Cholesterin

Biological Agents -> Cholesterol and Derivatives

Hormone and(or) waste-water effluent contaminant

Cosmetic ingredients (Cholesterol) -> CIR (Cosmetic Ingredient Review)

Emulsifying; Emollient; Stabilizing

1.067 @ 20 °C/4 °C

Pearly leaflets or plates from dilute alcohol; becomes anhydrous at 70-80 °C; density 1.03; practically insoluble in water (about 0.2 mg/100 ml H2O); slightly soluble in alcohol (1.29% w/w at 20 °C); more soluble in hot alcohol (100 g of saturated 96% alcoholic solution contains 28 g at 80 °C); one gram dissolves in 2.8 ml ether, in 4.5 ml chloroform, in 1.5 ml pyridine. Also soluble in benzene petroleum, oils, fats. Soluble in aqueous solution of bile salts; optical rotation (20 °C/D) = -31.5 deg (c = 2 in ether); optical rotation (20 °C/D) = -39.5 deg (c= 2 in chloroform). /Monohydrate/

Moderately soluble in hot alcohol; soluble in benzene, oils, fats and aq solns of bile salts

In water, 0.095 mg/l @ 30 °C.

9.5e-05 mg/mL

This chemical does not meet GHS hazard criteria for 97.8% (222 of 227) of all reports.

Not Classified

Aggregated GHS information provided per 227 reports by companies from 4 notifications to the ECHA C&L Inventory.

Chemical: Cholest-5-en-3-ol, (3.beta.)-

REACH registered substance: Cholesterol (EC: 200-353-2)

Cholesterol: Does not have an individual approval but may be used under an appropriate group standard

Drug products containing active ingredients offered over-the-counter (OTC) for the treatment of boils. (a) ... /Cholesterol has/ been present in OTC boil treatment drug products. There is a lack of adequate data to establish general recognition of the safety and effectiveness of these or any other ingredient for OTC use for the treatment of boils. ... Based on evidence currently available, any OTC drug product offered for the treatment of boils cannot be considered generally recognized as safe and effective. (b) Any OTC drug product that is labeled, represented, or promoted for the treatment of boils is regarded as a new drug within the meaning of section 201(p) of the Federal Food, Drug, and Cosmetic Act (the act), for which an approved application or abbreviated application under section 505 of the act and part 314 of this chapter is required for marketing. In the absence of an approved new drug application or abbreviated new drug application, such product is also misbranded under section 502 of the act. (c) Clinical investigations designed to obtain evidence that any OTC boil treatment drug product is safe and effective for the purpose intended must comply with the requirements and procedures governing the use of investigational new drugs set forth in part 312 of this chapter. (d) After May 7, 1991, any such OTC drug product that contains ... cholesterol ... initially introduced or initially delivered for introduction into interstate commerce that is not in compliance with this section is subject to regulatory action.

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Ideal plasma cholesterol (total free plust cholesterol ester) levels for adults should be <5200 uM or about <200 mg/dL. Chronically high values of >6200 uM (>240 mg/dL) are considered high risk and can lead to heart disease, atherosclerosis and stroke. The desirable LDL level is considered to be less than 100 mg/dL (2.6 mM)

Cardiologists recommend that individuals 20 or older should be screened for high cholesterol at least once every five years, with more frequent screenings for anyone deemed to be at high risk for heart disease. The USDA recommends that those wishing to reduce their cholesterol through a change in diet should aim to consume less than 7% of their daily energy needs from saturated fat and fewer than 200 mg of cholesterol per day. Statin drugs (which are HMG-CoA reductase inhibitors) are effective at reducing the amount of cholesterol produced in the liver. The National Institute for Health and Clinical Excellence (NICE) recommends statin treatment for adults with an estimated 10-year risk of developing cardiovascular disease that is greater than 20%. Several types of cholesterol-lowering medication are available, including niacin, bile acid resins, dietary fiber, psyllium and fibrates. But statins are the treatment of choice for most individuals.

