Displaying publications 61 - 80 of 257 in total

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  1. Fulltext Effect of vitamin E (Tri E®) on antioxidant enzymes and DNA damage in rats following eight weeks exercise
    Abd Hamid NA, Hasrul MA, Ruzanna RJ, Ibrahim IA, Baruah PS, Mazlan M, et al.
    Nutr J, 2011;10:37.
    PMID: 21513540 DOI: 10.1186/1475-2891-10-37
    Exercise is beneficial to health, but during exercise the body generates reactive oxygen species (ROS) which are known to result in oxidative stress. The present study analysed the effects of vitamin E (Tri E®) on antioxidant enzymes; superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (Cat) activity and DNA damage in rats undergoing eight weeks exercise.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  2. Fulltext Reactive oxygen species-induced impairment of endothelium-dependent relaxations in rat aortic rings: protection by methanolic extracts of Phoebe grandis
    Yeh-Siang L, Subramaniam G, Hadi AH, Murugan D, Mustafa MR
    Molecules, 2011 Apr 06;16(4):2990-3000.
    PMID: 21471938 DOI: 10.3390/molecules16042990
    Generation of reactive oxygen species plays a pivotal role in the development of cardiovascular diseases. The present study describes the effects of the methanolic extract of Phoebe grandis (MPG) stem bark on reactive oxygen species-induced endothelial dysfunction in vitro. Endothelium-dependent (acetylcholine, ACh) and -independent relaxation (sodium nitroprusside, SNP) was investigated from isolated rat aorta of Sprague-Dawley (SD) in the presence of the β-NADH (enzymatic superoxide inducer) and MPG extract. Superoxide anion production in aortic vessels was measured by lucigen chemiluminesence. Thirty minutes incubation of the rat aorta in vitro with β-NADH increased superoxide radical production and significantly inhibited ACh-induced relaxations. Pretreatment with MPG (0.5, 5 and 50 μg/mL) restored the ACh-induced relaxations (R(max): 92.29% ± 2.93, 91.02% ± 4.54 and 88.31 ± 2.36, respectively) in the presence of β-NADH. MPG was ineffective in reversing the impaired ACh-induced relaxations caused by pyrogallol, a non-enzymatic superoxide generator. Superoxide dismutase (a superoxide scavenger), however, reversed the impaired ACh relaxations induced by both β-NADH and pyrogallol. MPG also markedly inhibited the β-NADH-induced generation of the superoxide radicals. Furthermore, MPG scavenging peroxyl radicals generated by tBuOOH (10⁻⁴ M).These results indicate that MPG may improve the endothelium dependent relaxations to ACh through its scavenging activity as well as by inhibiting the NADH/NADPH oxidase induced generation of superoxide anions.
    Matched MeSH terms: Reactive Oxygen Species/metabolism*
  3. Mutations in mitochondrial NADH dehydrogenase subunit 1 (mtND1) gene in colorectal carcinoma
    Yusnita Y, Norsiah MD, Rahman AJ
    Malays J Pathol, 2010 Dec;32(2):103-10.
    PMID: 21329181 MyJurnal
    Mitochondrial Subunit ND1 (mtND1) gene is involved in the first step of the electron transport chain of oxidative phosphorylation (OXPHOS). Alteration of the electron transport components by mutations in mtDNA may compromise the normal electron flow. This could lead to an increase of bifurcation and generation of superoxidase radicals and increase oxidative stress in various types of cancer cells. Genomic DNA was extracted from thirty matched primary colorectal tumour tissues and matching non-tumour tissues. Blood samples were obtained from twenty-five normal people. The mtNDI coding region was amplified by step-down PCR. The purified products were then subjected to direct sequencing and subsequently, the DNA sequences obtained were compared with the revised Cambridge Reference Sequence (rCRS) and MITOMAP. From the analysis, the mtND1 gene showed 11 (45.8%) different mutations and also 13 (54.2%) polymorphisms. The heteroplasmic mutation A4123A/G (I273I/V) might have a pathogenic significance as it fulfills various pathogenic criteria. Three mutations, T3394C (Y30H), A3434G (Y43C) and C3497T (A64V) which occur in a highly conserved region were likely to alter the structure and function of the ND1 protein. We suggest that these mutations, and in combination with the polymorphic variance in mtDNA, may cause slight changes that generate subtly higher levels of toxic reactive oxygen species (ROS).
