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Micronutrients
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
The diffusion of Cl− ion through the cellular membrane is carried by anion channels, also called chloride channels (ClC or CLC). Chloride channels are proteinaceous pores in biological membranes that allow the passive diffusion of negatively charged ions along their electrochemical gradient. CLCs have roles in the control of electrical excitability, extra- and intracellular ion homeostasis, and transepithelial transport (17). The mutations in their genes conduct to diverse pathologies including neurodegeneration, leukodystrophy, mental retardation, deafness, blindness, myotonia, hyperaldosteronism, renal salt loss, proteinuria, kidney stones, male infertility, and osteopetrosis (17).
PerformLyte—A Prodosomed PL425 PEC Phytoceutical-Enriched Electrolyte Supplement—Supports Nutrient Repletion, Healthy Blood pH, Neuromuscular Synergy, Cellular and Metabolic Homeostasis
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Bernard W. Downs, Manashi Bagchi, Bruce S. Morrison, Jeffrey Galvin, Steve Kushner, Debasis Bagchi
Chloride: In human physiology, chloride ions help in the maintenance of regulating fluid balance, blood volume, electrolyte homeostasis, intracellular and extracellular fluid homeostasis, blood pressure, preservation of electrical neutrality, and pH of body fluids in a human body.125–127 The chloride ion is an important biomarker for a vast range of clinical conditions and, as a routine practice, is analytically determined in the sweat, urine, feces, and blood. Following intake of edible salt from diverse food sources, a human body gets chloride, which is absorbed in the intestine, while the excess amount gets excreted in the urine.125–128 However, excessive chloride levels indicate serious metabolic disorders, including metabolic acidosis or alkalosis, and a disruption in chloride channel expression and function, leading to multiple diseases and disorders in diverse organs.126–128
Neurons
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
A chloride channel of special interest is the cystic fibrosis transmembrane conductance regulator (CFTR) channel that is expressed in the membranes of epithelial cells that line the outer surfaces of organs. Mutations in the gene encoding the CFTR channel protein affects the regulation of epithelial fluid transport in the organs involved, resulting in cystic fibrosis characterized by abnormally thick mucus secretions mainly in the lungs but also in the pancreas, liver, kidneys, and intestine.
Emerging medicines to improve the basic defect in cystic fibrosis
Published in Expert Opinion on Emerging Drugs, 2022
Isabelle Fajac, Isabelle Sermet-Gaudelus
The CFTR protein is expressed at the apical membrane of many epithelial cells with direct relationships between abnormal expression or function, and CF pathology. When open or activated, the CFTR channel allows passive diffusion of chloride and bicarbonate ions down their electrochemical gradient. It has also many other roles such as inhibition of sodium transport through the epithelial sodium channel and regulation of other chloride channels [8]. CFTR mutations lead to a loss of CFTR activity due to either reduced quantity or impaired function of the protein. In the airways, a defective CFTR protein leads to impaired mucociliary clearance, infection and inflammation, bronchiectasis, and respiratory failure. To date, around 2,000 CFTR mutations have been described and around 250 variants have evidence supporting a disease-causing effect [9]. In the last decade, very innovative drugs called CFTR modulators that improve the defective CFTR protein function have been approved for marketing in patients with CF.
The protective effect of tanshinone IIa on endothelial cells: a generalist among clinical therapeutics
Published in Expert Review of Clinical Pharmacology, 2021
Jun Feng, Lina Liu, Fangfang Yao, Daixing Zhou, Yang He, Junshuai Wang
Intracellular chloride channel 1 (CLIC1), a unique chloride ion channel related to macrophage activation is both a sensor and an effector under oxidative stress and plays the primary role in diseases involving oxidative stress, such as tumors and neurodegenerative diseases, by regulating cell adhesion, cell cycle, apoptosis, and promotion of metastasis in tumor progression [79]. STS could induce Cl−secretion by CaCC in a mAChR-dependent manner to modulate ion transport in airway epithelial cells for the hydration of airways [80]. STS-induced dose-dependent relaxation of mouse tracheal rings in an epithelial cell-independent manner. STS also decreased CLIC1 expression, reduced lipid peroxidation, promoted antioxidant defensive systems and inflammatory levels, and resulted in a beneficial effect on anti-atherosclerosis [81]. These studies support the development and application of STS to affect vascular tone in pathological conditions, such as improving coronary blood flow in coronary heart disease.
Advances in genetic testing and optimization of clinical management in children and adults with epilepsy
Published in Expert Review of Neurotherapeutics, 2020
Marcello Scala, Amedeo Bianchi, Francesca Bisulli, Antonietta Coppola, Maurizio Elia, Marina Trivisano, Dario Pruna, Tommaso Pippucci, Laura Canafoglia, Simona Lattanzi, Silvana Franceschetti, Carlo Nobile, Antonio Gambardella, Roberto Michelucci, Federico Zara, Pasquale Striano
In the last two decades, significant advances have been accomplished in molecular genetics. The discovery of new causative genes for several epileptic disorders has remarkably improved the knowledge on the epileptogenesis. In particular, the identification of the genes encoding the subunits of voltage-gated channels (sodium, potassium, and chloride channels) and the subunits of the acetylcholine and GABA receptors have provided fundamental insights into the pathogenic mechanisms underlying several epileptic disorders. Accordingly, the development of new drugs specifically targeting mutated proteins and selectively addressing pathogenic mechanisms has opened new scenarios for personalized therapeutic approaches (precision medicine). As an example, the understanding of the pathophysiology of KCNT1-relatd epilepsies has supported the use of quinidine in these conditions [159]. Vipocentine, an alkaloid potentiating GABA-evoked currents, has been successfully used to treat Lennox-Gastaut syndrome caused by GABRB3 mutation [160]. The new compounds MPX-004 and MPX-007 have been developed to selectively block the NMDA receptors containing the NR2A subunit in patients with gain-of-function mutations in GRIN2A [151]. These improvements have also contributed to enhancing the pharmacogenomics, which represents a valuable tool for clinicians to predict the efficacy and tolerability of a specific drug in the single patient.