ascorbic-acid and Magnesium-Deficiency

Physicians' use of micronutrients to improve symptoms or outcomes in chronic illness has until recently been guided by limited data on the actions of individual agents in vitro or in animal studies. However several recently published clinical trials have provided information about which groups of patients are likely to benefit from which combination of micronutrients. Patients with chronic cardiac failure (CCF), particularly elderly individuals, have several reasons to be deficient in micronutrients including reduced intake, impaired gastrointestinal absorption and increased losses on the background of increased utilisation due for example to increased oxidative stress. Studies of nutritional supplementation in CCF patients have usually concentrated on specific agents. However given that many micronutrients have synergistic influences upon metabolic processes this strategy might merely lead to a shifting of a limiting step. Rather, a strategy of increasing the availability of multiple agents at once might be more logical. The aim of this article is to briefly review the experimental rationale for each of the micronutrients of potential benefit in chronic heart failure and examine the current clinical trial evidence supporting their use.

Topics: Animals; Antioxidants; Ascorbic Acid; Calcium; Carnitine; Copper; Dietary Supplements; Heart Failure; Humans; Magnesium; Magnesium Deficiency; Micronutrients; Niacin; Oxidative Stress; Phosphocreatine; Ubiquinone; Vitamin B Complex; Vitamin B Deficiency; Vitamin E; Zinc

Basic studies indicate magnesium deficiency as one of the important, but often neglected, risk factors aggravating the course of borderline disorders (BD). A clinical verification of this notion has been conducted.. Authors studied 62 patients with BD, aged 25-65 years, of inpatient and outpatient settings. Contents of magnesium and other blood electrolytes were determined.. Authors found an extremely high prevalence of very low levels of magnesium (Mg) in erythrocytes (<0.3 mmol/l) in patients with BD compared to controls (patients without BD, Mg (er.) 1.62±0.48 mmol/l). It has been shown that low Mg levels in the plasma and red blood cells are associated with a significantly increased risk of the following diagnoses: F07 «Personality and behavioral disorder due to brain disease, damage and dysfunction» (p<0.0016), F21 «Schizotypal disorder» (p<0.0005) and F34 «Persistent mood [affective] disorders» (p<0.0001). The use of Magne B6 Forte (4 tablets/day, 30 days, then 2 tablets/day for 1 year) resulted in a significant increase in the Mg levels in the plasma and erythrocytes, the compensation of anxiety and depressive symptoms, improvement of sleep and general health of the patients, reduced consumption of antidepressants (by 30%).. Administration of the drugs based on organic salts of magnesium per os improves the condition of patients and reduces their need in pharmacotherapy.. Цель исследования. Данные фундаментальных исследований указывают на дефицит магния при пограничных психических расстройствах (ППР) как на один из важных факторов риска развития, отягощающих их течение. Настоящая работа была направлена на клиническую проверку этого предположения. Материал и методы. Наблюдали 62 пациентов с ППР в возрасте 25-65 лет, проходящих лечение в психиатрическом стационаре и амбулаторно. В процессе клинического обследования изучали содержание магния и других электролитов в крови. Результаты. Установлена высокая частота сверхнизкого содержания магния в эритроцитах (<0,3 ммоль/л) у пациентов с ППР по сравнению с контролем (пациенты без ППР, уровень магния 1,62±0,48 ммоль/л). Отмечено, что низкий уровень магния в плазме и эритроцитах ассоциирован с достоверным повышением риска развития следующих заболеваний: F07 'Расстройства личности и поведения вследствие дисфункции головного мозга' (p<0,0016), F21 'Шизотипическое расстройство' (p<0,0005) и F34 'Хронические аффективные расстройства' (p<0,0001). Применение препарата магне В6 форте (4 таблетки в сутки 30 дней, затем 2 таблетки в сутки в течение 1 года) позволило увеличить уровень магния в плазме и эритроцитах, привести к компенсации тревожной и депрессивной симптоматики, улучшению сна и общего состояния пациентов, а также снижению потребности в антидепрессантах на 30%. Заключение. Использование препаратов на основе органических солей магния при перечисленных выше ППР дает возможность улучшить состояние пациентов и снизить их потребность в фармакотерапии.