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  4. Fulltext Piper sarmentosum as an antioxidant on oxidative stress in human umbilical vein endothelial cells induced by hydrogen peroxide
    Hafizah AH, Zaiton Z, Zulkhairi A, Mohd Ilham A, Nor Anita MM, Zaleha AM
    J Zhejiang Univ Sci B, 2010 May;11(5):357-65.
    PMID: 20443214 DOI: 10.1631/jzus.B0900397
    Endothelial cell death due to increased reactive oxygen species (ROS) may contribute to the initial endothelial injury, which promotes atherosclerotic lesion formation. Piper sarmentosum (PS), a natural product, has been shown to have an antioxidant property, which is hypothesized to inhibit production of ROS and prevent cell injury. Thus, the present study was designed to determine the effects of PS on the hydrogen peroxide (H(2)O(2))-induced oxidative cell damage in cultured human umbilical vein endothelial cells (HUVECs). In this experiment, HUVECs were obtained by collagenase perfusion of the large vein in the umbilical cord and cultured in medium M200 supplemented with low serum growth supplementation (LSGS). HUVECs were treated with various concentrations of H(2)O(2) (0-1000 micromol/L) and it was observed that 180 micromol/L H(2)O(2) reduced cell viability by 50% as denoted by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Using the above concentration as the positive control, the H(2)O(2)-induced HUVECs were concomitantly treated with various concentrations (100, 150, 250 and 300 microg/ml) of three different extracts (aqueous, methanol and hexane) of PS. Malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) levels showed a significant increase (P<0.05) in HUVECs compared to the negative control. However, PS extracts showed a protective effect on HUVECs from H(2)O(2)-induced cell apoptosis with a significant reduction in MDA, SOD, CAT and GPX levels (P<0.05). Furthermore, PS had exhibited ferric reducing antioxidant power with its high phenolic content. Hence, it was concluded that PS plays a beneficial role in reducing oxidative stress in H(2)O(2)-induced HUVECs.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  5. Amplifying the manganese scavenging potential of Streptococcus zooepidemicus to reactive oxygen species during production of hyaluronic acid
    Mashitah MD, Masitah H, Ramachandran KB
    Med J Malaysia, 2004 May;59 Suppl B:59-60.
    PMID: 15468818
    Streptococcus zooepidemicus (SZ) is an aerotolerant bacteria and its ability to survive under reactive oxidant challenge raises the question of the existence of a defense system. Thus growth, hyaluronic acid (HA) and hydrogen peroxide (H2O2) production by SZ in the presence of increasing concentration of Mn2+ were studied. The results suggested that the tested strain supported growth and HA production in cultures treated with 1 and 10 mM of Mn2+ regardless of H2O2 presence in the medium. This showed that SZ have acquired elaborate defense mechanisms to scavenge oxygen toxicity and thus protect cells from direct and indirect effect of this radical. In contrast, cells treated with 25 mM Mn2+ were sensitive, in which, the HA production was reduced considerably. Thus showing that the oxygen scavenger systems of the cells may be fully saturated at this concentration.
    Matched MeSH terms: Reactive Oxygen Species/metabolism*
  6. Pulmonary surfactant mitigates silver nanoparticle toxicity in human alveolar type-I-like epithelial cells
    Sweeney S, Leo BF, Chen S, Abraham-Thomas N, Thorley AJ, Gow A, et al.
    Colloids Surf B Biointerfaces, 2016 Sep 01;145:167-75.
    PMID: 27182651 DOI: 10.1016/j.colsurfb.2016.04.040
    Accompanying increased commercial applications and production of silver nanomaterials is an increased probability of human exposure, with inhalation a key route. Nanomaterials that deposit in the pulmonary alveolar region following inhalation will interact firstly with pulmonary surfactant before they interact with the alveolar epithelium. It is therefore critical to understand the effects of human pulmonary surfactant when evaluating the inhalation toxicity of silver nanoparticles. In this study, we evaluated the toxicity of AgNPs on human alveolar type-I-like epithelial (TT1) cells in the absence and presence of Curosurf(®) (a natural pulmonary surfactant substitute), hypothesising that the pulmonary surfactant would act to modify toxicity. We demonstrated that 20nm citrate-capped AgNPs induce toxicity in human alveolar type I-like epithelial cells and, in agreement with our hypothesis, that pulmonary surfactant acts to mitigate this toxicity, possibly through reducing AgNP dissolution into cytotoxic Ag(+) ions. For example, IL-6 and IL-8 release by TT1 cells significantly increased 10.7- and 35-fold, respectively (P<0.01), 24h after treatment with 25μg/ml AgNPs. In contrast, following pre-incubation of AgNPs with Curosurf(®), this effect was almost completely abolished. We further determined that the mechanism of this toxicity is likely associated with Ag(+) ion release and lysosomal disruption, but not with increased reactive oxygen species generation. This study provides a critical understanding of the toxicity of AgNPs in target human alveolar type-I-like epithelial cells and the role of pulmonary surfactant in mitigating this toxicity. The observations reported have important implications for the manufacture and application of AgNPs, in particular for applications involving use of aerosolised AgNPs.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  7. Effect of reduced graphene oxide-hybridized ZnO thin films on the photoinactivation of Staphylococcus aureus and Salmonella enterica serovar Typhi
