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Intracellular acidosis

Feng Cai, Feng Wang, Xin Hong, Xin-Hui Xie, Rui Shi, Zhi-Yang Xie, Xiao-Tao Wu
OBJECTIVES: Activation of acid-sensing ion channel 1a (ASIC1a) is responsible for tissue injury caused by acidosis in nervous systems. But its physiological and pathological roles in nucleus pulposus cells (NPCs) are unclear. The aim of this study is to investigate whether ASIC1a regulates the survival of NPCs in the acidic environment of degenerated discs. MATERIALS AND METHODS: NPCs were isolated and cultured followed by immunofluorescent staining and Western-blot analysis for ASIC1a...
August 2016: Iranian Journal of Basic Medical Sciences
X Gao, M Oba
The objective of this study was to examine whether lactating dairy cows with a greater or lower risk of subacute ruminal acidosis (SARA) have differences in volatile fatty acid (VFA) absorption rate, expression of genes involved in VFA metabolism and intracellular pH regulation in rumen epithelial cells, and in situ carbohydrate digestibility in the rumen. We fed 14 ruminally cannulated mid-lactating dairy cows (119 ± 47.2 d in milk; body weight 640 ± 47.9 kg) a high-grain diet consisting of 30% forage ad libitum, with an 18-d diet adaptation and a 7-d sample and data collection period...
September 13, 2016: Journal of Dairy Science
Lorissa Lamoureux, Jeejabai Radhakrishnan, Thomas G Mason, Jeffrey A Kraut, Raul J Gazmuri
Major myocardial abnormalities occur during cardiac resuscitation including intracellular acidosis - partly caused by CO2 accumulation - and activation of the Na(+)-H(+) exchanger isoform-1 (NHE-1). We hypothesized that a favorable interaction may result from NHE-1 inhibition during cardiac resuscitation followed by administration of a CO2-consuming buffer upon return of spontaneous circulation (ROSC). Ventricular fibrillation was electrically induced in 24 male rats and left untreated for 8 minutes followed by defibrillation after 8 minutes of CPR...
September 15, 2016: Journal of Applied Physiology
A Kollmann-Camaiora, E Alsina, A Domínguez, B Del Blanco, M J Yepes, J L Guerrero, A García
Malignant hyperthermia is a hypermetabolic syndrome that appears in susceptible patients after exposure to certain anaesthetic drugs (succinylcholine, inhalation anaesthetics). Its incidence in Spain is 1 in 40,000 adults, with a 10% mortality rate. It is induced by an abnormal regulation of the ryanodine receptors, producing a massive release of calcium from the sarcoplasmic reticulum in the striate muscle. Clinical manifestations include: CO2 increase, tachycardia, haemodynamic instability, metabolic and respiratory acidosis, profuse sweating, hyperpyrexia, CPK increase, myoglobinuria, kidney failure, disseminated intravascular coagulation (DIC), and ending in cardiac arrest...
September 12, 2016: Revista Española de Anestesiología y Reanimación
Takamasa Ishii, Yumi Takanashi, Koichi Sugita, Masaki Miyazawa, Rintaro Yanagihara, Kayo Yasuda, Hiromi Onouchi, Noboru Kawabe, Munehiro Nakata, Yorihiro Yamamoto, Phil S Hartman, Naoaki Ishii
The etiology of astrocyte dysfunction is not well understood even though neuronal defects have been extensively studied in a variety of neuronal degenerative diseases. Astrocyte defects could be triggered by the oxidative stress that occurs during physiological aging. Here, we provide evidence that intracellular or mitochondrial reactive oxygen species (ROS) at physiological levels can cause hippocampal (neuronal) dysfunctions. Specifically, we demonstrate that astrocyte defects occur in the hippocampal area of middle-aged Tet-mev-1 mice with the SDHC(V69E) mutation...