Topics: Adult; Aged; Anxiety; Ascorbic Acid; Depression; Erythrocytes; Female; Humans; Magnesium; Magnesium Deficiency; Male; Middle Aged; Personality Disorders; Sleep; Vitamin B 6

Topics: Adaptation, Psychological; Adult; Affective Symptoms; Ascorbic Acid; Chronic Disease; Humans; Magnesium; Magnesium Deficiency; Male; Stress, Psychological; Treatment Outcome; Vitamin B 6

We investigated the effects of ascorbic acid (AsA) supplementation on lipid peroxidation and the lipid content in the liver and serum of magnesium (Mg)-deficient rats. Eighteen 3-week-old male Sprague-Dawley strain rats were divided into 3 groups and maintained on a control diet (C group), a low-Mg diet (D group), or a low-Mg diet supplemented with AsA (DA group) for 42 d. At the end of this period, the final body weight, weight gain, and serum Mg concentrations were significantly decreased in the Mg-deficient rats. Further, dietary AsA supplementation had no effect on the growth, serum Mg concentration, Mg absorption, and Mg retention. The serum concentration of AsA was significantly lower in the D group than in the C group but was unaltered in the DA group. The levels of phosphatidylcholine hydroperoxide (PCOOH) in the serum and of triglycerides (TGs) and total cholesterol (TC) in the serum and liver were significantly higher in the D group than in the C group. The serum PCOOH, liver TG, and liver TC levels were decreased in the DA group. These results indicate that Mg deficiency increases the AsA requirement of the body and that AsA supplementation normalizes the serum levels of PCOOH and the liver lipid content in Mg-deficient rats, without altering the Mg status.

Topics: Animals; Ascorbic Acid; Body Weight; Dietary Supplements; Lipid Peroxidation; Lipids; Liver; Magnesium Deficiency; Male; Rats; Rats, Sprague-Dawley; Reference Standards

Topics: Animals; Ascorbic Acid; Behavior, Animal; Brain; Brain Ischemia; Disease Models, Animal; Drug Combinations; Female; Hemodynamics; Laser-Doppler Flowmetry; Magnesium; Magnesium Compounds; Magnesium Deficiency; Male; Neuroprotective Agents; Rats; Sodium Chloride; Vitamin B 6

The oxidation states of intracellular myoglobin and cytochrome oxidase aa3 were monitored by reflectance spectrophotometry in isolated perfused rat hearts subjected to an acutely magnesium deficient environment. After exposure to low extracellular [Mg2+]o (i.e., 0.3 mM) for 30 min, more than 80% of the oxymyoglobin converted to its deoxygenated form. The level of reduced cytochrome oxidase aa3 also increased about 80% in low [Mg2+]o. The deoxymyoglobin was converted further to a species identified as ferrylmyoglobin by its reaction with Na2S to form ferrous sulfmyoglobin which was optically visible. This process, set into motion by acute Mg deficiency, resulted from a direct accessibility of the exogenous peroxide to the cytosolic protein. The results suggest that a pathway leading to cardiac tissue damage, induced by magnesium deficiency, is probably involved in the generation of a ferrylmyoglobin radical which could be prevented by addition of ascorbate, which is known to be a one-electron reductant of this hypervalent form of myoglobin. In further studies, we also investigated whether addition of different concentrations of ascorbic acid (AA) to the perfusate could enhance myocardial function after exposure to low [Mg2+]o perfusion. Four concentrations of AA (0.5, 1, 5, 10 mM) were tested, and the results indicate that they exert their effects in a concentration-dependent manner; 1 mM AA was the most effective dose in improving aortic output in a Mg-deficient heart. Ferrylmyoglobin formation was found to be formed considerably before intracellular release of either creatine phosphokinase or lactic dehydrogenase. These studies may have wide implications as a new mechanism by which low extracellular Mg2+ can induce myocardial injury and subsequent cardiac failure.