    Teh SJ, Yeoh SL, Lee KM, Lai CW, Abdul Hamid SB, Thong KL
    J. Photochem. Photobiol. B, Biol., 2016 Aug;161:25-33.
    PMID: 27203568 DOI: 10.1016/j.jphotobiol.2016.05.013
    The immobilization of photocatalyst nanoparticles on a solid substrate is an important aspect for improved post-treatment separation and photocatalyst reactor design. In this study, we report the simple preparation of reduced graphene oxide (rGO)-hybridized zinc oxide (ZnO) thin films using a one-step electrochemical deposition, and investigated the effect of rGO-hybridization on the photoinactivation efficiency of ZnO thin films towards Staphylococcus aureus (S. aureus) and Salmonella enterica serovar Typhi (S. Typhi) as target bacterial pathogens. Field-emission scanning electron microscopy (FESEM) revealed the formation of geometric, hexagonal flakes of ZnO on the ITO glass substrate, as well as the incorporation of rGO with ZnO in the rGO/ZnO thin film. Raman spectroscopy indicated the successful incorporation of rGO with ZnO during the electrodeposition process. Photoluminescence (PL) spectroscopy indicates that rGO hybridization with ZnO increases the amount of oxygen vacancies, evidenced by the shift of visible PL peak at 650 to 500nm. The photoinactivation experiments showed that the thin films were able to reduce the bacterial cell density of Staph. aureus and S. Typhi from an initial concentration of approximately 10(8) to 10(3)CFU/mL within 15min. The rGO/ZnO thin film increased the photoinactivation rate for S. aureus (log[N/No]) from -5.1 (ZnO) to -5.9. In contrast, the application of rGO/ZnO thin film towards the photoinactivation of S. Typhi did not improve its photoinactivation rate, compared to the ZnO thin film. We may summarise that (1) rGO/ZnO was effective to accelerate the photoinactivation of S. aureus but showed no difference to improve the photoinactivation of S. Typhi, in comparison to the performance of ZnO thin films, and (2) the photoinactivation in the presence of ZnO and rGO/ZnO was by ROS damage to the extracellular wall.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  8. Fulltext Modulation of Hydrogen Peroxide-Induced Oxidative Stress in Human Neuronal Cells by Thymoquinone-Rich Fraction and Thymoquinone via Transcriptomic Regulation of Antioxidant and Apoptotic Signaling Genes
    Ismail N, Ismail M, Azmi NH, Abu Bakar MF, Basri H, Abdullah MA
    Oxid Med Cell Longev, 2016;2016:2528935.
    PMID: 26823946 DOI: 10.1155/2016/2528935
    Nigella sativa Linn. (N. sativa) and its bioactive constituent Thymoquinone (TQ) have demonstrated numerous pharmacological attributes. In the present study, the neuroprotective properties of Thymoquinone-rich fraction (TQRF) and TQ against hydrogen peroxide- (H2O2-) induced neurotoxicity in differentiated human SH-SY5Y cells were investigated. TQRF was extracted using supercritical fluid extraction while TQ was acquired commercially, and their effects on H2O2 were evaluated using cell viability assay, reactive oxygen species (ROS) assay, morphological observation, and multiplex gene expression. Both TQRF and TQ protected the cells against H2O2 by preserving the mitochondrial metabolic enzymes, reducing intracellular ROS levels, preserving morphological architecture, and modulating the expression of genes related to antioxidants (SOD1, SOD2, and catalase) and signaling genes (p53, AKT1, ERK1/2, p38 MAPK, JNK, and NF-κβ). In conclusion, the enhanced efficacy of TQRF over TQ was likely due to the synergism of multiple constituents in TQRF. The efficacy of TQRF was better than that of TQ alone when equal concentrations of TQ in TQRF were compared. In addition, TQRF also showed comparable effects to TQ when the same concentrations were tested. These findings provide further support for the use of TQRF as an alternative to combat oxidative stress insults in neurodegenerative diseases.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  9. Fulltext Life-span extension by pigmented rice bran in the model yeast Saccharomyces cerevisiae
    Sunthonkun P, Palajai R, Somboon P, Suan CL, Ungsurangsri M, Soontorngun N
    Sci Rep, 2019 12 02;9(1):18061.
