Sodium palmitate

278.41

278.222168

206-988-1

JQ43KP6296

DTXSID2041127

WHITE CRYSTALS|White to yellow powder

2915709000

40.13000

4.21760

White Powder

270 °C

340.6ºC at 760mmHg

154.1ºC

INSOL IN WATER, SPARINGLY SOL IN COLD ALC /PALMITIC ACID/|FREELY SOL IN HOT ALC, ETHER, CHLOROFORM /PALMITIC ACID/

2-8°C

Combustible

NONH for all modes of transport

1

36

22-24/25-26

RT4945000

Xi

P280-P305 + P351 + P338-P337 + P313

H319

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

Combustible

Combustible

Upper body obesity is associated with insulin resistance, hypertension, and endothelial dysfunction. /The authors/ examined forearm vascular function in response to vasodilator (endothelium-dependent and endothelium-independent) and vasoconstrictor stimuli in 8 normotensive, upper body/viscerally obese men with a positive family history of hypertension and 8 age-matched nonobese men ... Body composition and insulin regulation of free fatty acid (FFA) and glucose metabolism /were also measured/. Forearm blood flow was measured before and during brachial artery infusions of acetylcholine (Ach), sodium nitroprusside (NTP), and angiotensin II (+ / - nitric oxide synthase (NO)) synthase blockade with N(G)-monomethyl L-arginine (L-NMMA). On a separate day, baseline and insulin-regulated glucose ((3-(3)H)glucose) and FFA ((9,10-(3)H)palmitate) turnover were measured. The vasoconstrictor response to angiotensin II was greater (P<0.05) in obese men than in nonobese men, whereas endothelium-dependent vasodilation was similar. The slope of the angiotensin II dose-response curve correlated significantly with the basal plasma palmitate concentration. Basal and insulin-mediated glucose disposal was significantly reduced and FFA turnover significantly increased in viscerally obese men. No differences in endothelium-independent vasodilation or relationships between vascular responsivity and palmitate and glucose kinetics or body composition were found. Angiotensin II-stimulated forearm vasoconstriction is increased in viscerally obese normotensive men. /Palmitate/

STUDIES OF ACUTE ORAL TOXICITY IN RATS PLACE SIMPLE HOUSEHOLD SOAPS NEAR BORDERLINE BETWEEN TOXICITY CLASSES 1 & 2. 1= PRACTICALLY NONTOXIC: PROBABLE ORAL LETHAL DOSE (HUMAN) ABOVE 15,000 MG/KG; MORE THAN 1 QT (2.2 LB) FOR 70 KG PERSON (150 LB). /SOAPS/|STUDIES OF ACUTE ORAL TOXICITY IN RATS PLACE SIMPLE HOUSEHOLD SOAPS NEAR BORDERLINE BETWEEN TOXICITY CLASSES 1 & 2. 2= SLIGHTLY TOXIC: PROBABLE ORAL LETHAL DOSE (HUMAN) 5,000 to15,000 MG/KG; BETWEEN 1 PINT AND 1 QT FOR 70 KG PERSON (150 LB). /SOAPS/

Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. (See all compounds classified as Enzyme Inhibitors.)

Rat liver slices were incubated with (14)C-labeled sodium palmitate for 120 min at 37 °C. Lipid fractions extracted & separated by chromatography. Palmitate was maximally incorporated into phospholipid fractions after 5 min.|(14)C-1-Palmitate was injected into rabbit fetuses in utero. Fetal liver, blood, carcass & placenta checked for radioactivity. Highest total early specific activity in plasma, but later liver displayed most extensive incorporation. Phospholipid incorporation more rapid.

