ascorbic-acid and Acidosis

Topics: Acidosis; Animals; Ascorbic Acid; Blood Glucose; Brain; Dogs; Drug Therapy, Combination; Embryonic and Fetal Development; Female; Fetal Blood; Fetal Growth Retardation; Fetal Hypoxia; Glucose; Humans; Insulin; Insulin Secretion; Maltose; Maternal-Fetal Exchange; Oxygen Inhalation Therapy; Placenta; Placental Lactogen; Pregnancy; Sheep; Thiamine Pyrophosphate

Topics: Acid-Base Equilibrium; Acidosis; Alkalosis; Ascorbic Acid; Cell Division; Cell Membrane; Cystine; Cytosol; Electron Transport; Galactose; Glucose; Glutathione; Homeostasis; Humans; Hypoxia; Lactates; Lysosomes; Mitochondria; NAD; Neoplasms; Oxidation-Reduction; Oxygen Consumption; Proteins; Pyruvates; Sulfhydryl Compounds

Topics: Acidosis; Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Deoxyribonucleases; Glycogen; Guinea Pigs; Hydrogen-Ion Concentration; Iron; Lysosomes; Male; Membranes; Mitochondria; Muscles; Oxidation-Reduction; Testis

The aim of this work was to determine whether placental endoplasmic reticulum (ER) stress may contribute to the pathophysiology of gestational diabetes mellitus (GDM) and to test the efficacy of chemical chaperones and antioxidant vitamins in ameliorating that stress in a trophoblast-like cell line in vitro.. Placental samples were obtained from women suffering from GDM and from normoglycaemic controls and were frozen immediately. Women with GDM had 2 h serum glucose levels > 9.0 mmol/l following a 75 g oral glucose tolerance test and were treated with diet and insulin when necessary. Western blotting was used to assess markers of ER stress. To test the effects of hyperglycaemia on the generation of ER stress, a new trophoblast-like cell line, BeWo-NG, was generated by culturing in a physiological glucose concentration of 5.5 mmol/l (over 20 passages) before challenging with 10 or 20 mmol/l glucose.. All GDM patients were well-controlled (HbA1c 5.86 ± 0.55% or 40.64 ± 5.85 mmol/mol, n = 11). Low-grade ER stress was observed in the placental samples, with dilation of ER cisternae and increased phosphorylation of eukaryotic initiation factor 2 subunit α. Challenge of BeWo-NG with high glucose activated the same pathways, but this was as a result of acidosis of the culture medium rather than the glucose concentration per se. Addition of chemical chaperones 4-phenylbutyrate and tauroursodeoxycholic acid and vitamins C and E ameliorated the ER stress.. This is the first report of placental ER stress in GDM patients. Chemical chaperones and antioxidant vitamins represent potential therapeutic interventions for GDM.

Topics: Acidosis; Adult; Antioxidants; Ascorbic Acid; Blood Glucose; Blotting, Western; Cell Line; Diabetes, Gestational; Endoplasmic Reticulum Stress; Eukaryotic Initiation Factor-2; Female; Glucose; Humans; Phenylbutyrates; Phosphorylation; Placenta; Pregnancy; Taurochenodeoxycholic Acid; Unfolded Protein Response; Vitamin E

To describe a case of severe accidental cyanide poisoning following a single ingestion of amygdalin with therapeutic intent.. A 68-year-old patient with cancer presented to the emergency department shortly after her first dose (3 g) of amygdalin with a reduced Glasgow Coma Score, seizures, and severe lactic acidosis requiring intubation and ventilation. The patient also ingested 4800 mg of vitamin C per day. She responded rapidly to hydroxocobalamin treatment. The adverse drug reaction was rated probable on the Naranjo probability scale.. Amygdalin and laetrile (a synthetic form of amygdalin) are commonly used as complementary or alternative medicine (CAM) for the treatment of cancer. Vitamin C is known to increase the in vitro conversion of amygdalin to cyanide and reduce body stores of cysteine, which is used to detoxify cyanide. Amygdalin has been used for decades by patients with cancer who are seeking alternative therapies, and severe reactions have not been reported with this dose. An interaction with vitamin C is a plausible explanation for this life-threatening response.. This case highlights the fact that CAMs can produce life-threatening toxicity. This case also adds a further note of caution, namely, the potential for serious interactions between CAMs, particularly where there is no tradition of concomitant use.

