Magnesium Salicylate Research Articles

The Study of Propagation of Ultrasonic Waves and Molecular Interactions in the Solutions of Magnesium Salicylate Tetrahydrate

The Study of Propagation of Ultrasonic Waves and Molecular Interactions in the Solutions of Magnesium Salicylate Tetrahydrate

Development of quantitative HPTLC–Densitometry methods for the analysis of amiodarone HCl, carvedilol, doxylamine succinate, magnesium salicylate, metoprolol succinate, nebivolol HCl, and salicylamide using a model process developed earlier for the transfer of TLC screening methods

A model process, previously developed in a series of studies, allows for the transfer of thin-layer chromatography (TLC) methods for qualitative screening of counterfeit drug products published in the Global Pharma Health Fund (GPHF) Minilab manual and US Food and Drug Administration (FDA) Compendium of Unofficial Methods for Screening of Pharmaceuticals by TLC to quantitative high-performance TLC (HPTLC)–densitometry methods. This article describes HPTLC–densitometry methods developed and validated according to this model process for pharmaceutical products of amiodarone HCl, carvedilol, doxylamine succinate, magnesium salicylate, metoprolol succinate, nebivolol HCl, and salicylamide, for which qualitative screening methods have not been published in the Minilab manual or FDA Compendium. These methods use relatively inexpensive and nontoxic “green solvents” for sample and standard solution and mobile phase preparation, Merck Premium Purity silica gel 60 F254 plates, automated standard and sample solution bandwise application, and automated densitometry for the assessment of peak purity and identity and quantification. Corresponding to the quantitative HPTLC–densitometry methods, qualitative TLC screening methods for these drug products were developed and posted online with open access as supplements to the FDA Compendium.

Characterization of tribofilms derived from zinc dialkyldithiophosphate and salicylate detergents by X-ray absorbance near edge structure spectroscopy

Phosphorous and sulfur L- and K-edge X-ray absorption near edge structure (XANES) spectra were recorded to characterize the surface chemistry of the tribofilms derived from a commercial zinc dialkyldithiophosphate (ZDDP) and its blends with overbased calcium and magnesium salicylate detergents. The results show that the chemical structure of the tribofilms generated from the mixture of ZDDP and detergents is different from that of the tribofilm derived from ZDDP alone. However, the two kinds of detergents inhibit ZDDP from forming tribofilm, producing thinner polyphosphate films. Though XANES analysis does not provide definite evidence to the existence of magnesium element in the tribofilms, it is likely that calcium or magnesium has been incorporated therein. Moreover, ion exchange reaction and the formation of zinc polyphosphate film may occur simultaneously during sliding. However, calcium or magnesium (poly)phosphates do not contribute to reduce friction and wear of a steel–steel pair.

Determining binding sites of drugs on human serum albumin using FIA-QCM

A simple and effective method was developed for determining binding sites of drugs on human serum albumin (HSA) by independent binding or competitive displacement of bilirubin using flow injection analysis-quartz crystal microbalance (FIA-QCM) system. Both independent and competitive bindings were entirely monitored in real time. Bilirubin as a site I-binding ligand was pre-bound to HSA sensor so as to occupy the drug-binding site I. When the model site II-binding drugs (ibuprofen, ketoprofen and flurbiprofen) were injected into the bilirubin pre-bound HSA system, the frequency continuously decreased by 6 Hz, 4 Hz and 5 Hz, respectively, which was the same as that of their individual binding to HSA sensor. It indicated that the drug binding to site II was independent and did not interfere with bilirubin binding. However, when the model site I-binding drugs (iodipamide and magnesium salicylate) were introduced into the system, the frequency remained unchanged in the initial several minutes and then rapidly decreased by 4 Hz for iodipamide and increased by 4 Hz for magnesium salicylate. This phenomenon revealed site I-binding drugs competitively bound to HSA against bilirubin and displaced the pre-bound bilirubin. The results demonstrate FIA-QCM can be a valid approach for monitoring the dynamic interaction between drugs and HSA in real time further identifying drug-binding sites without the need of labels.