September 13, 2016: Aging Cell
Caroline de Andrade Kratz, Vitor de Salles Painelli, Kleiner Márcio de Andrade Nemezio, Rafael Pires da Silva, Emerson Franchini, Alessandro Moura Zagatto, Bruno Gualano, Guilherme Giannini Artioli
OBJECTIVES: In official judo competitions, athletes usually engage in 5-7 matches in the same day, performing numerous high-intensity efforts interspersed by short recovery intervals. Thus, glycolytic demand in judo is high and acidosis may limit performance. Carnosine is a relevant intracellular acid buffer whose content is increased with beta-alanine supplementation. Thus, we hypothesized that beta-alanine supplementation could attenuate acidosis and improve judo performance. DESIGN: Twenty-three highly-trained judo athletes were randomly assigned to receive either beta-alanine (6...
August 26, 2016: Journal of Science and Medicine in Sport
Kamel S Kamel, Martin Schreiber, Ana P C P Carlotti, Mitchell L Halperin
Diabetic ketoacidosis (DKA), a common cause of severe metabolic acidosis, remains a life-threatening condition due to complications of both the disease and its treatment. This Acid-Base and Electrolyte Teaching Case discusses DKA management, emphasizing complications of treatment. Because cerebral edema is the most common cause of mortality and morbidity, especially in children with DKA, we emphasize its pathophysiology and implications for therapy. The risk for cerebral edema may be minimized by avoiding a bolus of insulin, excessive saline resuscitation, and a decrease in effective plasma osmolality early in treatment...
September 3, 2016: American Journal of Kidney Diseases: the Official Journal of the National Kidney Foundation
Shing-Hong Lin, Martin Steinhoff, Akihiko Ikoma, Yen-Ching Chang, Yuan-Ren Cheng, Ravi Chandra Kopparaju, Satoshi Ishii, Wei-Hsin Sun, Chih-Cheng Chen
Itch and pain are closely related but are distinct sensations. Intradermal injection of acid generates pain in both rodents and humans; however, few studies have addressed the intriguing question of whether acid (protons) can evoke itch like other algogens by spatial contrast activation of single nociceptors. Here, we report that (i) citric acid (0.2 mol/L) pH-dependently induced a scratching response in mice when applied intradermally to nape or cheek skin, (ii) acidified buffer elevated intracellular calcium levels in dorsal root ganglion pruriceptors, and (iii) injection of intradermal citric acid (pH 3...
August 24, 2016: Journal of Investigative Dermatology
Carlos Sanhueza, Joaquín Araos, Luciano Naranjo, Eric Barros, Mario Subiabre, Fernando Toledo, Jaime Gutiérrez, Delia I Chiarello, Fabián Pardo, Andrea Leiva, Luis Sobrevia
Nitric oxide plays several roles in cellular physiology, including control of the vascular tone and defence against pathogen infection. Neuronal, inducible and endothelial nitric oxide synthase (NOS) isoforms synthesize nitric oxide. Cells generate acid and base equivalents, whose physiological intracellular concentrations are kept due to membrane transport systems, including Na(+) /H(+) exchangers and Na(+) /HCO3 (-) transporters, thus maintaining a physiological pH at the intracellular (~7.0) and extracellular (~7...
July 29, 2016: Journal of Cellular and Molecular Medicine
David J Collier, Chris B Wolff, Anne-Marie Hedges, John Nathan, Rod J Flower, James S Milledge, Erik R Swenson
Acetazolamide is the standard carbonic anhydrase (CA) inhibitor used for acute mountain sickness (AMS), however some of its undesirable effects are related to intracellular penetrance into many tissues, including across the blood-brain barrier. Benzolamide is a much more hydrophilic inhibitor, which nonetheless retains a strong renal action to engender a metabolic acidosis and ventilatory stimulus that improves oxygenation at high altitude and reduces AMS. We tested the effectiveness of benzolamide versus placebo in a first field study of the drug as prophylaxis for AMS during an ascent to the Everest Base Camp (5340 m)...