    PMID: 31792269 DOI: 10.1038/s41598-019-54448-9
    Benefits of whole grains as dietary supplements and active ingredients in health products have been promoted. Despite being neglected as an agricultural byproduct of polished rice, pigmented rice bran has emerged as a promising source of natural anti-aging compounds. Indeed, the extract of red rice bran Hom Dang cultivar contained rich phenolic acids and flavonoids. It displayed high antioxidant activities in vitro and in vivo assays. Using yeast model, extract and bioactive compounds, quercetin and protocatechuic acid found in the rice bran pericarp, effectively reduced levels of intracellular reactive oxygen species (ROS), restored plasma membrane damages and prolonged life-span of pre-treated wild-yeast cells. Importantly, these molecules modulated life span-extension through a mechanism of ROS reduction that resembles to that operated under the highly conserved Tor1- and Sir2-dependent signaling pathways, with the human homologs TORC1 and SIRT1, respectively. The key longevity factors Sch9 and Rim15 kinases, Msn2/4 regulators and a novel transcription factor Asg1, the antioxidant enzymes superoxide dismutases and glutathione peroxidases played important role in mediating longevity. Yeast clearly provides an instrumental platform for rapid screening of compounds with anti-aging efficacies and advances knowledge in the molecular study of ageing.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  10. Fulltext Synergetic Influence of Bismuth Oxide Nanoparticles, Cisplatin and Baicalein-Rich Fraction on Reactive Oxygen Species Generation and Radiosensitization Effects for Clinical Radiotherapy Beams
    Talik Sisin NN, Abdul Razak K, Zainal Abidin S, Che Mat NF, Abdullah R, Ab Rashid R, et al.
    Int J Nanomedicine, 2020;15:7805-7823.
    PMID: 33116502 DOI: 10.2147/IJN.S269214
    Purpose: This study aimed to quantify synergetic effects induced by bismuth oxide nanoparticles (BiONPs), cisplatin (Cis) and baicalein-rich fraction (BRF) natural-based agent on the reactive oxygen species (ROS) generation and radiosensitization effects under irradiation of clinical radiotherapy beams of photon, electron and HDR-brachytherapy. The combined therapeutic responses of each compound and clinical radiotherapy beam were evaluated on breast cancer and normal fibroblast cell line.

    Methods: In this study, individual BiONPs, Cis, and BRF, as well as combinations of BiONPs-Cis (BC), BiONPs-BRF (BB) and BiONPs-Cis-BRF (BCB) were treated to the cells before irradiation using HDR brachytherapy with 0.38 MeV iridium-192 source, 6 MV photon beam and 6 MeV electron beam. The individual or synergetic effects from the application of the treatment components during the radiotherapy were elucidated by quantifying the ROS generation and radiosensitization effects on MCF-7 and MDA-MB-231 breast cancer cell lines as well as NIH/3T3 normal cell line.

    Results: The ROS generated in the presence of Cis stimulated the most substantial amount of ROS compared to the BiONPs and BRF. Meanwhile, the combination of the components had induced the higher ROS levels for photon beam than the brachytherapy and electron beam. The highest ROS enhancement relative to the control is attributable to the presence of BC combination in MDA-MB-231 cells, in comparison to the BB and BCB combinations. The radiosensitization effects which were quantified using the sensitization enhancement ratio (SER) indicate the highest value by BC in MCF-7 cells, followed by BCB and BB treatment. The radiosensitization effects are found to be more prominent for brachytherapy in comparison to photon and electron beam.

    Conclusion: The BiONPs, Cis and BRF are the potential radiosensitizers that could improve the efficiency of radiotherapy to eradicate the cancer cells. The combination of these potent radiosensitizers might produce multiple effects when applied in radiotherapy. The BC combination is found to have the highest SER, followed by the BCB combination. This study is also the first to investigate the effect of BRF in combination with BiONPs (BB) and BC (BCB) treatments.