Kinetics of the Thermal Decomposition of Magnesium Salicylate Powder in Air

Simultaneous thermogravimetry-differential thermal analysis (TG-DTA) was used to study the kinetics and the degradation of magnesium salicylate(C 14 H 10 MgO 6 ) in air. The results show that the decomposition proceeds through two steps. The kinetics of the first decomposition step was studied. The activation energies were calculated by using the Friedman and Flynn Wall Ozawa(FWO) methods, and the most probable kinetic model function was estimated using the multiple linear regression method. The values of the correlated kinetic parameters for the first decomposition step are E = 152.97 kJ/mol, lg( A /S −1 ) = 10.78, f (α) = (1−α) n (1 + K cat α), n = 0.691, and K cat = 1. 3048.

Acute Effects of a Weight Loss Supplement on Resting Metabolic Rate and Anaerobic Exercise Performance

This project examined a nutritional supplement that is advertised to stimulate marked weight loss and increase perceived energy that contains a proprietary blend of vitamin B12, hypercium extract, caffeine, gugglesterones, magnesium salicylate, bitter orange extract, guarana, theobromine, yohimbine extract, L-tyrosine, citrin K, psyllium husk, valerian root, ho shou wu, turkey rhubarb, cascara sagrada, senna extract, and piper nigrum. This weight loss supplement (WLS) is a combination of capsules that consist of morning, afternoon, and evening formulations. PURPOSE: The purpose of this study was to elucidate the effects of the WLS on resting metabolic rate (RMR: kcal/day), respiratory exchange ratio (RER), heart rate (HR: BPM), blood pressure (BP: mmHg), and anaerobic exercise performance (W). METHODS: Ten healthy young males underwent determination of RMR, RER, HR, and BP at baseline, and again one hour after taking each of the WLS capsules in randomized double blind cross over manner. After the second RMR, RER, HR, and BP measurements, the subjects engaged in a 30s Wingate bicycle test. RESULTS: There were no differences (P >0.05) in RMR between placebo (2151 ± 68), morning (2167 ± 61), afternoon (2156 ± 43), or evening (2109 ± 57) capsules. There were no differences in RER between placebo (0.72 ± 0.01), morning (0.72 ± 0.01), afternoon (0.73 ± 0.02), or evening (0.72 ± 0.01) capsules. There were no differences in HR between placebo (53 ± 3), morning (52 ± 3), afternoon (51 ± 3), or evening (51 ±3) capsules and no differences in BP between placebo (119 ± 4 / 82 ± 6), morning (125 ± 3 / 75 ± 2), afternoon (125 ± 2 / 77 ± 2), or evening (122 ±3/79 ± 2). There were no differences in absolute peak anaerobic power during the Wingate bicycle test between placebo (756 ± 25), morning (773 ± 35), afternoon (711 ± 30), or evening (739 ±41) capsules. There were also no differences in relative peak anaerobic power or minimum absolute peak anaerobic power. There were no differences in fatigue index during the Wingate bicycle test between placebo (46 ± 3), morning (50 ± 4), afternoon (41 ± 4), or evening (46 ± 4) capsules. There were no differences in baseline blood lactate concentrations, but the morning WLS capsule caused a greater increase in [blood lactate] after the Wingate test than the other treatments. DISCUSSION: Despite containing demonstrated stimulatory components, the current data suggest that the WLS does not promote body mass reduction, increase RMR, BP, HR, anaerobic exercise performance, or alter RER. The lack of effects could be due to an inadequate dosage of the stimulant or a counteractive effect caused by the proprietary blend of ingredients.

Trusty or Rusty? Oxidation Rate of Nails

In this Activity, students investigate the process of rusting using supermarket chemicals: unflavored gelatin, table salt and backache pain reliever tablets. A gelatin mixture is prepared and steel nails are placed in the gelatin and allowed to react with atmospheric oxygen. Ferric ion produced by the oxidation is made visible as a garnet-colored complex by magnesium salicylate present in the backache tablets. Factors that accelerate or retard the rate of iron oxidation are studied.