High plasma levels lead to hyperlipidemia or hypercholesterolemia which over a long period of time can lead to athersoclerosis, heart disease, stroke, poor kidney function. Extremely low levels of cholesterol (hypocholesterolemia) can lead to depression, cancer and cerebral hemorrhage. Chronically high levels of cholesterol are associated with at least 5 inborn errors of metabolism including: Cerebrotendinous Xanthomatosis, Cholesteryl ester storage disease, Congenital Lipoid Adrenal Hyperplasia, Hypercholesterolemia and Zellweger syndrome.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 16,000(SRC), determined from a water solubility of 0.095 mg/l(2) and a regression-derived equation(3), indicates that cholesterol is expected to be immobile in soil(SRC). Volatilization of cholesterol from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.7X10-4 atm-cu m/mole(SRC), using a fragment constant estimation method(4). However, volatilization from moist soil surfaces is expected to be attenuated by adsorption(SRC). Cholesterol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 7.8X10-10 mm(SRC), determined from a fragment constant method(5).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 16,000(SRC), determined from a water solubility of 0.095 mg/l(2) and a regression-derived equation(3), indicates that cholesterol is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 1.7X10-4 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 8.9 hours and 11 days, respectively(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment(SRC). The estimated volatilization half-life from a model pond is 145 years if adsorption is considered(5). According to a classification scheme(6), an estimated BCF of 270(SRC), from an estimated log Kow(2) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is high(SRC).

Drug products containing active ingredients offered over-the-counter (OTC) for the treatment of boils. (a) ... /Cholesterol has/ been present in OTC boil treatment drug products. There is a lack of adequate data to establish general recognition of the safety and effectiveness of these or any other ingredient for OTC use for the treatment of boils. ... Based on evidence currently available, any OTC drug product offered for the treatment of boils cannot be considered generally recognized as safe and effective. (b) Any OTC drug product that is labeled, represented, or promoted for the treatment of boils is regarded as a new drug within the meaning of section 201(p) of the Federal Food, Drug, and Cosmetic Act (the act), for which an approved application or abbreviated application under section 505 of the act and part 314 of this chapter is required for marketing. In the absence of an approved new drug application or abbreviated new drug application, such product is also misbranded under section 502 of the act. (c) Clinical investigations designed to obtain evidence that any OTC boil treatment drug product is safe and effective for the purpose intended must comply with the requirements and procedures governing the use of investigational new drugs set forth in part 312 of this chapter. (d) After May 7, 1991, any such OTC drug product that contains ... cholesterol ... initially introduced or initially delivered for introduction into interstate commerce that is not in compliance with this section is subject to regulatory action.

Cell degeneration in Alzheimer's disease is mediated by a toxic mechanism that involves interaction of the AbetaP peptide with the plasma membrane of the target cell. PC12 cells become resistant to the cytotoxic action of AbetaP when incubated in a medium that enriches cholesterol levels of the surface membrane. On the other hand, making cholesterol-deficient membranes by either cholesterol extraction with cyclodextrin or by inhibiting de novo synthesis of cholesterol makes PC12 cells more vulnerable to the action of AbetaP. Increasing cholesterol content of PS liposomes also suppresses AbetaP-dependent liposome aggregation. /The authors/ suggest that by modifying the fluidity of the neuronal membranes, cholesterol may modulate the incorporation and pore formation of AbetaP into cell membranes. This idea is supported by the finding that the enhanced cytotoxicity generated by lowering the membrane cholesterol content can be reversed by AbetaP calcium channel blockers Zn2+ and tromethamine.

Cholesterol itself in the animal system is the precursor of bile acids, steroid hormones, and provitamin D3.