    Matched MeSH terms: Reactive Oxygen Species/metabolism*
  11. Fulltext TRPC3-Nox2 axis mediates nutritional deficiency-induced cardiomyocyte atrophy
    Sudi SB, Tanaka T, Oda S, Nishiyama K, Nishimura A, Sunggip C, et al.
    Sci Rep, 2019 07 05;9(1):9785.
    PMID: 31278358 DOI: 10.1038/s41598-019-46252-2
    Myocardial atrophy, characterized by the decreases in size and contractility of cardiomyocytes, is caused by severe malnutrition and/or mechanical unloading. Extracellular adenosine 5'-triphosphate (ATP), known as a danger signal, is recognized to negatively regulate cell volume. However, it is obscure whether extracellular ATP contributes to cardiomyocyte atrophy. Here, we report that ATP induces atrophy of neonatal rat cardiomyocytes (NRCMs) without cell death through P2Y2 receptors. ATP led to overproduction of reactive oxygen species (ROS) through increased amount of NADPH oxidase (Nox) 2 proteins, due to increased physical interaction between Nox2 and canonical transient receptor potential 3 (TRPC3). This ATP-mediated formation of TRPC3-Nox2 complex was also pathophysiologically involved in nutritional deficiency-induced NRCM atrophy. Strikingly, knockdown of either TRPC3 or Nox2 suppressed nutritional deficiency-induced ATP release, as well as ROS production and NRCM atrophy. Taken together, we propose that TRPC3-Nox2 axis, activated by extracellular ATP, is the key component that mediates nutritional deficiency-induced cardiomyocyte atrophy.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  12. Silver nanoparticles: Advanced and promising technology in diabetic wound therapy
    Choudhury H, Pandey M, Lim YQ, Low CY, Lee CT, Marilyn TCL, et al.
    Mater Sci Eng C Mater Biol Appl, 2020 Jul;112:110925.
    PMID: 32409075 DOI: 10.1016/j.msec.2020.110925
    Wounds associated with diabetes mellitus are the most severe co-morbidities, which could be progressed to cause cell necrosis leading to amputation. Statistics on the recent status of the diabetic wounds revealed that the disease affects 15% of diabetic patients, where 20% of them undergo amputation of their limb. Conventional therapies are found to be ineffective due to changes in the molecular architecture of the injured area, urging novel deliveries for effective treatment. Therefore, recent researches are on the development of new and effective wound care materials. Literature is evident in providing potential tools in topical drug delivery for wound healing under the umbrella of nanotechnology, where nano-scaffolds and nanofibers have shown promising results. The nano-sized particles are also known to promote healing of wounds by facilitating proper movement through the healing phases. To date, focuses have been made on the efficacy of silver nanoparticles (AgNPs) in treating the diabetic wound, where these nanoparticles are known to exploit potential biological properties in producing anti-inflammatory and antibacterial activities. AgNPs are also known to activate cellular mechanisms towards the healing of chronic wounds; however, associated toxicities of AgNPs are of great concern. This review is an attempt to illustrate the use of AgNPs in wound healing to facilitate this delivery system in bringing into clinical applications for a superior dressing and treatment over wounds and ulcers in diabetes patients.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  13. The pyranoxanthone inophyllin A induces oxidative stress mediated-apoptosis in Jurkat T lymphoblastic leukemia cells
    Chan KM, Hamzah R, Rahaman AA, Jong VY, Khong HY, Rajab NF, et al.
    Food Chem Toxicol, 2012 Aug;50(8):2916-22.
    PMID: 22613213 DOI: 10.1016/j.fct.2012.04.048
    Inophyllin A (INO-A), a pyranoxanthone isolated from the roots of Calophyllum inophyllum represents a new xanthone with potential chemotherapeutic activity. In this study, the molecular mechanism of INO-A-induced cell death was investigated in Jurkat T lymphoblastic leukemia cells. Assessment of phosphatidylserine exposure confirmed apoptosis as the primary mode of cell death in INO-A-treated Jurkat cells. INO-A treatment for only 30 min resulted in a significant increase of tail moment which suggests that DNA damage is an early apoptotic signal. Further flow cytometric assessment of the superoxide anion level confirmed that INO-A induced DNA damage was mediated with a concomitant generation of reactive oxygen species (ROS). Investigation on the thiols revealed an early decrease of free thiols in 30 min after 50 μM INO-A treatment. Using tetramethylrhodamine ethyl ester, a potentiometric dye, the loss of mitochondrial membrane potential (MPP) was observed in INO-A-treated cells as early as 30 min. The INO-A-induced apoptosis progressed with the simultaneous activation of caspases-2 and -9 which then led to the processing of caspase-3. Taken together, these data demonstrate that INO-A induced early oxidative stress, DNA damage and loss of MMP which subsequently led to the activation of an intrinsic pathway of apoptosis in Jurkat cells.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  14. Fulltext Dengue Virus-Induced Reactive Oxygen Species Production in Rat Microglial Cells
    Suwanprinya L, Morales NP, Sanvarinda P, Dieng H, Okabayashi T, Morales Vargas RE
    Jpn J Infect Dis, 2017 07 24;70(4):383-387.
