary pathogenesis of IDD. It was also revealed that allicin could be a promising therapeutic approach against AOPP-mediated oxidative stress during IDD progression.

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Bimodal Behavior of Ascorbic Acid in Musca domestica Larvae

Biointerface Research in Applied Chemistry ◽

10.33263/briac124.51995216 ◽

2021 ◽

Vol 12 (4) ◽

pp. 5199-5216

Keyword(s):

Oxidative Stress ◽

Ascorbic Acid ◽

Musca Domestica ◽

Food Supplement ◽

Water Soluble ◽

Dependent Manner ◽

Concentration Dependent Manner ◽

Dietary Antioxidant ◽

High Concentrations ◽

Normal Food

Ascorbic acid (Vitamin C) is an excellent water-soluble dietary antioxidant, well known to protect the biomolecules from oxidative stress-linked damages. It is reported to show a contrary behavior by inflicting pro-oxidant effects under varied, altered circumstances. The present work is an attempt to study the antioxidant and pro-oxidant behavior of ascorbic acid in Musca domestica larvae. Its pro-oxidant properties were tested by exposing the larvae to various concentrations of ascorbic acid. For confirming its oxidant scavenging properties, its effects on the antioxidant enzyme profiles were studied in both the normal and stress-induced M. domestica larvae. Oxidative stress was induced by adding D-Galactose (D-Gal) to the normal food supplement of the larvae. Outcomes of the study demonstrate that ascorbic acid acts as an efficient antioxidant when added in lower concentrations, but at high concentrations, it induces oxidative stress in the larvae, thus acting as a pro-oxidant. At the concentration of 10 mM, ascorbic acid significantly reduced the oxidative stress induced by D-Gal (p < 0.05) and maintained the percent pupal survival and percent eclosion. In conclusion, we suggest that ascorbic acid may function as an antioxidant and pro-oxidant in a concentration-dependent manner under normal physiological conditions.

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Ketogenic diet decreases oxidative stress and improves mitochondrial respiratory complex activity

Journal of Cerebral Blood Flow & Metabolism ◽

10.1177/0271678x15610584 ◽

2016 ◽

Vol 36 (9) ◽

pp. 1603-1613 ◽

Cited By ~ 52

Author(s):

Tiffany Greco ◽

Thomas C Glenn ◽

David A Hovda ◽

Mayumi L Prins

Keyword(s):

Oxidative Stress ◽

Mitochondrial Dysfunction ◽

Ketogenic Diet ◽

Cerebral Metabolism ◽

Antioxidant Properties ◽

Male Rats ◽

Dependent Manner ◽

Complex Activity ◽

Post Injury ◽

Beneficial Effects

Cerebral metabolism of ketones after traumatic brain injury (TBI) improves neuropathology and behavior in an age-dependent manner. Neuroprotection is attributed to improved cellular energetics, although other properties contribute to the beneficial effects. Oxidative stress is responsible for mitochondrial dysfunction after TBI. Ketones decrease oxidative stress, increase antioxidants and scavenge free radicals. It is hypothesized that ketogenic diet (KD) will decrease post-TBI oxidative stress and improve mitochondria. Postnatal day 35 (PND35) male rats were given sham or controlled cortical impact (CCI) injury and placed on standard (STD) or KD. Ipsilateral cortex homogenates and mitochondria were assayed for markers of oxidative stress, antioxidant expression and mitochondrial function. Oxidative stress was significantly increased at 6 and 24 h post-injury and attenuated by KD while inducing protein expression of antioxidants, NAD(P)H dehydrogenase quinone 1 (NQO1) and superoxide dismutase (SOD1/2). Complex I activity was inhibited in STD and KD groups at 6 h and normalized by 24 h. KD significantly improved Complex II–III activity that was reduced in STD at 6 h. Activity remained reduced at 24 h in STD and unchanged in KD animals. These results strongly suggest that ketones improve post-TBI cerebral metabolism by providing alternative substrates and through antioxidant properties, preventing oxidative stress-mediated mitochondrial dysfunction.

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Pro-oxidant activity of zuclopenthixol in vivo: differential effect of the drug on brain oxidative status of scopolamine-treated rats

Human & Experimental Toxicology ◽

10.1191/0960327104ht470oa ◽

2004 ◽

Vol 23 (9) ◽

pp. 439-445 ◽

Cited By ~ 9

Author(s):

Amani E Khalifa

Keyword(s):

Oxidative Stress ◽

Combined Treatment ◽

Antioxidant Properties ◽

Oxidative Status ◽

Interactive Effects ◽

Acute Administration ◽

Treatment Conditions ◽

Brain Oxidative Stress ◽

Oxidant Effect

Several clinical studies implicated oxidative stress in the pathophysiology of both psychosis and dementia. As dementia is commonly associated with psychosis, antipsychotic medications are of importance in the pharmacotherapy of dementia particularly as a number of antipsychotics were reported to demonstrate neuronal pro-oxidant and/or antioxidant properties. Impairment of learning and memory, as the most characteristic manifestation of dementia, could be induced in experimental animals by acute administration of scopolamine (SCO) with a resultant elevation in brain oxidative status. This study investigated the potential pro-oxidant and/or antioxidant activity of the antipsychotic drug zuclopenthixol acetate, as its effect on brain oxidative status has yet to be evaluated. A 2×3 between-subjects factorial design was used to investigate the simultaneous and interactive effects of zuclopenthixol (0.7 and 1.4 mg/kg i.p.) and SCO on rat brain malondialdehyde, glutathione, glutathione peroxidase and superoxide dismutase levels/activities. Results revealed a significant pro-oxidant effect for both zuclopenthixol and SCO alone conditions. In addition, combined treatment of zuclopenthixol and SCO was found to be significantly different compared to either treatment conditions with regard to their effect on different brain oxidative stress indices. Such findings may have valuable implications in the pharmacotherapy of both psychosis and dementia.

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