Cholesterol is the substrate for steroid biosynthesis. Conversion of cholesterol to pregnenolone occurs in the mitochondria, and oxidative reactions catalyzed by P450 enzymes occur in the smooth endoplasmic reticulum and mitochondria. Sources of cholesterol include lipoprotein uptake from serum (LDL and HDL), de novo synthesis from acetate via the acetyl coenzyme A pathway, and hydrolysis of cholesteryl ester (CE) by neutral CE hydrolase (nCEH). The storage pool in the form of lipid droplets is derived principally from the conversion of free cholesterol to CE catalyzed by acyl coenzyme A: cholesterol acyltransferase (ACAT). Direct uptake of CE from serum to the storage pool is minimal in the rat.

Cholesterol introduced into the cecum of rats is changed to lithocholic and isolithocholic acids, which are partly excreted in the feces. In the guinea pig, the gut bacteria can metabolize cholesterol to estradiol and estrone, which are excreted in the urine.

Cholesterol is metabolized in the liver, the main metabolic pathway being conversion to the two primary bile acids, cholic acid and chenodeoxycholic acid. These, after conjugation with either glycine or taurine, pass into the intestine via the bile, where they may be further metabolized by bacterial enzymes to yield the secondary bile acids, deoxycholic acid and lithocholic acid. Cholesterol is also converted to other neutral sterols; in the liver, reduction yields cholestanol. In the intestine, the main metabolites produced by bacterial enzymes are coprostanol (a stereoisomer of cholestanol) and cholestanone. Although both bile acids and neutral sterols undergo enterohepatic recirculation, there is a net loss daily of about 250 mg cholesterol as bile acids and about 500 mg as neutral sterols.

For more Metabolism/Metabolites (Complete) data for CHOLESTEROL (6 total), please visit the HSDB record page.

Cholesterol is not readily biodegradable and is primarily eliminated in the feces as bile acids. Only the liver possesses the enzymes to degrade significant amounts. Cholesterol and its oxidized metabolites (oxysterols) are transferred back from peripheral tissues in lipoprotein complexes to the liver for catabolism by conversion to oxysterols and bile acids. The latter are exported into the intestines to aid digestion. Until recently, it was believed that approximately 90% of cholesterol elimination from the body occurred via bile acids in humans. However, experiments with animal models now suggest that a significant amount is secreted directly into the intestines by a process known as trans-intestinal cholesterol efflux.

Found in all body tissues, especially in the brain, spinal cord, and in animal fats or oils. Main constituent of gallstones.

Cholesterol is distributed universally in all animal tissues. It can be derived either from intestinal absorption of dietary cholesterol or from synthesis de novo within the body.

The fraction of dietary cholesterol absorbed is dependent on the intake; after reaching a plateau, the amount absorbed decreases with increased dietary intake. Most people in western societies ingest between 500 and 800 mg/day and absorb from 300 to 400 mg/day.

Cholesterol is absorbed from the gut via lymph. The primary site of absorption of dietary cholesterol is the proximal small intestine. Cholesterol is absorbed from the intestine after incorporation into chylomicrons, which are mixed micelles composed of triglycerides, phospholipids, protein and free and esterified cholesterol.

For more Absorption, Distribution and Excretion (Complete) data for CHOLESTEROL (6 total), please visit the HSDB record page.

CIR ingredient: Cholesterol

Main sterol of higher animals found in all body tissues; Used as an emulsifying agent for pharmaceuticals; [Merck Index] Also used as a raw material for syntheses; [HSDB]

Used in pharmaceutical and dermal preparations as an emulsifying agent.

... Important as raw material for syntheses involving microbiological degradation of the side chain.

Found in many foods (meats, eggs, milk, cheese, fish, shellfish) derived from animal products. Essential for membrane integrity. Used in steroid hormone synthesis.

Prepared commercially from the spinal cord of cattle by petroleum ether extraction of the nonsaponifiable matter. Also produced from wool grease.

Cholesterol is commercially prepared from bovine spinal cord and wool grease by extraction with petroleum ether. The extracted material is then purified by repeated bromination.