    PMID: 28003593 DOI: 10.7883/yoken.JJID.2016.236
    Encephalitis has been described worldwide as a severe complication in patients infected by dengue virus. Reactive oxygen species (ROS) production is a key mechanism involved in the neuronal damage caused by viral encephalitis. In the present study, the capability of dengue virus serotypes 2 (DENV2) and DENV4 to induce ROS production was investigated in a rat microglial cell line, HAPI cells. The cells were infected with DENV2 and DENV4 at a multiplicity of infection of 0.1 for a 2-h adsorption period. Japanese encephalitis virus (JEV) was used as the reference. DENV2- and DENV4-induced microglial activation and significantly increased ROS production corresponded to decreased cell viability. The activity of DENV4 was significantly higher than the activities of DENV2 and JEV at 48 and 72 h post infection. DENV4 partly induced ROS production via an iron-induced Fenton reaction, as demonstrated by the treatment with an iron chelator, deferiprone. Despite the induction of increased inducible nitric oxide synthase expression and nitric oxide (NO) production by JEV, DENV2, and DENV4 did not induce NO production, suggesting the activation of different pathways in response to infections by different viruses. In conclusion, DENV2 and DENV4 have the capability to induce ROS production and activate microglia, which have been reported as the key components of neuronal damage.
    Matched MeSH terms: Reactive Oxygen Species/metabolism*
  15. Triphenyltin(IV) benzoates with diazenyl/imino scaffold exhibiting remarkable apoptosis mediated by reactive oxygen species
    Basu Baul TS, Dutta D, Duthie A, Prasad R, Rana NK, Koch B, et al.
    J Inorg Biochem, 2017 08;173:79-92.
    PMID: 28505480 DOI: 10.1016/j.jinorgbio.2017.04.020
    The cytotoxic potency of a series of triphenyltin(IV) compounds of general composition [Ph3Sn(Ln)] (1-6) has been probed in vitro employing MDA-MB-231 (human breast cancer) and HeLa (human cervical cancer) cell lines, where Ln=L1-3; isomeric 2/3/4-{(E)-2-[4-(dimethylamino)phenyl]diazenyl}benzoates and L4-6are their corresponding isoelectronic imino analogues 2/3/4-[(E)-{[4-(dimethylamino)phenyl]methylidene}amino]benzoates. Compounds 1-6 have been characterized by elemental analysis and their spectroscopic properties were studied using IR and NMR (1H,13C,119Sn) techniques. The molecular structures of a pro-ligand 2-[(E)-{[4-(dimethylamino)phenyl]methylidene}amino]benzoic acid (HL4) and two representative molecules, Ph3Sn(L2) 2 and Ph3Sn(L5) 5, have been determined by X-ray crystallography. Structural analyses of 2 and 5 revealed distorted tetrahedral geometries within C3O donor sets owing to monodentate modes of coordination of the respective carboxylate ligands, close intramolecular Sn…O(carbonyl) interactions notwithstanding. Cytotoxic studies in vitro in MDA-MB-231 and HeLa cell lines revealed high activity, in sub-micromolar range, for all investigated compounds. Among these, 1 and 3 exhibited potent cytotoxicity most effectively towards MDA-MB-231 cells with a IC50value of 1.19 and 1.44μM, respectively, whereas 5 showed remarkable activity towards HeLa cells with a IC50value of 0.88μM, yet the series of compounds had minimal cytotoxic effect on normal HEK 293 (human embryonic kidney) cell line. The underlying investigation suggested that the compounds exert potent antitumor effect by elevating intracellular reactive oxygen species generation and cause delay in cell cycle by inhibiting cells at G2/M phase. The results presented herein suggest further development of this class of triphenyltin(IV) compounds-based drugs as potential anti-cancer therapies should be pursued.