Nonprescription Analgesics and Their Use in Solid-Organ Transplantation: A Review

To review the pharmacology, adverse events, drug interactions, and use of the nonprescription analgesics in solid-organ transplant recipients. Studies evaluating nonprescription analgesics in solid-organ transplantation were considered for evaluation. English-language studies were selected for inclusion. Nonprescription analgesics (aspirin, choline salicylate, magnesium salicylate, sodium salicylate, ibuprofen, ketoprofen, naproxen sodium, and acetaminophen) are the most commonly purchased over-the-counter agents in the United States. These agents, although generally considered safe, have been associated with a number of toxicities. The salicylates and nonsteroidal anti-inflammatory drugs have been associated with gastrointestinal damage, hematologic changes, liver and kidney dysfunction, and breathing difficulties. Acetaminophen has been shown to induce hematologic changes and liver and renal dysfunction. A closer look at the nonprescription analgesics reveals their potential for harm when used by solid-organ transplant recipients. In this patient population, the salicylates and nonsteroidal anti-inflammatory drugs should generally be avoided if possible, because of their potential toxicities, especially renal dysfunction. Low-dose aspirin, for the prevention of cardiovascular and cardiocerebral events, appears to be safe, but patients must still be followed closely. Acetaminophen is generally considered the nonprescription analgesic and antipyretic of choice in transplant recipients because of its favorable toxicity profile. However, it is imperative that patients and transplant practitioners are aware that this agent is not without toxicities and proper monitoring is advised.

Nonprescription analgesics and their use in solid-organ transplantation: a review

To review the pharmacology, adverse events, drug interactions, and use of the nonprescription analgesics in solid-organ transplant recipients. Studies evaluating nonprescription analgesics in solid-organ transplantation were considered for evaluation. English-language studies were selected for inclusion. Nonprescription analgesics (aspirin, choline salicylate, magnesium salicylate, sodium salicylate, ibuprofen, ketoprofen, naproxen sodium, and acetaminophen) are the most commonly purchased over-the-counter agents in the United States. These agents, although generally considered safe, have been associated with a number of toxicities. The salicylates and nonsteroidal anti-inflammatory drugs have been associated with gastrointestinal damage, hematologic changes, liver and kidney dysfunction, and breathing difficulties. Acetaminophen has been shown to induce hematologic changes and liver and renal dysfunction. A closer look at the nonprescription analgesics reveals their potential for harm when used by solid-organ transplant recipients. In this patient population, the salicylates and nonsteroidal anti-inflammatory drugs should generally be avoided if possible, because of their potential toxicities, especially renal dysfunction. Low-dose aspirin, for the prevention of cardiovascular and cardiocerebral events, appears to be safe, but patients must still be followed closely. Acetaminophen is generally considered the nonprescription analgesic and antipyretic of choice in transplant recipients because of its favorable toxicity profile. However, it is imperative that patients and transplant practitioners are aware that this agent is not without toxicities and proper monitoring is advised.

Safety Assessment of Salicylic Acid, Butyloctyl Salicylate, Calcium Salicylate, C12-15 Alkyl Salicylate, Capryloyl Salicylic Acid, Hexyldodecyl Salicylate, Isocetyl Salicylate, Isodecyl Salicylate, Magnesium Salicylate, MEA-Salicylate, Ethylhexyl Salicylate, Potassium Salicylate, Methyl Salicylate, Myristyl Salicylate, Sodium Salicylate, TEA-Salicylate, and Tridecyl Salicylate

Safety Assessment of Salicylic Acid, Butyloctyl Salicylate, Calcium Salicylate, C12-15 Alkyl Salicylate, Capryloyl Salicylic Acid, Hexyldodecyl Salicylate, Isocetyl Salicylate, Isodecyl Salicylate, Magnesium Salicylate, MEA-Salicylate, Ethylhexyl Salicylate, Potassium Salicylate, Methyl Salicylate, Myristyl Salicylate, Sodium Salicylate, TEA-Salicylate, and Tridecyl Salicylate

Safety Assessment of Salicylic Acid, Butyloctyl Salicylate, Calcium Salicylate, C12–15 Alkyl Salicylate, Capryloyl Salicylic Acid, Hexyldodecyl Salicylate, Isocetyl Salicylate, Isodecyl Salicylate, Magnesium Salicylate, MEA-Salicylate, Ethylhexyl Salicylate, Potassium Salicylate, Methyl Salicylate, Myristyl Salicylate, Sodium Salicylate, TEA-Salicylate, and Tridecyl Salicylate

Safety Assessment of Salicylic Acid, Butyloctyl Salicylate, Calcium Salicylate, C12–15 Alkyl Salicylate, Capryloyl Salicylic Acid, Hexyldodecyl Salicylate, Isocetyl Salicylate, Isodecyl Salicylate, Magnesium Salicylate, MEA-Salicylate, Ethylhexyl Salicylate, Potassium Salicylate, Methyl Salicylate, Myristyl Salicylate, Sodium Salicylate, TEA-Salicylate, and Tridecyl Salicylate