The metabolism of radiolabeled acetone, acetate, or palmitate was studied in pregnant and nonpregnant guinea-pigs. Fasted pregnant guinea-pigs and guinea-pigs that were not pregnant were injected intracardially with carbon-14 C-(14) labeled acetone, sodium-acetate, or sodium-palmitate. Doses ranged from 0.4 to 2.2 milligrams per kilogram. Expired carbon-dioxide was collected and assayed for radioactivity. C-(14) content of lipids, and blood and urine total acetone bodies were measured. ... In the palmitate treated animals, specific carbon-dioxide activities were twice as great in the pregnant guinea-pigs. Liver lipid C-(14) content of the group that were not pregnant was twice that of the pregnant group. The authors conclude that pregnant guinea-pigs used C-(14) more for biosynthesis than for carbon-dioxide excretion, while the opposite is true for guinea-pigs that were not pregnant.|Fat cells isolated from rat epididymal adipose tissue were incubated with albumin-bound (14)C-palmitate. Incorporation of (14)C into (14)CO2, and glycerides was measured. Some evidence is presented to suggest that the exogenous palmitate pool is in isotopic equilibrium with intracellular precursors for these metabolic processes. Precautions were taken to minimize dilution of the exogenous palmitate pool by fatty acids released from the cells. (14)CO2 production from (1-(14)C)-palmitate was 3 times that from (16-(14)C)-palmitate. Octanoate increased this differential oxidation of palmitate carbons and also inhibited palmitate oxidation without similarly affecting esterification. Glucose increased palmitate esterification in cells from fed or starved rats. Insulin potentiated this effect of glucose. Glucose influenced palmitate oxidation in a more complex manner, dependent upon the glucose concentration. Both the observation that esterification constitutes 99% of the metabolic flux of fatty acid and the manner in which glucose, insulin, or starvation influence palmitate esterification and oxidation suggested that factors controlling esterification may alter oxidation as a secondary effect, but not vice versa. It is suggested that oxidation and esterification compete for a single intracellular precursor, possibly extramitochondrial long chain fatty acyl COA. /Palmitate/

Vascular dysfunction is a major complication of metabolic disorders such as diabetes and obesity. The current studies were undertaken to determine whether inflammatory responses are activated in the vasculature of mice with diet-induced obesity, and if so, whether Toll-Like Receptor-4 (TLR4), a key mediator of innate immunity, contributes to these responses. Mice lacking TLR4 (TLR4(-/-)) and wild-type (WT) controls were fed either a low fat (LF) control diet or a diet high in saturated fat (HF) for 8 weeks. In response to HF feeding, both genotypes displayed similar increases of body weight, body fat content, and serum insulin and free fatty acid (FFA) levels compared with mice on a LF diet. In lysates of thoracic aorta from WT mice maintained on a HF diet, markers of vascular inflammation both upstream (IKK-beta activity) and downstream of the transcriptional regulator, NF-kappa-B (ICAM protein and IL-6 mRNA expression), were increased and this effect was associated with cellular insulin resistance and impaired insulin stimulation of endothelial nitric oxide synthase (eNOS). In contrast, vascular inflammation and impaired insulin responsiveness were not evident in aortic samples taken from TLR4(-/-) mice fed the same HF diet, despite comparable increases of body fat mass. Incubation of either aortic explants from WT mice or cultured human microvascular endothelial cells with the saturated FFA, palmitate (100 mol/L), similarly activated IKK-beta, inhibited insulin signal transduction and blocked insulin-stimulated NO production. Each of these effects was subsequently shown to be dependent on both TLR4 and NF-kappa-B activation. These findings identify the TLR4 signaling pathway as a key mediator of the deleterious effects of palmitate on endothelial NO signaling, and are the first to document a key role for TLR4 in the mechanism whereby diet-induced obesity induces vascular inflammation and insulin resistance. /Palmitate/|Insulin stimulates its own secretion and synthesis by pancreatic beta-cells. Although the exact molecular mechanism involved is unknown, changes in beta-cell insulin signalling have been recognized as a potential link between insulin resistance and its impaired release, as observed in non-insulin-dependent diabetes. However, insulin resistance is also associated with elevated plasma levels of free fatty acids (FFA) that are well known modulators of insulin secretion by pancreatic islets. This information led us to investigate the effect of FFA on insulin receptor signalling in pancreatic islets. Exposure of pancreatic islets to palmitate caused up-regulation of several insulin-induced activities including tyrosine phosphorylation of insulin receptor and pp185. This is the first evidence that short exposure of these cells to 100 microM palmitate activates the early steps of insulin receptor signalling. 2-Bromopalmitate, a carnitine palmitoyl-CoA transferase-1 inhibitor, did not affect the effect of the fatty acid. Cerulenin, an acylation inhibitor, abolished the palmitate effect on protein levels and phosphorylation of insulin receptor. This result supports the proposition that protein acylation may be an important mechanism by which palmitate exerts its modulating effect on the intracellular insulin signalling pathway in rat pancreatic islets.|Accumulation of long-chain fatty acids in the heart has been proposed to play a role in the development of heart failure and diabetic cardiomyopathy. Several animal models with increased cardiomyocyte lipid accumulation suggest a link between the accumulation of lipid, cardiomyocyte cell death and the development of cardiomyopathy. In this review, we discuss the mechanism through which fatty acid accumulation may contribute to the development or progression of heart failure by initiation of apoptotic cell death. Long-chain saturated fatty acids induce apoptosis through a mechanism involving the generation of reactive intermediates. Reactive intermediate production occurs in concert with de novo ceramide synthesis, but ceramide production is not required for cell death. Cardiomyocyte dysfunction and death from reactive intermediates generated by long-chain saturated fatty acids may contribute to the pathogenesis of human heart disease. /Long-chain Fatty Acids/