June 2016: Pharmacology Research & Perspectives
Ming-Hua Li, Tian-Dong Leng, Xue-Chao Feng, Tao Yang, Roger P Simon, Zhi-Gang Xiong
An important contributor to brain ischemia is known to be extracellular acidosis, which activates acid-sensing ion channels (ASICs), a family of proton-gated sodium channels. Lines of evidence suggest that targeting ASICs may lead to novel therapeutic strategies for stroke. Investigations of the role of ASICs in ischemic brain injury have naturally focused on the role of extracellular pH in ASIC activation. By contrast, intracellular pH (pHi) has received little attention. This is a significant gap in our understanding because the ASIC response to extracellular pH is modulated by pHi, and activation of ASICs by extracellular protons is paradoxically enhanced by intracellular alkalosis...
August 26, 2016: Journal of Biological Chemistry
Jian Zhang, Xiaoling Li, Herman Kwansa, Yun Tai Kim, Liye Yi, Gina Hong, Shaida A Andrabi, Valina L Dawson, Ted M Dawson, Raymond C Koehler, Zeng-Jin Yang
Tissue acidosis is a key component of cerebral ischemic injury, but its influence on cell death signaling pathways is not well defined. One such pathway is parthanatos, in which oxidative damage to DNA results in activation of poly(ADP-ribose) polymerase and generation of poly(ADP-ribose) polymers that trigger release of mitochondrial apoptosis-inducing factor. In primary neuronal cultures, we first investigated whether acidosis per sé is capable of augmenting parthanatos signaling initiated pharmacologically with the DNA alkylating agent, N-methyl-N'-nitro-N-nitrosoguanidine...
July 5, 2016: Journal of Cerebral Blood Flow and Metabolism
Ahlam I Salameh, Christian A Hübner, Walter F Boron
The anion exchanger AE3, expressed in hippocampal (HC) neurons but not astrocytes, contributes to intracellular pH (pHi ) regulation by facilitating the exchange of extracellular Cl(-) for intracellular HCO3 (-) . The human AE3 polymorphism A867D is associated with idiopathic generalized epilepsy. Moreover, AE3 knockout (AE3(-/-) ) mice are more susceptible to epileptic seizure. The mechanism of these effects has been unclear because the starting pHi in AE3(-/-) and wild-type neurons is indistinguishable. The purpose of the present study was to use AE3(-/-) mice to investigate the role of AE3 in pHi homeostasis in HC neurons, co-cultured with astrocytes...
June 29, 2016: Journal of Physiology
Evan J Myers, Lu Yuan, Melanie A Felmlee, Yuan-Yuan Lin, Yan Jiang, Yu Pei, Ou Wang, Mei Li, Xiao-Ping Xing, Aniko Marshall, Wei-Bo Xia, Mark D Parker
KEY POINTS: The inheritance of two defective alleles of SLC4A4, the gene that encodes the widely-expressed electrogenic sodium bicarbonate cotransporter NBCe1, results in the bicarbonate-wasting disease proximal renal tubular acidosis (pRTA). In the present study, we report the first case of compound-heterozygous inheritance of pRTA (p.Arg510His/p.Gln913Arg) in an individual with low blood pH, blindness and neurological signs that resemble transient ischaemic attacks. We employ fluorescence microscopy on non-polarized (human embryonic kidney) and polarized (Madin-Darby canine kidney) renal cell lines and electrophysiology on Xenopus oocytes to characterize the mutant transporters (R510H and Q913R)...
June 24, 2016: Journal of Physiology
Jeffrey A Kraut, Nicolaos E Madias
Mortality rates associated with severe lactic acidosis (blood pH<7.2) due to sepsis or low-flow states are high. Eliminating the triggering conditions remains the most effective therapy. Although recommended by some, administration of sodium bicarbonate does not improve cardiovascular function or reduce mortality. This failure has been attributed to both reduction in serum calcium concentration and generation of excess carbon dioxide with intracellular acidification. In animal studies, hyperventilation and infusion of calcium during sodium bicarbonate administration improves cardiovascular function, suggesting that this approach could allow expression of the positive aspects of sodium bicarbonate...
