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The Role of Metallothionein in Oxidative Stress  [PDF]
Branislav Ruttkay-Nedecky,Lukas Nejdl,Jaromir Gumulec,Ondrej Zitka,Michal Masarik,Tomas Eckschlager,Marie Stiborova,Vojtech Adam,Rene Kizek
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms14036044
Abstract: Free radicals are chemical particles containing one or more unpaired electrons, which may be part of the molecule. They cause the molecule to become highly reactive. The free radicals are also known to play a dual role in biological systems, as they can be either beneficial or harmful for living systems. It is clear that there are numerous mechanisms participating on the protection of a cell against free radicals. In this review, our attention is paid to metallothioneins (MTs) as small, cysteine-rich and heavy metal-binding proteins, which participate in an array of protective stress responses. The mechanism of the reaction of metallothioneins with oxidants and electrophilic compounds is discussed. Numerous reports indicate that MT protects cells from exposure to oxidants and electrophiles, which react readily with sulfhydryl groups. Moreover, MT plays a key role in regulation of zinc levels and distribution in the intracellular space. The connections between zinc, MT and cancer are highlighted.
Role of autophagy in liver physiology and pathophysiology  [cached]
Wen-Xing Ding
World Journal of Biological Chemistry , 2010,
Abstract: Autophagy is a highly conserved intracellular degradation pathway by which bulk cytoplasm and superfluous or damaged organelles are enveloped by double membrane structures termed autophagosomes. The autophagosomes then fuse with lysosomes for degradation of their contents, and the resulting amino acids can then recycle back to the cytosol. Autophagy is normally activated in response to nutrient deprivation and other stressors and occurs in all eukaryotes. In addition to maintaining energy and nutrient balance in the liver, it is now clear that autophagy plays a role in liver protein aggregates related diseases, hepatocyte cell death, steatohepatitis, hepatitis virus infection and hepatocellular carcinoma. In this review, I discuss the recent findings of autophagy with a focus on its role in liver pathophysiology.
Separation and Identification of Metallothionein Isoforms and Sub-isoforms by Liquid Chromatography

LU Suge,SHEN Jincan,ZHUANG Zhixia,WANG Xiaoru,

色谱 , 2005,
Abstract: A method has been established for the separation and identification of metallothionein (MT) isoforms and sub-isoforms by liquid chromatography. A mixture of rabbit liver MT was separated on a DEAE A-25 weak anion-exchange chromatographic (AEC) column. Inductively coupled plasma-mass spectrometer (ICP-MS) was used for off-line detection of Zn in each fraction. The two main MT isoforms, MT-1 and MT-2, were isolated. The collected MT isoform fractions were then desalted by a homemade Sephadex G-25 size exclusion chromatographic (SEC) column. Afterwards, the sample was separated on a C_(18) reversed-phase column with UV detection at 210 nm. Different separation conditions were discussed and several sub-isoforms of MT were well separated at pH 2.0. The sub-isoforms were finally characterized by on-line HPLC-ESI-MS. The isoforms and sub-isoforms were well separated on a reversed-phase column under optimized chromatographic conditions and the detection results of ESI-MS were in agreement with the data found in literature. The method developed can be well used for the separation of metallothionein isoforms and sub-isoforms.
Identification of two metallothionein isoforms by molecular cloning of their cDNAs in fresh-water fish, crucian carp (Carassius-cuvieri)
Hongwei Ren,Muto Norio,Itoh Norio,Meimin Yu,Binggeng Ru,Tanaka Keiichi
Chinese Science Bulletin , 2001, DOI: 10.1007/BF03183209
Abstract: Generally, there are two major isoforms of metallothionein (MT) in mammals. In this study two cDNAs of metallothionein, MT-A and MT-B, in a fresh-water fish, crucian carp (Carassius cuvieri), were cloned by the rapid amplification of cDNA ends (RACE). The homology of their reading frame is about 92.3%. The sequence analysis of both cDNAs gave the structures of coding regions corresponding to 60 amino acid residues, and the structures of complete 3′-untranslated regions in which a significant difference in the size of their 3′-untranslated regions (130 bp for MT-A and 280 bp for MT-B) exists. The results of amino acid sequencing of both MT-1 and MT-2 purified by HPLC are identical to those deduced from MT cDNA genes, indicating that MT-1 is from MT-A gene and MT-2 is from MT-B gene respectively. No blocking in the N-terminal of MT-2 isoform was the first case found in vertebrates, most of which were blocked by acetylation. These results suggest that there were differential controls at the transcription level and after translation of these two MT isoforms. And this gives a clue to understand the diversities of their functions.