Topics: Acidosis; Aged; Amygdalin; Antineoplastic Agents, Phytogenic; Antioxidants; Ascorbic Acid; Complementary Therapies; Cyanides; Drug Interactions; Female; Glasgow Coma Scale; Hematinics; Humans; Hydroxocobalamin; Seizures

The objective was to determine the long-term clinical outcome and the effects of treatment of patients with glutathione synthetase (GS) deficiency (n = 28).. The diagnosis was based on demonstration of a marked decrease in GS activity in erythrocytes or cultured fibroblasts in all patients and was supported by finding a decrease in erythrocyte or fibroblast glutathione, presence of 5-oxoprolinuria, or both. The treatment varied but usually included correction of acidosis and supplementation with vitamins C and/or E.. Sixteen patients were severely affected with neurologic symptoms such as seizures and psychomotor retardation; 7 had died at the time of the study. None of the severely affected patients had been treated with both vitamins C and E from the neonatal period. No significant difference was found in GS activity between patients with or without neurologic symptoms or in erythrocyte or fibroblast glutathione levels. Five patients had recurrent bacterial infections.. On the basis of clinical symptoms, patients with GS deficiency can be classified into 3 phenotypes: mild, moderate, and severe. Our results indicate that early supplementation with vitamins C and E may improve the long-term clinical outcome.

Topics: Acidosis; Adult; Anemia, Hemolytic; Ascorbic Acid; Child; Child, Preschool; Erythrocytes; Female; Fibroblasts; Genes, Recessive; Glutathione Synthase; Humans; Infant; Infant, Newborn; Male; Mutation; Nervous System Diseases; Psychomotor Disorders; Time Factors; Vitamin E

Oxidative stress in brain tissue was measured experimentally in situ using microdialysis to sample the extracellular environment for a lipid peroxidation breakdown product and antioxidants. The extracellular concentrations of the lipid peroxidation product malonaldehyde (MDA) and the antioxidants ascorbic acid (AA) and uric acid (UA) were measured in rat cortex and striatum in vivo using microdialysis coupled to HPLC with UV detection. Tissue acidosis following ischaemia and epileptic seizures may contribute to neuronal damage, which may be mediated by reactive oxygen species. Perfusion of microdialysis probes with acidic artificial cerebrospinal fluid (pH 6) led to a significant increase in the sampled concentration of MDA and the antioxidant ascorbic acid. Simultaneous perfusion of ascorbate (5 mM) with acidic ACSF (pH 6) completely attenuated the rise in lipid peroxidation. This study provides in vivo evidence for acidosis induced oxidative stress in brain tissue and an antioxidant action of ascorbate. The methodology described here can provide direct in vivo information in respect of oxidative stress in experimental situations. The method could equally be applied to the assessment of oxidative stress in a number of pathological models not necessarily confined to the CNS.

Topics: Acidosis; Animals; Antioxidants; Ascorbic Acid; Brain; Chromatography, High Pressure Liquid; Lipid Peroxidation; Male; Malondialdehyde; Microdialysis; Oxidative Stress; Rats; Rats, Inbred Strains; Spectrophotometry, Ultraviolet; Uric Acid

Cortical homogenates were prepared from rat brain in Krebs-Ringer phosphate media adjusted to pH 7, 6 or 5 and incubated for 1 hr under aerotic or anaerobic conditions in the presence of dipyridyl, an iron chelator. Low molecular weight species (LMWS) iron was measured spectrophotometrically after passing of the homogenates through a 10,000-Mr ultrafiltration membrane. Following aerobic incubation, LMWS iron reached 1.24 micrograms/g tissue at pH 7, and increased 1.7-fold at pH 6 and 3.1-fold at pH 5. Anoxia enhanced significantly the amount of ultrafiltrable iron at the three pH values, the LMWS iron level being increased by 190% at pH 7, by 113% at pH 6, and by 77% at pH 5. Addition of the ultrafiltrates to brain membranes caused significant rises in the production of lipid peroxides assessed by the thiobarbituric acid test, indicating that LMWS iron was in a form capable for catalysing oxygen-derived free radical-mediated lipid peroxidation. It was concluded that decompartmentalization of intracellular iron may be an important factor in the initiation of peroxidative damage to ischemic cells.