    Matched MeSH terms: Reactive Oxygen Species/metabolism*
  16. Rutin loaded liquid crystalline nanoparticles inhibit lipopolysaccharide induced oxidative stress and apoptosis in bronchial epithelial cells in vitro
    Paudel KR, Wadhwa R, Mehta M, Chellappan DK, Hansbro PM, Dua K
    Toxicol In Vitro, 2020 Oct;68:104961.
    PMID: 32771431 DOI: 10.1016/j.tiv.2020.104961
    Airway inflammation and infections are the primary causes of damage in the airway epithelium, that lead to hypersecretion of mucus and airway hyper-responsiveness. The role of reactive oxygen species (ROS) and their components in the pathophysiological mechanisms of airway inflammation have been well-studied and emphasized for the past several decades. Rutin, a potent bioflavonoid, is well-known for its antioxidant, anti-inflammatory, especially in bronchial inflammation. However, poor solubility and rapid metabolism have led to its low bioavailability in biological systems, and hence limit its application. The present study aims to investigate the beneficial effects of rutin-loaded liquid crystalline nanoparticles (LCNs) against lipopolysaccharide (LPS) induced oxidative damage in human bronchial epithelial cell line (BEAS-2-B) cells in vitro. LPS was used to stimulate BEAS-2-B cells, causing the generation of nitric oxide (NO) and other reactive oxygen species (ROS) that had led to cellular apoptosis. The levels of NO and ROS were detected by, Griess reagent kit and dichlorodihydrofluorescein diacetate (DCFH-DA) respectively, whereas, cell apoptosis was studied by Annexin V-FITC and PI staining. The findings revealed that rutin-loaded LCNs significantly reduced NO, ROS levels and prevented apoptosis in BEAS-2B cells. The observations and findings provide a mechanistic understanding of the effectiveness of rutin-loaded LCNs in protecting the bronchial cells against airway inflammation, thus possessing a promising therapeutic option for the management of airway diseases.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  17. Thymoquinone induces apoptosis and increase ROS in ovarian cancer cell line
    Taha MM, Sheikh BY, Salim LZ, Mohan S, Khan A, Kamalidehghan B, et al.
    Cell Mol Biol (Noisy-le-grand), 2016 May 30;62(6):97-101.
    PMID: 27262811
    Nigella sativa is also known for its properties as a traditional herbal healing for many ailments. In this study, the anticancer properties of thyomquinone (TQ), the active ingredient of N. sativa, were studied using ovarian cancer cell line (Caov-3 cells). The anti-proliferative activity of TQ was determined using MTT and the apoptosis was investigated using Flowcytometry and Annexin-V Assays. Multiparameteric cytotoxicity bioassays were used to quantify the changes in cell permeability and mitochondrial membrane potential. Reactive oxygen species (ROS) and apoptosis-involved cell markers were examined to verify cell death mechanism. The MTT-assay showed that TQ induces anti-proliferative activity on Caov-3 with an IC50 of 6.0±0.03 μg/mL, without any cytotoxic activity towards WRL-68 normal hepatocytes. A significant induction of early phase of apoptosis was shown by annexin-V analysis. Treatment of Caov-3 cells with TQ induces decreases in plasma membrane permeability and mitochondrial membrane potential. Visible decrease in the nuclear area was also observed. A significant decrease is observed in Bcl-2 while Bax is down-regulated. TQ-triggered ROS-mediated has found to be associated with Hsp70 dysregulation, an indicator of oxidative injury. We found that TQ induced anti-cancer effect involves intrinsic pathway of apoptosis and cellular oxidative stress. Our results considered collectively indicated that thyomquinone may be a potential agent for ovarian cancer drug development.
    Matched MeSH terms: Reactive Oxygen Species/metabolism*
  18. Phenylpropanoids isolated from Piper sarmentosum Roxb. induce apoptosis in breast cancer cells through reactive oxygen species and mitochondrial-dependent pathways
    Hematpoor A, Paydar M, Liew SY, Sivasothy Y, Mohebali N, Looi CY, et al.
    Chem Biol Interact, 2018 Jan 05;279:210-218.