Safety Assessment of Salicylic Acid, Butyloctyl Salicylate, Calcium Salicylate, C12-15 Alkyl Salicylate, Capryloyl Salicylic Acid, Hexyldodecyl Salicylate, Isocetyl Salicylate, Isodecyl Salicylate, Magnesium Salicylate, MEA-Salicylate, Ethylhexyl Salicylate, Potassium Salicylate, Methyl Salicylate, Myristyl Salicylate, Sodium Salicylate, TEA-Salicylate, and Tridecyl Salicylate

Safety Assessment of Salicylic Acid, Butyloctyl Salicylate, Calcium Salicylate, C12-15 Alkyl Salicylate, Capryloyl Salicylic Acid, Hexyldodecyl Salicylate, Isocetyl Salicylate, Isodecyl Salicylate, Magnesium Salicylate, MEA-Salicylate, Ethylhexyl Salicylate, Potassium Salicylate, Methyl Salicylate, Myristyl Salicylate, Sodium Salicylate, TEA-Salicylate, and Tridecyl Salicylate

Bioavailability and pharmacokinetics of magnesium after administration of magnesium salts to humans.

Therapeutically, magnesium salts represent an important class of compounds and exhibit various pharmacologic actions. Examples of magnesium salts are ionic magnesium and magnesium citrate in nephrolithiasis, magnesium salicylate in rheumatoid arthritis, magnesium hydroxide as an antacid as well as a cathartic, and magnesium mandelate as urinary antiseptic. Various anions attached to the cation magnesium, such as oxide, chloride, gluconate, and lactate, affect the delivery of the amounts of elemental magnesium to the target site and thereby produce different pharmacodynamic effects. This review examines the bioavailability and pharmacokinetics of various magnesium salts and correlates pharmacodynamic action with the structure-activity relationship.

In reply

Editors note: The above letter was referred to the authors of the original paper, and their reply follows. In reply: Salicylate intoxication is an important limitation of these preparations. Making this problem worse in older people is the common problem of renal insufficiency resulting in drug accumulation. Older patients may also take over-the-counter salicylate preparations without the physician's knowledge. In this setting, it is important to provide substantial patient and caregiver education to reduce the risk of salicylate intoxication and to check salicylate levels periodically in those at high risk.1 Doctor Romano is correct in asserting that the maximum safe dose of choline magnesium salicylate (Trilisate, and others) is 3 grams per day. Higher doses may lead to salicylism and other toxic outcomes.1 Doctor Romano is also correct in clarifying the comment in the table about toxicities of choline magnesium salicylate. Choline magnesium trisalicylate does not have a clinical effect on platelet aggregation at normal clinical doses of 1.5 to 3 grams/24 hours.2,3 This is also true with COX-2-specific NSAIDs, rofecoxib and celecoxib. However, there are not sufficient data to suggest that choline magnesium trisalicylate is any less apt to interfere with renal plasma flow. All NSAIDs, including COX-2-specific NSAIDs, affect renal plasma flow to some degree. Clinical trails with celecoxib have shown renal effects similar to those of other NSAIDs.4

Intensive hydrogen bonding in a monomeric magnesium salicylate tetrahydrate

Intensive hydrogen bonding in a monomeric magnesium salicylate tetrahydrate

Effect of choline magnesium trisalicylate on prostacyclin production by isolated vascular tissue of the rat

Choline Magnesium Trisalicylate (Trilisate), in therapeutic concentrations of 5, 10, 15 and 30 mg/100 ml, did not significantly affect production of prostacyclin-like (PGI 2) substance by rat aortic tissue in vitro. The ED 50 for inhibition of aorta PGI 2-like substance production by Trilisate was 1,200 mg/100 ml. This is approximately 40 times the maximum therapeutic blood concentration achieved in humans. Choline or Magnesium salicylate produced slight but insignificant inhibition of PGI 2-like substance production by rat aortic tissue in vitro. The ED 50 for ibuprofen (Motrin) for inhibition of PGI 2-like production of rat aortic rings was 0.65–0.92 mg/100 ml. Injection of Choline Magnesium Trisalicylate into rats (124, 250, 500 mg/kg I.P.) did not affect the normal production of PGI 2-like substance of aortic tissue obtained one hour after in vivo treatment. These results suggest this anti-inflammatory salicylate does not adversely affect PGI 2-like production by blood vessels, in concentrations associated with therapeutic effects in man.