September 2016: American Journal of Kidney Diseases: the Official Journal of the National Kidney Foundation
M D Carretta, A I Hidalgo, J Burgos, L Opazo, L Castro, M A Hidalgo, C D Figueroa, A Taubert, C Hermosilla, R A Burgos
Increased short-chain fatty acid (SCFA) production is associated with subacute ruminal acidosis (SARA) and activation of inflammatory processes. In humans and rodents, SCFAs modulate inflammatory responses in the gut via free fatty acid receptor 2 (FFA2). In bovines, butyric acid is one of the most potent FFA2 agonists. Its expression in bovine neutrophils has recently been demonstrated, suggesting a role in innate immune response in cattle. This study aimed to evaluate if butyric acid modulates oxidative and non-oxidative functions or if it can potentiate other inflammatory mediators in bovine neutrophils...
August 2016: Veterinary Immunology and Immunopathology
Jinxiang Zheng, Feng Zhou, Terry Su, Lei Huang, Yeda Wu, Kun Yin, Qiuping Wu, Shuangbo Tang, Jonathan C Makielski, Jianding Cheng
Increasing evidence observed in clinical phenotypes show that abrupt breathing disorders during sleep may play an important role in the pathogenesis of sudden unexplained nocturnal death syndrome (SUNDS). The reported Brugada syndrome causing mutation R1512W in cardiac sodium channel α subunit encoded gene SCN5A, without obvious loss of function of cardiac sodium channel in previous in vitro study, was identified as the first genetic cause of Chinese SUNDS by us. The R1512W carrier was a 38-year-old male SUNDS victim who died suddenly after tachypnea in nocturnal sleep without any structural heart disease...
June 2016: Medicine (Baltimore)
Alejandro Orlowski, Verónica C De Giusti, María C Ciancio, María S Espejo, Ernesto A Aiello
The sodium/bicarbonate cotransporter (NBC) transports extracellular Na(+) and HCO3(-) into the cytoplasm upon intracellular acidosis, restoring the acidic pHi to near neutral values. Two different NBC isoforms have been described in the heart, the electroneutral NBCn1 (1Na(+):1HCO3(-)) and the electrogenic NBCe1 (1Na(+):2HCO3(-)). Certain non-genomic effects of aldosterone (Ald) were due to an orphan G protein-couple receptor 30 (GPR30). We have recently demonstrated that Ald activates GPR30 in adult rat ventricular myocytes, which transactivates the epidermal growth factor receptor (EGFR) and in turn triggers a reactive oxygen species (ROS)- and PI3K/AKT-dependent pathway, leading to the stimulation of NBC...
June 1, 2016: Channels
Özlem Ünal, R Köksal Özgül, Didem Yücel, Dilek Yalnızoğlu, Ayşegül Tokatlı, H Serap Sivri, Burcu Hişmi, Turgay Coşkun, Ali Dursun
Association of 3-methylglutaconic aciduria with impaired oxidative phosphorylation, deafness, encephalopathy, leigh-like lesions on brain imaging, progressive spasticity and dystonia defined as a distinct entity under the name of MEGDEL syndrome. It is an autosomal recessive disorder due to mutation in the serine active site-containing protein 1 (SERAC1). SERAC1 is localized at the interface between the mitochondria and the endoplasmic reticulum in the mitochondria-associated membrane fraction that is essential for phospholipid exchange...
July 2015: Turkish Journal of Pediatrics
Ryan B Shartau, Dane A Crossley, Zachary F Kohl, Colin J Brauner
The nests of embryonic turtles naturally experience elevated CO2 (hypercarbia), which leads to increased blood PCO2  and a respiratory acidosis, resulting in reduced blood pH [extracellular pH (pHe)]. Some fishes preferentially regulate tissue pH [intracellular pH (pHi)] against changes in pHe; this has been proposed to be associated with exceptional CO2 tolerance and has never been identified in amniotes. As embryonic turtles may be CO2 tolerant based on nesting strategy, we hypothesized that they preferentially regulate pHi, conferring tolerance to severe acute acid-base challenges...
July 1, 2016: Journal of Experimental Biology
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