Ergosterol
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Ergosterol
structure -
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CAS No:
57-87-4
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Formula:
C28H44O
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Chemical Name:
Ergosterol
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Synonyms:
Ergosta-5,7,22-trien-3-ol,(3β,22E)-;Ergosterol;(3β,22E)-Ergosta-5,7,22-trien-3-ol;Ergosterin;Provitamin D2;Provitamin D;24-Methylcholesta-5,7,22-trien-3β-ol;24R-Methylcholesta-5,7,22E-trien-3β-ol;24α-Methyl-22E-dehydrocholesterol;(24R)-Ergosta-5,7,22-trien-3β-ol;(22E,24R)-Ergosta-5,7,22-trien-3β-ol;3β-Hydroxyergosta-5,7,22-triene;18844-74-1;37571-51-0;2170258-75-8
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CAS No:
Description
Ergosterol is the primary sterol found in fungi, with antioxidative, anti-proliferative, and anti-inflammatory effects.
Solid
Ergosterol is a phytosterol consisting of ergostane having double bonds at the 5,6-, 7,8- and 22,23-positions as well as a 3beta-hydroxy group. It has a role as a fungal metabolite and a Saccharomyces cerevisiae metabolite. It is a 3beta-sterol, an ergostanoid and a member of phytosterols.|A steroid of interest both because its biosynthesis in FUNGI is a target of ANTIFUNGAL AGENTS, notably AZOLES, and because when it is present in SKIN of animals, ULTRAVIOLET RAYS break a bond to result in ERGOCALCIFEROL.|A steroid occurring in FUNGI. Irradiation with ULTRAVIOLET RAYS results in formation of ERGOCALCIFEROL (vitamin D2).
Ergosterol Basic Attributes
396.64800
396.65
200-352-7
Z30RAY509F
Small hydrated plates from alcohol, in hydrated needles from ether. The best crystalized form contains 1 1/2 mol H2O|Platelets from water, alcohol; needles from ethyl ether|Colorless crystals
29334900
Characteristics
20.23000
7.33080
Solid
1.04 g/cm3
170 °C
250 °C @ Press: 0.01 Torr
216.3ºC
-112.5 ° (C=1, THF)
Practically insoluble in water
2-8ºC
1.04X10-9 mm Hg at 25 deg C (est)
Specific optical rotation: -135 deg (in chloroform)
MP: 157-158 °C; Specific optical rotation: -75 deg at 19 °C/D ( c = 2.1 in CHCl3) /22,23-Dihydro acetate/|A plant sterol widely distributed in nature|Hydroxyl radical reaction rate constant = 3.51X-10 cu cm/molec-sec at 25 °C (est)
Safety Information
II
6.1
UN 2811
3
R28
S28-S36/37-S45
T+
Stable, but may be light or air sensitive. Incompatible with acids, strong oxidizing agents.
P261-P281-P305 + P351 + P338-P311
H302-H315-H319-H331-H336-H351-H361d-H372
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.
|Danger|H300 (13.33%): Fatal if swallowed [Danger Acute toxicity, oral]|P264, P270, P273, P301+P310, P321, P330, P405, and P501|Aggregated GHS information provided by 46 companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.
Ergosterol concentrations in digested sludges collected from four French municipal wastewater treatment plants in Lyon (Saint Fons, 11/18/1993) and Paris (Asnieres/Oise, 8/26/1991; Acheres, 1/26/1993; Evry 6/8/1993) were at <0.1, <0.1, <0.1, and 0.02 mg/g dried matter, respectively(1).
SOIL: Ergosterol concentrations in Italian agricultural soils subjected to 3 different treatments (sewage sludge applications, irrigation by saline waters, and contamination by flood waters containing industrial and municipal sludge) were 2, 4.7, and 5 mg/kg in samples from Cremona, Bari, and Naples, respectively(1).
RURAL/REMOTE: The ergosterol concentration in subtropical air from an unspecified location was estimated as approximately 230 pg/sq m(SRC), based upon the weighted-average concentration in fungal spores commonly encountered in subtropical ambient air of 0.191 pg/spore(1).