Molecular functions of metallothionein and its role in hematological malignancies  [cached]
Takahashi Shinichiro
Journal of Hematology & Oncology , 2012, DOI: 10.1186/1756-8722-5-41
Abstract: Metallothionein (MT) was reported to be a potential negative regulator of apoptosis, and various reports have suggested that it may play roles in carcinogenesis and drug resistance, in at least a portion of cancer cells. The author summarizes the current understanding of the molecular functions of MT for tumor cell growth and drug resistance. These activities are regulated through intracellular metal ion modulation and free radical scavenging. Compared with analyses of solid tumors, few studies have analyzed the roles of MT in hematological malignancies. This review mainly describes the functions of MT in hematopoietic cells. Furthermore, through expression analyses of leukemias and lymphomas, the roles of MT in the biology of these diseases are particularly focused upon.
The Role of Hippocampus in the Pathophysiology of Depression  [PDF]
M. ?a?da? Eker,?zlem Donat Eker
Psikiyatride Guncel Yaklasimlar , 2009,
Abstract: Hippocampus, as a part of the limbic cortex, has a variety of functions ranging from mating behavior to memory besides its role in the regulation of emotions. The hippocampus has reciprocal interactions of with other brain regions which act in the pathophysiology of major depressive disorder (MDD). Moreover, since the hippocampus is a scene for the neurogenesis, which can be seen as a response to antidepressant treatment, the hippocampus became a focus of attention in neuroimaging studies of MDD. It has been shown that brain derived neurotrophic factor (BDNF), that is responsible from the neurogenesis, is associated with the response to the antidepressants and antidepressant drugs are ineffective if neurogenesis is hindered.Hippocampal atrophy is expected with the decrease of neurogenesis as a result of the lower BDNF levels with the deleterious effects of glucocorticoids in depression. Recurrent and severe depression seems to cause such a volume reduction though first episode MDD subjects do not differ from healthy individuals in respect to their hippocampal volumes (HCVs) measured by magnetic resonance imaging methods. One may argue regarding these findings that the atrophy in the hippocampus may be observed in the long term and the decrease in BDNF levels may predispose the volume reduction. Although it has been postulated that smaller HCV as a result of genetic and environmental factors and prior to the illness, may cause a vulnerability to MDD, sufficient evidence has not been accumulated yet and the view that HCV loss develops as depression progresses is widely accepted. Findings that serum BDNF (sBDNF) is lower in MDD patients though HCVs of patients do not differ from healthy individuals and the positive correlation of sBDNF with HCV seen only in the patient group support this view. It can be assumed that depressed patients have sensitivity for the fluctuations in BDNF levels. Follow-up studies which consider effects of hipotalamo-pituiter-adrenal axis dysregulation and monoamine systems are needed to further elucidate the role of BDNF in the pathogenesis of MDD. Results of these studies may lead the way for the treatment of resistant or recurrent depressive disorder.
The Pivotal Role of Airway Smooth Muscle in Asthma Pathophysiology  [PDF]
Anna?g Ozier,Benoit Allard,Imane Bara,Pierre-Olivier Girodet,Thomas Trian,Roger Marthan,Patrick Berger
Journal of Allergy , 2011, DOI: 10.1155/2011/742710
Abstract: Asthma is characterized by the association of airway hyperresponsiveness (AHR), inflammation, and remodelling. The aim of the present article is to review the pivotal role of airway smooth muscle (ASM) in the pathophysiology of asthma. ASM is the main effector of AHR. The mechanisms of AHR in asthma may involve a larger release of contractile mediators and/or a lower release of relaxant mediators, an improved ASM cell excitation/contraction coupling, and/or an alteration in the contraction/load coupling. Beyond its contractile function, ASM is also involved in bronchial inflammation and remodelling. Whereas ASM is a target of the inflammatory process, it can also display proinflammatory and immunomodulatory functions, through its synthetic properties and the expression of a wide range of cell surface molecules. ASM remodelling represents a key feature of asthmatic bronchial remodelling. ASM also plays a role in promoting complementary airway structural alterations, in particular by its synthetic function. 