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Organic acids and related compounds/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist respirations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Activated charcoal is not effective ... . Do not attempt to neutralize because of exothermic reaction. Cover skin burns with dry, sterile dressings after decontamination ... . /Organic acids and related compounds/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Early intubation, at the first sign of upper airway obstruction, may be necessary. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Organic acids and related compounds/

/HUMAN EXPOSURE STUDIES/ Changes in contractility of newborn and adult hearts with different substrates were studied under oxygenation and hypoxia. Under oxygenation, insulin (50 mU/L) and low doses of fatty acids (sodium palmitate 0.12 mM) increased the differential ventricular pressure (DVP), while higher doses of fatty acids (from 0.3 to 1.5 mM) decreased it. However, when both low doses of fatty acids and insulin were added simultaneously, tension development decreased. Hypoxia reduced DVP, and low doses of fatty acids restored cardiac force. The contractile response to extracellular glucose concentrations changed during development, and sensitivity to high doses of fatty acids increased with age. ...|/ALTERNATIVE and IN VITRO TESTS/ In adult cardiomyocytes, glucose uptake was also inhibited by sodium palmitate under oxygenation when cardiac metabolism is fatty acid dependent, but not under hypoxia, when it consumes carbohydrates. Newborn cardiomyocytes consumed more glucose than adult cells, they did not respond to insulin, and palmitate did not completely inhibit glucose uptake neither under oxygenation nor under hypoxia. Substrate availability modified glucose uptake and contractility by independent mechanisms.|/SIGNS AND SYMPTOMS/ BY INTRAUTERINE INJECTION (AS IN SOME CRIMINAL ABORTIONS), SOAPS CAUSE HEMOLYSIS, EMBOLI, HYPERPYREXIA, SHOCK, RENAL DAMAGE, & OFTEN PROMPT DEATH. /SOAPS/|/SIGNS AND SYMPTOMS/ THEY ARE...LESS LETHAL THAN SYNTHETIC ANIONIC DETERGENTS & EVEN LESS THAN MOST NONIONIC DETERGENTS. HOWEVER, SOAPS WITH APPRECIABLE CONTENT OF FREE ALKALI...ARE LESS BENIGN. /SOAPS/

Acid, Hexadecanoic

Soap, cleaning compound, and toilet preparation manufacturing|Hexadecanoic acid, sodium salt (1:1): ACTIVE|/IT IS A/ SUBSTANCE WHICH MIGRATES TO FOOD FROM PACKAGING MATERIALS.|listed /as a cosmetic ingredient/

EPA Safer Chemical Functional Use Classes -> Surfactants|Safer Chemical Classes -> Green circle - The chemical has been verified to be of low concern|Cosmetics -> Cleansing; Emulsifying; Surfactant; Viscosity controlling