Topics: 2,2'-Dipyridyl; Acidosis; Animals; Ascorbic Acid; Brain Chemistry; Ferrous Compounds; Hydrogen-Ion Concentration; Hypoxia, Brain; Iron; Lipid Peroxidation; Lipid Peroxides; Male; Oxygen; Rats; Rats, Inbred Strains

The effect of urinary intestinal diversion on bone mineral metabolism was investigated in 78 rats. The animals were divided into sham-operated controls and diverted animals. The diverted animals were given either no supplement, sodium bicarbonate or ascorbic acid for an eight month period. Dual photon densitometry and bone mineral content were determined. Urinary intestinal diversion resulted in a minimal systemic acidosis and little alteration in baseline renal function but a significant decrease in bone calcium content. Oral bicarbonate and ascorbic acid administration prevented the demineralization.

Topics: Acidosis; Animals; Ascorbic Acid; Bicarbonates; Bone and Bones; Calcium; Colon, Sigmoid; Female; Magnesium; Minerals; Phosphorus; Rats; Rats, Inbred Strains; Sodium; Sodium Bicarbonate; Urinary Diversion

Seventeen infants under 2 months of age are described who presented with methaemoglobinaemia and acute diarrhoea during a period of 2 years. No infants beyond this age presented with such characteristics. In none of them was one of the known mechanisms of methaemoglobin formation found. All infants recovered with conventional therapy. Methaemoglobin associated with diarrhoea relapsed in three infants before they were 2 months old. Twenty-six similar cases have been reported in the literature. The mechanism of methaemoglobinaemia in these infants is unclear.

Topics: Acidosis; Ascorbic Acid; Diarrhea, Infantile; Female; Fluid Therapy; Humans; Infant; Infant, Newborn; Male; Methemoglobinemia; Methylene Blue

Topics: Acidosis; Ascorbic Acid; Child, Preschool; Cyanosis; Diagnosis, Differential; Fluid Therapy; Humans; Infant, Newborn; Male; Methemoglobinemia; Methylene Blue

Experiments with normal animals (10 sheep and 15 cows) revealed that the intravenous injection of bovicystan led to a considerable and dependable rise of the blood sugar for 2 to 36 hours the peak being at the 6th hour. The treatment of 95 freshly calved cows on 8 farms with signs of subclinical ketosis (ketonemia 22.4 +/- 1.9 mg%, ketonuria up to dilution of 1:2-1:16 and hypoglycemia 26.7 +/- 2.6 mg%) resulted in a 92.6 per cent total curative effect, consisting in the full inhibition of ketonuria, drop of the ketone bodies in the blood up to 16.5 +/- 1.2 mg%, on an average, and rise of the blood sugar up to 47.7 +/- 1.2 mg%, on an average. In 27.4 per cent of the treated cows ketonuria disappeared after the first injection, in 50.5 per cent - after the second one, and in 14.7 per cent only did ketonuria faded after the third injection of the preparation within a period of 24 hours. At the 48th hour following the last introduction of bovicystan there was an increase in the blood serum level of carotene and lactose, and a decrease in the level of inorganic phosphorus. One to three weeks after treatment with bovicystan in some 27.6 to 33.0 per cent of the cows on 2 of the farms signs of subclinical ketosis reappeared.

Topics: Acidosis; Animals; Ascorbic Acid; Blood Glucose; Cattle; Cattle Diseases; Cysteamine; Dexamethasone; Drug Combinations; Drug Evaluation; Drug Evaluation, Preclinical; Female; Ketosis; Sheep; Time Factors

Topics: Acidosis; Ascorbic Acid; Blood; Cholesterol; Gastrointestinal Diseases; Glycosuria; Humans; Hydrogen-Ion Concentration; Hyperglycemia; Kidney Calculi; Oxalates; Prothrombin; Vitamin B 12

In order to investigate whether or not there is a causal relationship between the metabolic acidosis and the ocular hypotension induced by acetazolamide, we undertook to correlate over a period of time the blood-acidifying and ocular-hypotonizing effects of administering the lowest intravenous effective dose of acetazolamide; to treat the metabolic acidosis induced by acetazolamide by means of the intravenous introduction of bases, and pulmonary hyperventilation (respiratory alkalosis); to evaluate the effects on the intraocular pressure (IOP) by neutralizing the acetazolamide-induced metabolic acidosis by means of a continuous infusion of sodium bicarbonate; to determine the relationship between the metabolic acidosis induced by blood-acidifying agents, which do not inhibit carbonic anhydrase, and the IOP; and to determine the changes in the acid-base status of the aqueous humor induced by acetazolamide and other blood-acidifying drugs. We found that the hypertonic buffering solution of sodium bicarbonate could reduce the IOP by itself through an osmotic mechanism. On the basis of our results, we believe that a causal relationship exists between the metabolic acidosis induced by acetazolamide, and by other drugs that have a blood-acidifying effect as the result of other mechanisms, and ocular hypotension, bothin the animal and in the glaucomatous patient.