1. Introduction The pathophysiology of asthma is characterized by the association of airway hyperresponsiveness (AHR), inflammation, and remodelling [1–3]. AHR is defined by an increased airway narrowing to a wide range of stimuli and is responsible for recurrent episodes of wheezing and breathlessness. Airway smooth muscle (ASM) is considered as the main cell type involved in AHR [4, 5]. Bronchial inflammation in asthma involves the recruitment of various inflammatory cells including eosinophils, mast cells and T lymphocytes [1]. However, the microlocalization of these cell types is different within the asthmatic ASM layer [6], suggesting complex interactions between inflammatory cells and ASM cells. Bronchial remodelling is described as an increased thickening of the bronchial wall due to various structural alterations including epithelial changes [7], subepithelial membrane thickening, enhanced extracellular matrix (ECM) deposition [8], mucous gland and goblet cell hypertrophy and hyperplasia [9], neoangiogenesis [10], and increase in ASM mass [11, 12]. This latter appears to be a key feature of bronchial remodelling since increased ASM mass is associated with a decrease in lung function in asthma [13–15]. The aim of the present article is thus to review the pivotal role of ASM in the pathophysiology of asthma. 2. Role of ASM in Airway Hyperresponsiveness AHR is usually described as either nonspecific or specific AHR (Table 1). Nonspecific AHR is a common feature of asthma, although it is also found in some patients suffering from chronic
Pathophysiology of Graves’ Ophthalmopathy: A Literature Review  [PDF]
Mariela Carolina Santos Carballo, Bianca Paiva Cunha de Sá, Denise Rosso Tenório Wanderley Rocha, Alberto Krayyem Arbex
Open Journal of Endocrine and Metabolic Diseases (OJEMD) , 2017, DOI: 10.4236/ojemd.2017.71008
Abstract: Graves’ ophthalmopathy (GO), an autoimmune condition associated with Graves’ disease (GD), occurs at a prevalence of nearly 40% in patients diagnosed with GD. Ocular involvement is probably due to the presence of autoantibodies in the orbital tissues, regardless of the control state of thyroid hormones in individuals with GD, even during euthyroid or hypothyroid states, which are associated with thyroid hormone treatment. In addition to the immunological role present in the pathophysiology of GO, the genetic component, proteins and cytokines, minerals (e.g., selenium), and environmental factors (e.g., smoking) also contribute to its development and occurrence of clinical manifestations in varying degrees. Until now, the interaction of causal, intermediary, and triggering factors of GO is still unclear, so the purpose of this article is to review literature on the theme.
The Role of Lactic Acid Bacteria in the Pathophysiology and Treatment of Irritable Bowel Syndrome (IBS)  [PDF]
Julia K?nig, Ignacio Rangel, Robert J. Brummer
Food and Nutrition Sciences (FNS) , 2013, DOI: 10.4236/fns.2013.411A005

Irritable bowel syndrome (IBS) is a multifactorial chronic disorder characterized by various abdominal complaints and a worldwide prevalence of 10% - 20%. Although its etiology and pathophysiology are complex and still not completely understood, aberrations along the microbe-gut-brain axis are known to play a central role. IBS is characterized by interrelated alterations in intestinal barrier function, gut microbe composition, immune activation, afferent sensory signaling and brain activity. Pharmaceutical treatment is generally ineffective and, hence, most therapeutic strategies are based on non-drug approaches. A promising option is the administration of probiotics, in which lactic acid bacteria strains are considered specifically beneficial. This review aims to provide a concise, although comprehensive, overview of the role of lactic acid bacteria in the pathophysiology and treatment of IBS.

The role of sigma-1 receptors in the pathophysiology of neuropsychiatric diseases
Masatomo Ishikawa, Kenji Hashimoto
Journal of Receptor, Ligand and Channel Research , 2010, DOI: http://dx.doi.org/10.2147/JRLCR.S8453
Abstract: ole of sigma-1 receptors in the pathophysiology of neuropsychiatric diseases Review (11161) Total Article Views Authors: Masatomo Ishikawa, Kenji Hashimoto Published Date December 2009 Volume 2010:3 Pages 25 - 36 DOI: http://dx.doi.org/10.2147/JRLCR.S8453 Masatomo Ishikawa, Kenji Hashimoto Division of Clinical Neuroscience, Chiba University for Forensic Mental Health, Chiba, Japan Abstract: The endoplasmic reticulum protein sigma-1 receptors, first regarded as opioid receptors and later confused as the phencyclidine (PCP) binding sites of the N-methyl-D-aspartate (NMDA) receptor, are now confirmed to be independent receptors. They are involved in the modulation of various neurotransmitter systems and have a high affinity for diverse classes of psychotropic drugs. Accumulating evidence suggests that the sigma-1 receptors are implicated in higher-ordered brain functions and play important roles in the pathophysiology of neuropsychiatric diseases such as schizophrenia, depression, anxiety disorders, and dementia. Recently, sigma-1 receptors have been shown to function at the molecular level as “receptor chaperones.” This mechanism may unify the explanation of the role of sigma-1 receptors in the pathophysiology of neuropsychiatric diseases. With the development of the positron emission tomography (PET) ligand [11C]SA4503, it has become possible to visualize sigma-1 receptors and estimate the sigma-1 receptor occupancy of drugs in the human brain. This approach may provide additional information on the function of sigma-1 receptors. This article reviews the function of sigma-1 receptors and attempts to reinterpret their role in the pathophysiology of neuropsychiatric diseases based on their new description as “receptor chaperones.”
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