Toxicity
MURINE LEUKEMIA CELLS (L1210) GROWN IN MEDIUM CONTAINING ERGOSTEROL (40 UG/ML) THEN EXPOSED BRIEFLY TO AMPHOTERICIN B (0-10 UG/ML) WERE MORE SENSITIVE TO THE ANTIBIOTIC THAN WERE CONTROLS.|AFTER 4-HR GROWTH PERIOD IN PRESENCE OF 5X10-9 MOLES KETOCONAZOLE, ACETATE INCORPORATION INTO ERGOSTEROL BY CANDIDA ALBICANS WAS INHIBITED APPROXIMATELY 50%.|INHIBITION OF ERGOSTEROL BIOSYNTHESIS IN CANDIDA ALBICANS BY THE ANTIFUNGAL AGENT MICONAZOLE NITRATE WAS INVESTIGATED AFTER IN VITRO CONTACT WITH THE DRUG FOR 1, 4, 16, & 24 HR.|The functions and biosynthesis of sterols have been effective targets for fungal control in different areas, including pharmaceutical and agricultural applications. Fungi are among the organisms that synthesize sterols, principally ergosterol. In this paper, the effect of dibutyryl-cAMP (db-cAMP) on ergosterol level and the interaction of drugs that would change the concentration of cAMP with antifungal drugs have been investigated. Sterols were extracted from Candida albicans, and ergosterol was measured using the gas chromatography method. The interaction of different agents was measured by the broth dilution method. It was found that phosphodiesterase inhibitors reverse the inhibitory activity of azole antifungal drugs. Evaluating the ergosterol level of C. albicans incubated with db-cAMP revealed that it increased ergosterol level. Further experiments provided evidence attributing the observed interaction between azoles and phosphodiesterase inhibitors to the relationship between ergosterol and cAMP. The possible significance of this interaction includes potentiation of antifungal activity of drugs by manipulating the cAMP level.|For more Interactions (Complete) data for ERGOSTEROL (6 total), please visit the HSDB record page.
/AQUATIC SPECIES/ In crustaceans, cholesterol is an essential nutrient, which they must directly obtain from their food or by bioconversion from other dietary sterols. Eukaryotic phytoplankton contain a great variety of sterols that differ from cholesterol in having additional substituents or different positions and/or number of double bonds in the side chain or in the sterol nucleus. ... This study ... investigated to what extent these structural features affect the growth and reproduction of Daphnia galeata in standardized growth experiments with the cyanobacterium Synechococcus elongatus supplemented with single sterols as food source. The results indicated that delta 5 (sitosterol, stigmasterol, desmosterol) and delta 5.7 (7-dehydrocholesterol, ergosterol) sterols meet the nutritional requirements of the daphnids, while the delta 7 sterol lathosterol supports somatic growth and reproduction to a significantly lower extent than cholesterol. Dihydrocholesterol (delta 0) and lanosterol (delta 8) did not improve the growth of D. galeata, and growth was ad versely affected by the delta 4 sterol allocholesterol. Sterols seem to differ in their allocation to somatic growth and reproduction. Thus, structural differences of dietary sterols have pronounced effects on life-history traits of D. galeata.
Ergosterol is a plant sterol that is widely distributed in nature(1). Twelve species and strains of fungal spores and yeast cells commonly found in the subtropical ambient air as well as mold spores(3) were shown to contain ergosterol(2).
Ergosterol's production and use as a vitamin and pharmaceutical intermediate(1) may result in its release to the environment through various waste streams(SRC).
TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 2.5X10+6(SRC), determined from a structure estimation method(2), indicates that ergosterol is expected to be immobile in soil(SRC). Volatilization of ergosterol from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.6X10-4 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Ergosterol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.0X10-9 mm Hg at 25 °C(SRC), determined from a fragment constant method(4). However, adsorption to soil is expected to attenuate volatilization(SRC). The soil microbe Nocardia erthopolis was able to grow on ergosterol(5).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 2.5X10+6(SRC), determined from a structure estimation method(2), indicates that ergosterol 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 1.6X10-4 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 9 hours and 11 days, respectively(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The estimated volatilization half-life from a model pond is 2.1X10+4 years if adsorption is considered(5). According to a classification scheme(6), an estimated BCF of 1,600(SRC), from an estimated log Kow of 8.86(7) and a regression-derived equation(8), suggests the potential for bioconcentration in aquatic organisms is very high, provided the compound is not metabolized by the organism(SRC). Aquatic biodegradation data were not available(SRC, 2009).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), ergosterol, which has an estimated vapor pressure of 1.0X10-9 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely in the particulate phase in the ambient atmosphere. Particulate-phase ergosterol may be removed from the air by wet or dry deposition(SRC). When irradiated with uv light, ergosterol develops powerful vitamin D2 activity(5) and therefore the compound is expected to be susceptible to direct photolysis by sunlight(SRC).
Ergosterol is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(1). When irradiated with uv light, ergosterol develops powerful vitamin D2 activity with a main irradiation product being lumisterol(2); therefore the compound is expected to be susceptible to direct photolysis by sunlight(SRC).
An estimated BCF of 1,600 was calculated in fish for ergosterol(SRC), using an estimated log Kow of 8.86(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is very high(SRC), provided the compound is not metabolized by the organism(SRC).