Topics: Acetazolamide; Acid-Base Equilibrium; Acidosis; Alkalosis, Respiratory; Animals; Ascorbic Acid; Buffers; Calcium Chloride; Dose-Response Relationship, Drug; Glaucoma; Humans; Hydrochlorothiazide; Intraocular Pressure; Osmolar Concentration; Rabbits

Topics: Acidosis; Adrenocortical Hyperfunction; Ascorbic Acid; Ascorbic Acid Deficiency; Peptic Ulcer; Postoperative Care; Postoperative Complications; Preoperative Care

Topics: Acid-Base Equilibrium; Acidosis; Animals; Ascorbic Acid; Blood; Blood Pressure; Carbon Dioxide; Cats; Decamethonium Compounds; Depression, Chemical; Diaphragm; Hydrochloric Acid; Hydrogen-Ion Concentration; In Vitro Techniques; Muscle Contraction; Pancuronium; Partial Pressure; Phrenic Nerve; Rats; Succinylcholine; Tibia; Trimethadione

Topics: Acidosis; Animals; Ascorbic Acid; Bicarbonates; Calcium; Carbon Dioxide; Dogs; Hydrochloric Acid; Hydrogen-Ion Concentration; Injections, Intravenous; Lactates; Oxygen; Pyruvates; Tetracycline

Topics: Acidosis; Ammonium Chloride; Ascorbic Acid; Betaine; Evaluation Studies as Topic; Humans; Hydrochloric Acid; Hydrogen-Ion Concentration; Lysine; Pepsin A; Urinary Calculi; Urinary Tract Infections; Urine

Topics: Acetazolamide; Acid-Base Equilibrium; Acidosis; Animals; Aqueous Humor; Ascorbic Acid; Bicarbonates; Calcium Chloride; Carbonic Anhydrase Inhibitors; Dichlorphenamide; Glaucoma; Humans; Hydrogen-Ion Concentration; Intraocular Pressure; Rabbits; Time Factors

Topics: Acidosis; Animals; Ascorbic Acid; Calcium Chloride; Carbonic Anhydrase Inhibitors; Diabetic Ketoacidosis; Glaucoma; Humans; Intraocular Pressure; Methods; Rabbits

Topics: Acidosis; Adult; Aged; Ascorbic Acid; Female; Glucose; Humans; Insulin; Intestinal Neoplasms; Lung Neoplasms; Male; Middle Aged; Ovarian Neoplasms; Premedication; Pyridoxine; Stomach Neoplasms; Thiamine; Thiamine Pyrophosphate; Uterine Neoplasms

Topics: Acid-Base Equilibrium; Acidosis; Administration, Oral; Animals; Aqueous Humor; Ascorbic Acid; Bicarbonates; Chronic Disease; Glaucoma; Humans; Hydrogen-Ion Concentration; Hypotension; Intraocular Pressure; Osmosis; Rabbits

Topics: Acidosis; Adrenal Glands; Animals; Ascorbic Acid; Catecholamines; Ethionine; Exercise Test; Guinea Pigs; Humans; Liver; Liver Diseases; Male; Mandelic Acids; Sleep Wake Disorders

Topics: Acidosis; Alloxan; Animals; Ascorbic Acid; Diabetes Mellitus, Experimental; Dietary Fats; Drug Synergism; Injections; Injections, Intravenous; Injections, Subcutaneous; Insulin; Ketosis; Pharmacology; Rats; Research

Topics: Acidosis; Ascorbic Acid; Blood Chemical Analysis; Electrolytes; Fasting; Humans; Hydrogen-Ion Concentration; Urine

Topics: Acidosis; Animals; Ascorbic Acid; Cattle; Female; Ketoses; Ketosis

Topics: Acidosis; Alkalosis; Ascorbic Acid; Diuresis; Diuretics; Food; Humans; Metabolism; Niacin; Niacinamide; Riboflavin; Thiamine