Physicochemical Properties of Magnesium Salicylate

Magnesium salicylate tetrahydrate is a nonhygroscopic, crystalline powder, whereas anhydrous magnesium salicylate is amorphous and very hygroscopic. Magnesium salicylate tetrahydrate tablets formulated with gelatin as a binder showed a dissolution half-life (t1/2) of 12 min, whereas a formulation using pregelatinized starch as a binder showed a t1/2 of 33 min. The optimum level of calcium stearate in the formulation was determined by the oscilloscope tracings of compressional and ejectional forces from an instrumented rotary tableting machine. Increasing the level of calcium stearate from 1 to 1.5 and 2% resulted in dissolution t1/2 values of 12, 18, and 21 min, respectively, and a higher incidence of softer tablets and capping.

Theophylline Magnesium Salicylate, a New Xanthine Compound

Interaction of 1 mole of magnesium salicylate and 2 moles of theophylline in water precipitated a crystalline compound, identified as theophylline magnesium salicylate pentahydrate from analytical and supportive physicochemical data. Similarly, barium salicylate and theophylline produced theophylline barium salicylate. No precipitates were formed with calcium salicylate or strontium salicylate under the same conditions. Theophylline magnesium salicylate is not a mixture of components and differs in composition from the known theophylline calcium salicylate dihydrate. Unlike the latter compound, it is not alkaline.

Comparative plasma salicylate and urine salicylurate levels following administration of aspirin, magnesium salicylate, and choline magnesium trisalicylate

Eighteen healthy volunteers were administered single doses of commercially available solid dosage forms of aspirin, magnesium salicylate (I), and choline magnesium trisalicylate (II), equivalent to ∼500mg of salicylic acid, in a randomized, complete crossover design. Plasma salicylate and urine salicylurate levels were measured by high-pressure liquid chromatography at frequent intervals following dosing; the resultant profiles, areas under the curve (AUC), and percentages of dose excreted as salicylurate were statistically analyzed by an analysis of variance. The plasma salicylate levels following the two dosage forms containing I and II were virtually identical when corrected for small differences in the dose. The plasma salicylic acid level following aspirin was ∼10% lower during the 1.5–3.0-hr interval due to a portion of unhydrolyzed aspirin, but the dose-corrected AUC for the products tested did not differ significantly (p < 0.05). During the 24hr following dosing, 66.5 ± 12.1, 68.4 ± 7.1, and 60.9 ± 14.1% of the salicylic acid were excreted as urine salicylurate for aspirin, I, and II, respectively, with no significant difference (p < 0.05). Based on this study, there are no significant differences in the rate and extent of absorption of salicylate following the three dosage forms tested, and the elimination kinetics of salicylic acid are not altered by these dosage forms.

Drug therapy reviews: Antirheumatic agents

The pathophysiology, symptoms and drug treatment of rheumatic disease are reviewed. Antirheumatic drugs reviewed are salicylates (including aspirin, sodium salicylate, choline salicylate, choline magnesium salicylate, salsalate), phenylpropionic acid derivatives (fenoprofen, ibuprofen, naproxen), indole derivatives (sulindac, tolmetin and indomethacin), pyrazolone derivatives (phenylbutazone, oxyphenbutazone), gold compounds, penicillamine, antimalarials mefenamic acid, corticosteroids and immunosuppressives. Simple analgesic therapy (acetaminophen, aspirin, propoxyphene) is used in the early stage of the disease. As the disease progresses, aspirin remains the drug of choice for antiinflammatory activity but the phenylpropionic acid or indole derivatives may be preferred in patients unable to tolerate salicylates. If such nonsteroidal antiinflammatory agents are not effective, parenteral therapy with gold compounds or oral penicillamine usually is indicated. Indomethacin or phenylbutazone, then antimalarials, are resorted to next. Corticosteroids or immunosuppressives are reserved for patients who are unsuccessfully controlled or who have major side effects with the other drugs. Mefenamic acid occupies a very secondary place in rheumatoid arthritis treatment.