Topics: Animals; Ascorbic Acid; Coronary Disease; Electron Transport Complex IV; Magnesium Deficiency; Male; Metmyoglobin; Mitochondria, Heart; Myocardium; Myoglobin; Perfusion; Rats; Rats, Wistar; Spectrophotometry

Supplementation with dietary Mg at a minimum level of 0.06% seems to be essential to prevent the hypercalcinosis of the kidney and hepatopancreas in a fish, the common carp. Mg deficiency appears to have no effect on the Mg level in kidneys and hepatic tissue, whereas the Fe level in those tissues was significantly diminished by increasing dietary Mg supplementation up to 3.2 g.kg-1. Both hypercalcinosis and accumulation of Fe in soft tissues were more pronounced in fish offered diets high in protein (44%) compared to fish on low dietary protein (25%). The ascorbic acid in the hepatopancreas and kidney was greatly depleted in fish fed the high-protein diets, and this depletion did not correlate with the dietary Mg level nor with a high level of tissue Ca. However, the increased Ca concentration in the kidney coincided with the greatest depletion of ascorbate in fish fed a high-protein diet. The concentration of ascorbate in the brain was much less affected by a low level of vitamin C in the diets than in other tissues. Depletion of ascorbate in soft tissues did not correspond to fish growth but might be rather related to the metabolic rate imposed by the dietary nutrients. It is suggested that the Mg and ascorbic acid requirements in the carp are considerably elevated by the increased dietary protein level.

Topics: Animals; Antioxidants; Ascorbic Acid; Brain; Calcium; Carps; Diet; Glutathione; Iron; Kidney; Magnesium; Magnesium Deficiency; Nutritional Requirements; Pancreas

The effects of a high dose of ascorbic acid superimposed on a low magnesium diet were studied for the first time. Young male guinea pigs were fed for six weeks two diets containing 3000 or 600 ppm magnesium: half in each group was supplemented with a daily oral dose of either 3 mg or 100 mg ascorbic acid per 100 g body weight. No treatment effects were found in serum copper and ceruloplasmin, spleen copper, bone calcium, kidney magnesium, and brain calcium and magnesium contents. Both bone copper and brain ascorbic acid contents of the group fed the normal ascorbic acid/low magnesium diet were lower (p less than 0.01) than the combined means of the other three groups; the high ascorbic acid/low magnesium treatment resulted in normalization of bone copper and brain ascorbic acid levels. Irrespective of ascorbic acid level, the low magnesium diet decreased the bone magnesium and increased the kidney calcium contents (p less than 0.01); this effect on kidney was nearly doubled by the high ascorbic acid intake (p less than 0.01). The results indicated that the main effects were due to the magnesium deficit.

Topics: Animals; Ascorbic Acid; Bone and Bones; Brain; Calcium; Ceruloplasmin; Copper; Guinea Pigs; Kidney; Magnesium; Magnesium Deficiency; Male; Spleen; Tissue Distribution

The effect of feeding a magnesium (Mg)-deficient diet for 9-34 days to weanling and young male rats on urinary and tissue ascorbate levels were studied. The concentrations of ascorbic acid in the liver and kidney were significantly reduced in the rats receiving a Mg-deficient diet as compared to those receiving a Mg-supplemented diet. The response to trichloro-2-methyl-2-propanol stimulation of urinary ascorbic acid was found to be considerably suppressed by dietary deficiency of Mg, suggesting that the decrease was not due to feed intake. In in vitro studies, the enzymatic synthesis of the vitamin from glucuronolactone or gulonolactone by liver extracts from Mg-deficient rats was significantly decreased as compared with Mg-supplemented rats. These results suggest that Mg-deficient rats have a reduced capacity to synthesize ascorbate which in turn produces a decrease in ascorbic acid concentrations in the liver.

Topics: Animals; Ascorbic Acid; Calcium; Chlorobutanol; Kidney; Liver; Magnesium; Magnesium Deficiency; Male; Rats; Rats, Inbred Strains