Using a structure estimation method based on molecular connectivity indices(1), the Koc of ergosterol can be estimated to be 2.5X10+6(SRC). According to a classification scheme(2), this estimated Koc value suggests that ergosterol is expected to be immobile in soil.
The Henry's Law constant for ergosterol is estimated as 1.6X10-4 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that ergosterol is expected to volatilize from water surfaces(2). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(2) is estimated as 9 hours(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is estimated as 11 days(SRC). Ergosterol's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). The volatilization half-life from a model pond is about 2.1X10+4 years when adsorption is considered(4). Ergosterol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.0X10+9 mm Hg(SRC), determined from a fragment constant method(3).
Vitamin D is excreted into breast milk in limited amounts. A direct relationship exists between maternal serum levels of vitamin D and the concentration in breast milk. Chronic maternal ingestion of large doses may lead to greater than normal vitamin D activity in the milk and resulting hypercalcemia in the infant. /Vitamin D/
Occupational exposure to ergosterol may occur through inhalation and dermal contact with this compound at workplaces where ergosterol is produced or used. Monitoring and use data indicate that limited general population exposure to ergosterol may occur via inhalation of ambient air and ingestion of contaminated water and consumer products containing ergosterol. (SRC)
Drug Information
Very high levels of vitamin D have been used to treat maternal hypoparathyroidism during pregnancy. In two studies, 15 mothers were treated with doses averaging 107,000 IU/day throughout their pregnancies to maintain maternal calcium levels within the normal range. All of the 27 children were normal at birth & during follow up examinations, ranging up to 16 years. /Vitamin D/|... Irradiated ergosterol from yeast became the major vitamin D source for food fortification and the treatment of rickets, leading to a public health campaign to eradicate rickets by the 1930s. /Irradiated ergosterol/
Vitamin D is excreted into breast milk in limited amounts. A direct relationship exists between maternal serum levels of vitamin D & the concn in breast milk. Chronic maternal ingestion of large doses may lead to greater than normal vitamin D activity in the milk & resulting hypercalcemia in the infant. /Vitamin D/
Precursor forms of vitamins. (See all compounds classified as Provitamins.)
Vitamin D is excreted into breast milk in limited amounts. A direct relationship exists between maternal serum levels of vitamin D & the concn in breast milk. Chronic maternal ingestion of large doses may lead to greater than normal vitamin D activity in the milk & resulting hypercalcemia in the infant. /Vitamin D/|The results of experiments on rats given the ergosterol-containing diet for a long time indicate that ergosterol was incorporated in liver tissues in trace amounts which are not comparable with ergosterol concentrations exerting an effect in model experiments. Ergosterol was not detected in the liver after 3-day experiments. At the same time it was established that the proportion of unchanged ergosterol in rat feces was about 16% of the amount administered per os. The products of a possible ergosterol transformation (dehydroneoergosterol-24-methyl-1,3,5 (10), 6,8 (9), 22-hexaen-3 beta-ol; 24-methylcholesta-7,24 (28)-dien-3 beta-ol; 4-cholesta-7,22,25 (?)-trien-3 beta-ol; 4-methylcholesta-7,22 (?)-dien-3 beta-ol, and so forth were identified in feces.
... The metabolism of ergosterol by cytochrome P450scc /is demonstrated/ in either a reconstituted system or isolated adrenal mitochondria. The major reaction product was identified as 17alpha,24-dihydroxyergosterol. Purified P450scc also generated hydroxyergosterol as a minor product, which is probably an intermediate in the synthesis of 17alpha,24-dihydroxyergosterol. In contrast to cholesterol and 7-dehydrocholesterol, cleavage of the ergosterol side chain was not observed. NMR analysis clearly located one hydroxyl group to C24, with evidence that the second hydroxyl group is at C17. 17alpha,24-Dihydroxyergosterol inhibited cell proliferation of HaCaT keratinocytes and melanoma cells. Thus, in comparison with cholesterol and 7-dehydrocholesterol, the 24-methyl group and the C22-C23 double bond of ergosterol prevent side chain cleavage by P450scc and change the enzyme's hydroxylase activity from C22 and C20, to C24 and C17, generating bioactive product.|In order to investigate the effect of the different stereochemistry of C-24 on the microbial C-26 oxidation of sterol side-chain the genetically modified Mycobacterium sp. BCS 396 strain was used to transform erogsterol. Ergosterol was converted to 3-oxo-4,22-ergostadien-26-oic acid methyl ester, 3-oxo-1,4,22-ergostatrien-26-oic acid methyl ester, and 3-oxo-1,4,22-ergostatrien-26-oic acid, the structures of which have been determined by IR, 1H NMR, 13C NMR, and mass spectroscopy. The X-ray structure of 3-oxo-4,22-ergostadien-26-oic acid methyl ester revealed that oxidation at C-26 of the ergostane side-chain generates a chiral center with S-configuration at C-25 as a result of chiral induction of the C-24 center.