Stearic acid metabolism via beta-oxidation, omega-oxidation, and (omega-1)-oxidation has been demonstrated in rat liver. Removal of a single acetate moiety can occur to produce palmitic acid, and both this and stearic acid may be desaturated, producing oleic and palmitoleic acids, respectively. After (l4)C stearic acid was injected into rats, about 50 percent of the liver (14)C was recovered as oleic acid, indicating that extensive desaturation occurs. Desaturation occurs only to a small extent extrahepatically but has been detected in adipose tissue and in cells of mammary tissue. Stearic acid is also incorporated into phospholipids, di- and triglycerides, cholesterol, cholesterol esters, and other sterol esters.
Proposed mechanisms for fatty acid uptake by different tissues range from passive diffusion to facilitated diffusion or a combination of both. Fatty acids taken up by the tissues can either be stored in the form of triglycerides (98% of which occurs in adipose tissue depots) or they can be oxidized for energy via the beta-oxidation and tricarboxylic acid cycle pathways of catabolism.
The beta-oxidation of fatty acids occurs in most vertebrae tissues (except the brain) using an enzyme complex for the series of oxidation and hydration reactions resulting in the cleavage of acetate groups as acetyl-CoA (coenzyme A). An additional isomerization reaction is required for the complete catabolism of oleic acid. Alternate oxidation pathways can be found in the liver (omega-oxidation) and in the brain (alpha-oxidation).
Fatty acid biosynthesis from acetyl-CoA takes place primarily in the liver, adipose tissue, and mammary glands of higher animals. Successive reduction and dehydration reactions yield saturated fatty acids up to a 16-carbon chain length. Stearic acid is synthesized by the condensation of palmitoyl-CoA and acetyl-CoA in the mitochondria, and oleic acid is formed via a mono-oxygenase system in the endoplasmic reticulum.
Animal cells can de novo synthesize palmitic and stearic fatty acid and their n-9 derivatives. However, de novo synthesis requires the utilization of energy. Palmitic acid (C16) is the immediate precursor of stearic acid (C18). In animal cells, oleic acid is created by the dehydrogenation (desaturation) of stearic acid. Oleic acid is further elongated and desaturated into a family of n-9 fatty acids. The demand for energy used to synthesize n-9 fatty acids can be reduced in cell culture by providing palmitic and stearic acids. In addition, since palmitic and stearic acid are saturated, they are not peroxidized during delivery to the cells.
IDENTIFICATION AND USE: Stearic acid is a solid. It is used in suppositories, coating enteric pills, ointments and for coating bitter remedies. It is also used in manufacturing stearates of aluminum, zinc, and other metals, stearin soap for a liniment invented by Paracelsus, candles, phonograph records, insulators, modeling compounds, impregnating plaster of Paris, in vanishing creams and other cosmetics. Stearic acid is used in animal cell culture. HUMAN STUDIES: The greatest danger from ingestion of large quantities of stearic acid is intestinal obstruction. Skin sensitization is unusual. Aspiration or inhalation of stearic acid could cause chemical pneumonitis. Implantation of stearic acid will cause foreign body reaction. ANIMAL STUDIES: Skin lotion formulations containing 2.8% stearic acid administered at doses of 15 g/kg by gavage to groups of 10 rats resulted in 1 death. Normal behavior and appearance were observed, and there were no gross alterations in surviving rats. No ocular irritation was produced in 6 rabbits by commercial grade stearic acid, whereas mild conjunctival erythema was produced in 3 of 6 rabbits by commercial grade triple-pressed stearic acid. Treatment with 35% stearic acid in corn oil and 50% stearic acid in petrolatum was primarily producing mild conjunctival erythema, which had subsided within 2 days. Intravenous infusion of large doses of stearic acid were thrombogenic in rats, rabbits, and dogs, causing blood platelet aggregation and acute heart failure. When diets containing 5 to 50% stearic acid (as the monoglyceride) were fed to weanling mice for 3 weeks, depression of weight gain was seen above the 10% dietary level. Mortality occurred only with the 50% diet. The effects were less noticeable in adult mice. Rats fed 5% stearic acid as part of a high-fat diet for 6 weeks, or 6% stearic acid for 9 weeks, showed a decreased blood clotting time and hyperlipemia. Rats fed 50 g/kg/day stearic acid for 24 weeks developed reversible lipogranulomas in adipose tissue. No significant pathological lesions were observed in rats fed 3000 ppm stearic acid orally for about 30 weeks, but anorexia, increased mortality, and a greater incidence of pulmonary infection were observed. Single intraperitoneal doses of stearic acid in mice, ranging from approximately 15 to 500 mg/kg, caused no fatalities, but at the highest dose level caused a loss of body weight. In cats, low doses of stearic acid produced elevated pulmonary but decreased systemic blood pressure. Doses greater than 5 mg caused apnea, a fall in blood pressure, and convulsions leading to death. Stearic acid was tested for mutagenicity using the Ames test with Salmonella typhimurium strains TA98, TA100, TA1535, TA1537, and TA1538. Stearic acid had no mutagenic activity over background in the strains tested with and without metabolic activation.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
A4：不能归类为人类致癌物。
A4: Not classifiable as a human carcinogen.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌物分类
对人类不具有致癌性（未被国际癌症研究机构IARC列名）。
No indication of carcinogenicity to humans (not listed by IARC).
来源:Toxin and Toxin Target Database (T3DB)
毒理性
暴露途径
该物质可以通过吸入其气溶胶和通过吞食被吸收进人体。
The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.
来源:ILO-WHO International Chemical Safety Cards (ICSCs)
毒理性
副作用
ACGIH 致癌物 - 未分类。
ACGIH Carcinogen - Not Classifiable.
来源:Haz-Map, Information on Hazardous Chemicals and Occupational Diseases
A mild moisturizing body wash with stearic acid, a key component of corneum lipids, and emollient soybean oil has been introduced in the market place. The objectives of this study are to determine the amount and the location of the stearic acid in the corneum after in vivo cleansing by the formulation. Clinical cleansing studies for one and five consecutive days were carried out with the formulation containing soybean oil or petroleum jelly (PJ). The free stearic acid in it was replaced by the fully deuterated variant. The amounts of stearic acid in 10 consecutive corneum tape strips were measured by liquid chromatograph-mass spectroscopy. Separately, electron paramagnetic resonance (EPR) measurements were taken with a porcine skin after a wash by the soybean oil formulation with its free fatty acid replaced by its spin probe analogue, 5-doxyl stearic acid. Deuterated stearic acid was detected in all 10 consecutive layers of stratum corneum and the total amount after five washes with the soybean oil formulation was 0.33 ug/sq cm. The spin probe in cleanser-treated skin was incorporated in a partially ordered hydrophobic region similar to corneum lipids. The probe mobility increased in the temperature region where lipid disorder was expected. The estimated total fatty acid delivered to skin from cleansing is comparable to the amount of fatty acid in a corneum layer. The delivered fatty acid is most likely incorporated in the corneum lipid phase.
It has been noted by several investigators that increasing fatty acid chain length slightly decreased their digestibility; stearic acid was the most poorly absorbed of the common fatty acids.
Oleic, palmitic, myristic, and stearic acids are primarily transported via the lymphatic system, and lauric acid is transported by the lymphatic and (as a free fatty acid) portal systems.
Radioactivity has been traced to the heart, liver, lung, spleen, kidney, muscle, intestine, adrenal, blood, and lymph, and adipose, mucosal, and dental tissues after administration of radioactive oleic, palmitic, and stearic acids.
