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  • Open Access

    ARTICLE

    Melatonin ameliorates docetaxel-induced mitochondrial oxidative toxicity and cytokine generation in the laryngo-tracheal epithelial cell

    SINEM GÖKÇE KÜTÜK1, MUSTAFA NAZIROĞLU2,3,*

    BIOCELL, Vol.45, No.1, pp. 177-188, 2021, DOI:10.32604/biocell.2021.013531

    Abstract A protective action of melatonin (MELAT) on docetaxel (DCT)-induced inflammation, apoptosis, and reactive free oxygen radical (fROS) generation values via blocking of TRPM2 calcium-permeable channel was investigated in different cells except for laryngo-tracheal epithelial (LT-Epi) cells. Hence, the protective action of MELAT on DCT-induced oxidative toxicity and inflammation in LT-Epi tissue and cells of mice were investigated in the current study. MELAT treatment ameliorated DCTinduced mitochondrial ROS in the LT-Epi cells by reducing the generation of fROS (cytosolic and mitochondrial), lipid peroxidation, and depolarization of the mitochondrial membrane, while increasing reduced glutathione (GSH), GSH peroxidase, and total antioxidant status. In… More >

  • Open Access

    REVIEW

    Nuclear regulation of mitochondrial functions during oocyte development

    TIANQI WANG, WANXI YANG*

    BIOCELL, Vol.44, No.4, pp. 469-478, 2020, DOI:10.32604/biocell.2020.014708

    Abstract Mitochondria are important in eukaryotic cells due to their functions in energy production and regulation over other cellular activities. Oocytes are produced by a long and precisely controlled process, the dysfunction of which leads to impaired female fertility. As oocytes mature, mitochondria are constantly under the regulation of nuclear genes, the process of which can be modulated by extracellular signals. Understanding how nuclear genes regulate mitochondrial functions is important for studying animal reproduction and human fertility. As more and more genes regulating mitochondrial functions in oocytes are being revealed, new approaches for improving female fertility in both human and animals… More >

  • Open Access

    ARTICLE

    YB-1 downregulation attenuates UQCRC1 protein expression level in H9C2 cells and decreases the mitochondrial membrane potential

    HUIFANG CHEN1,2, XIAOYING ZHOU2, ZONGHONG LONG2, XIANGLONG TANG2, HONG LI2,*

    BIOCELL, Vol.44, No.3, pp. 371-379, 2020, DOI:10.32604/biocell.2020.08893

    Abstract UQCRC1 is one of the 10 mitochondrial complex III subunits, this protein has a role in energy metabolism, myocardial protection, and neurological diseases. The upstream mechanism of the UQCRC1 protective effect on cardiomyocytes is currently unavailable. In order to explore the upstream molecules of UQCRC1 and elucidate the protective mechanism of UQCRC1 on cardiomyocytes in more detail, we focused on the nuclease-sensitive elementbinding protein 1 (YB-1). We hypothesized YB-1 acts as an upstream regulatory molecule of UQCRC1. This study found that YB-1 RNAi significantly reduces the expression of the UQCRC1 protein level (p < 0.05) and obviously decreases the mitochondrial… More >

  • Open Access

    ARTICLE

    Mitochondrial DNA mutation “m.3243A>G”—Heterogeneous clinical picture for cardiologists (“m.3243A>G”: A phenotypic chameleon)

    Katharina Niedermayr1, Gerhard Pölzl2, Sabine Scholl‐Bürgi1, Christine Fauth3, Ulrich Schweigmann1, Edda Haberlandt1, Ursula Albrecht1, Manuela Zlamy1, Wolfgang Sperl4, Johannes A. Mayr4, Daniela Karall1

    Congenital Heart Disease, Vol.13, No.5, pp. 671-677, 2018, DOI:10.1111/chd.12634

    Abstract Objective: In general, a mitochondrial disorder is diagnosed on the basis of symptom combinations and confirmed by genetic findings. However, patients carrying the m.3243A>G mutation in the mitochondrial tRNA leucine 1 (MT‐TL1) do not always meet all the proposed criteria for the most frequently encountered mitochondrial syndrome “MELAS,” an acronym for Mitochondrial Encephalomyopathy, Lactic Acidosis, and at least one Stroke‐like episode. We here present various phenotypic characteristics of the mitochondrial mutation m.3243A>G with particular focus on cardiac manifestations.
    Methods and Results: We followed nine patients (1 month to 68 years old; median 42 years; four female and five male) from… More >

  • Open Access

    ARTICLE

    An extract of Hypericum perforatum induces wound healing through inhibitions of Ca2+ mobilizations, mitochondrial oxidative stress and cell death in epithelial cells: Involvement of TRPM2 channels

    Fuat USLUSOY1, Mustafa NAZIROĞLU2,3,*

    BIOCELL, Vol.43, No.4, pp. 271-283, 2019, DOI:10.32604/biocell.2019.08333

    Abstract The wound is induced by several mechanical and metabolic factors. In the etiology of the wound recovery, excessive oxidative stress, calcium ion (Ca2+) influx, and apoptosis have important roles. Ca2+-permeable TRPM2 channel is activated by oxidative stress. Protective roles of Hypericum perforatum extract (HP) on the mechanical nerve injury-induced apoptosis and oxidative toxicity through regulation of TRPM2 in the experimental animals were recently reported. The potential protective roles in HP treatment were evaluated on the TRPM2-mediated cellular oxidative toxicity in the renal epithelium (MPK) cells. The cells were divided into three groups as control, wound, and wound + HP treatment… More >