    PMID: 29174417 DOI: 10.1016/j.cbi.2017.11.014
    The aim of the present study is to isolate bioactive compounds from the roots of Piper sarmentosum and examine the mechanism of action using human breast cancer cell line (MDA-MB-231). Bioassay guided-fractionation of methanolic extract led to the isolation of asaricin (1) and isoasarone (2). Asaricin (1) and isoasarone (2) had significant cytotoxicity towards MDA-MB-231. MCF-10A (human normal breast epithelial cells) cells are less sensitive than MDA-MB-231, but they respond to the treatment with the same unit of measurement. Both compounds increase reactive oxygen species (ROS), decrease mitochondrial membrane potential (MMP) and enhance cytochrome c release in treated MDA-MB-231 cells. Isoasarone (2) markedly elevated caspase -8 and -3/7 activities and caused a decline in nuclear NF-κB translocation, suggesting extrinsic, death receptor-linked apoptosis pathway. Quantitative PCR results of MDA-MB-231 treated with asaricin (1) and isoasarone (2) showed altered expression of Bcl-2: Bax level. The inhibitory potency of these isolates may support the therapeutic uses of these compounds in breast cancer.
    Matched MeSH terms: Reactive Oxygen Species/metabolism*
  19. Chemical evaluation and cytotoxic mechanism investigation of Clinacanthus nutans extract in lymphoma SUP-T1 cells
    Lu MC, Li TY, Hsieh YC, Hsieh PC, Chu YL
    Environ Toxicol, 2018 Dec;33(12):1229-1236.
    PMID: 30188005 DOI: 10.1002/tox.22629
    Clinacanthus nutans has been used as herbal medicine with antidiabetic, blood pressure lowering, and diuretic properties in Singapore, Thailand, and Malaysia. The in vitro cellular study showed the chloroform extract possessed significant cytotoxicity against leukemia K562 and lymphoma Raji cells. The clinical study reported that administration of plant could treat or prevent relapse in 12 cancer patients. However, detailed mechanism of the anticancer effects and chemical profiles are not thoroughly studied. The chemical study did show that the acetone extract (MHA) exerted the highest antiproliferative effect on human leukemia MOLT-4 cells and lymphoma SUP-T1 cells in dose-dependent cytotoxicity. We found that the use of MHA increased apoptosis by 4.28%-43.65% and caused disruption of mitochondrial membrane potential (MMP) by 11.79%-26.93%, increased reactive oxygen species (ROS) by 19.54% and increased calcium ion by 233.83%, as demonstrated by annexin-V/PI, JC-1, H2 DCFDA, and Flou-3 staining assays, respectively. MHA-induced ER stress was confirmed by increase expression of CHOP and IRE-1α with western blotting assay. In conclusion, we identified good bioactivity in Clinacanthus nutans and recognize its potential effect on cancer therapy, but further research is needed to determine the use of the plant.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
  20. Peroxiredoxin of Arthrospira platensis derived short molecule YT12 influences antioxidant and anticancer activity
    Sannasimuthu A, Ramani M, Pasupuleti M, Saraswathi NT, Arasu MV, Al-Dhabi NA, et al.
    Cell Biol Int, 2020 Nov;44(11):2231-2242.
    PMID: 32716104 DOI: 10.1002/cbin.11431
    This study demonstrates both the antioxidant and anticancer potential of the novel short molecule YT12 derived from peroxiredoxin (Prx) of spirulina, Arthrospira platensis (Ap). ApPrx showed significant reduction in reactive oxygen species (ROS) against hydrogen peroxide (H2 O2 ) stress. The complementary DNA sequence of ApPrx contained 706 nucleotides and its coding region possessed 546 nucleotides between position 115 and 660. Real-time quantitative reverse transcription polymerase chain reaction analysis confirmed the messenger RNA expression of ApPrx due to H2 O2 exposure in spirulina cells at regular intervals, in which the highest expression was noticed on Day 20. Cytotoxicity assay was performed using human peripheral blood mononuclear cells, and revealed that at 10 μM, the YT12 did not exhibit any notable toxicity. Furthermore, ROS scavenging activity of YT12 was performed using DCF-DA assay, in which YT12 scavenged a significant amount of ROS at 25 μM in H2 O2 -treated blood leukocytes. The intracellular ROS in human colon adenocarcinoma cells (HT-29) was regulated by oxidative stress, where the YT12 scavenges ROS in HT-29 cells at 12.5 μM. Findings show that YT12 peptide has anticancer activity, when treated against HT-29 cells. Through the MTT assay, YT12 showed vital cytotoxicity against HT-29 cells. These finding suggested that YT12 is a potent antioxidant molecule which defends ROS against oxidative stress and plays a role in redox balance.
    Matched MeSH terms: Reactive Oxygen Species/metabolism
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