  • Open Access

    ARTICLE

    Knockdown of apoptosis-inducing factor disrupts function of respiratory complex

    MIROSLAV VAŘECHA1*, DANIELA PÁCLOVÁ2, JIŘINA PROCHÁZKOVÁ2, PAVEL MATULA1, DUŠAN CMARKO3, AND MICHAL KOZUBEK1

    BIOCELL, Vol.36, No.3, pp. 121-126, 2012, DOI:10.32604/biocell.2012.36.121

    Abstract Recent findings suggest that apoptotic protein apoptosis-inducing factor (AIF) may also play an important non-apoptotic function inside mitochondria. AIF was proposed to be an important component of respiratory chain complex I that is the major producer of superoxide radical. The possible role of AIF is still controversial. Superoxide production could be used as a valuable measure of complex I function, because the majority of superoxide is produced there. Therefore, we employed superoxide-specific mitochondrial fluorescence dye for detection of superoxide production. We studied an impact of AIF knockdown on function of mitochondrial complex I by analyzing superoxide production in selected cell… More >

  • Open Access

    ARTICLE

    Mechanisms involved in the cytotoxic effects of berberine on human colon cancer HCT-8 cells

    LI-NA XU1#, BI-NAN LU2#, MING-MING HU1, YOU-WEI XU1, XU HAN1, YAN QI1, JIN-YONG PENG1,3*

    BIOCELL, Vol.36, No.3, pp. 113-120, 2012, DOI:10.32604/biocell.2012.36.113

    Abstract Berberine, a constituent of some traditional Chinese medicinal plants, has been reported to have cytotoxicity effects on different human cancer cell lines. There is no available information about the effects and mechanism of action of berberine on human colon cancer cell line HCT-8. In this paper, the cytotoxicity of berberine on HCT-8 cancer cells was investigated by MTT assay, fluorescence microscopy and flow cytometry analysis. Our data revealed that berberine could significantly inhibit the growth of HCT-8 cells in a dose- and time-dependent manner. Morphology of apoptotic cells was studied with acridine orange/ ethidium bromide staining. The concentrations of lactate… More >

  • Open Access

    REVIEW

    Review: Mitochondrial apoptotic pathways

    NORA MOHAMAD, ALICIA GUTIÉRREZ, MARIEL NÚÑEZ, CLAUDIA COCCA, GABRIELA MARTÍN*, GRACIELA CRICCO, VANINA MEDINA, ELENA RIVERA, ROSA BERGOC*.

    BIOCELL, Vol.29, No.2, pp. 149-161, 2005, DOI:10.32604/biocell.2005.29.149

    Abstract Apoptosis or programmed cell death (PCD) is a physiological process characteristic of pluricellular organisms leading to self-destruction of the cell. It is therefore involved in development, homeostasis and host defense. However, a significant difference has been shown between mammalian cell apoptosis and non-mammalian cell apoptosis: mitochondria are implicated only in the former. Execution of PCD includes the release of several proapoptotic proteins from the intermembrane space of mitochondria. They could exert their actions through a caspase dependent as well as a caspase independent way. On the other hand, regulation of PCD is mainly given by the Bcl-2 family members, which… More >

  • Open Access

    ARTICLE

    Heart mitochondrial dysfunction in diabetic rats

    S.S. Bombicino*, D.E. Iglesias, I.A. Rukavina Mikusic, A. Boveris, L.B. Valdez

    BIOCELL, Vol.40, No.1, pp. 7-10, 2016, DOI:10.32604/biocell.2016.40.007

    Abstract Diabetic cardiomyopathy, i.e. the ventricular dysfunction in the absence of hypertension or coronary arterial disease, is a common complication of diabetes mellitus that leads to a heightened risk of heart failure and death among diabetic patients. This contractile dysfunction could be associated to mitochondrial dysfunction, in which mitochondrial biogenesis could emerge as a compensatory mechanism triggered in response to hyperglycemia. It has been proposed that nitric oxide synthase activities with enhanced NO production are involved in this process. Alterations in the contractile response and lusitropic reserve were observed in streptozotocin diabetic rats after β-adrenergic stimuli. Additionally, tissue O2 consumption was… More >

  • Open Access

    ARTICLE

    Autophagy, apoptosis and organelle features during cell exposure to cadmiumč

    Cristiane Dos Santos VERGILIO, Edésio José Tenório De MELO*

    BIOCELL, Vol.37, No.2, pp. 45-54, 2013, DOI:10.32604/biocell.2013.37.045

    Abstract Cadmium (Cd) induces several effects in different tissues, but our knowledge of the toxic effects on organelles is insufficient. To observe the progression of Cd effects on organelle structure and function, HuH-7 cells (human hepatic carcinoma cell line) were exposed to CdCl2 in increasing concentrations (1 μM – 20 μM) and exposure times (2 h – 24 h). During Cd treatment, the cells exhibited a progressive decrease in viability that was both time- and dose-dependent. Cd treated cells displayed progressive morphological changes that included cytoplasm retraction and nuclear condensation preceding a total loss of cell adhesion. Treatment with 10 μM… More >

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