|The results of experiments on rats given the ergosterol-containing diet for a long time indicate that ergosterol was incorporated in liver tissues in trace amounts which are not comparable with ergosterol concentrations exerting an effect in model experiments. Ergosterol was not detected in the liver after 3-day experiments. At the same time it was established that the proportion of unchanged ergosterol in rat feces was about 16% of the amount administered per os. The products of a possible ergosterol transformation (dehydroneoergosterol-24-methyl-1,3,5 (10), 6,8 (9), 22-hexaen-3 beta-ol; 24-methylcholesta-7,24 (28)-dien-3 beta-ol; 4-cholesta-7,22,25 (?)-trien-3 beta-ol; 4-methylcholesta-7,22 (?)-dien-3 beta-ol, and so forth were identified in feces.|Metabolism of orally administered ergosterol (Erg) ... in rats and ... vitamin D biological activity were investigated. Most of orally administered Erg ... /was/ excreted in feces and the remaining sterols were absorbed through intestine. The absorbed sterols were not transported in skin as the intact forms but metabolized into brassicasterol and cholesterol, respectively, within 25 hr. Neither increment of intestinal calcium absorption nor plasma calcium concentrations were observed by oral administration of Erg ... to vitamin D-deficient rats...|The chick-oviduct assay was used to investigate the effects of dietary ergosterol on the response to oral progestogens and estrogens. Progestogens alone had no effect on the oviduct but the hypertrophy due to estrogen was greatly enhanced by simultaneous treatment with progestogen at all dose levels tested. Ergosterol had no effect on any of the responses of the oviduct studied.
... A new member of the F-box family, Pof14, which forms a canonical, F-box dependent SCF (Skp1, Cullin, F-box protein) ubiquitin ligase complex /is described/. The Pof14 protein has intrinsic instability that is abolished by inactivation of its Skp1 interaction motif (the F-box), Skp1 or the proteasome, indicating that Pof14 stability is controlled by an autocatalytic mechanism. Pof14 interacts with the squalene synthase Erg9, a key enzyme in ergosterol metabolism, in a membrane-bound complex that does not contain the core SCF components. pof14 transcription is induced by hydrogen peroxide and requires the Pap1 transcription factor and the Sty1 MAP kinase. Pof14 binds to and decreases Erg9 activity in vitro and a pof14 deletion strain quickly loses viability in the presence of hydrogen peroxide due to its inability to repress ergosterol synthesis. A pof14 mutant lacking the F-box and an skp1-3 ts mutant behave as wild type in the presence of oxidant showing that Pof14 function is independent of SCF. This indicates that modulation of ergosterol level plays a key role in adaptation to oxidative stress.|The continuous use of triazoles can result in the development of drug resistance. Azole-resistant clinical isolates, spontaneous and induced mutants of Aspergillus fumigatus have been documented. The azoles block the ergosterol biosynthesis pathway by inhibiting the enzyme 14-alpha-demethylase, product of the CYP51. Fungal azole resistance involves both amino acid changes in the target site that alter drug-target interactions and those that decrease net azole accumulation. The reduced intracellular accumulation has also been correlated with overexpression of multidrug resistance (MDR) efflux transporter genes of the ATP-binding cassette (ABC) and the major facilitator superfamily (MFS) classes. About 20 genes are involved in the A. fumigatus ergosterol biosynthesis pathway. There are several duplicated genes in this pathway. Interestingly, erg3 and erg11 showed two copies in A. fumigatus. In general, Aspergillus spp. have proportionally more MFS transporter encoding genes than Saccharomyces cerevisiae, S. pombe, and Neurospora crassa. The drug H+ (12 and 14 spanners) sub-families are also proportionally greater than in the other species. Although the numbers of ABC transporter encoding genes are comparable, again the Aspergillus spp. have more ABC transporters related to multidrug permease than the other fungal species.|The human pathogen Candida albicans is responsible for a large proportion of infections in immunocompromised individuals, and the emergence of drug-resistant strains is of medical concern. Resistance to antifungal azole compounds is often due to an increase in drug efflux or an alteration of the pathway for synthesis of ergosterol, an important plasma membrane component in fungi. However, little is known about the transcription factors that mediate drug resistance. In Saccharomyces cerevisiae, two highly related transcriptional activators, Upc2p and Ecm22p, positively regulate the expression of genes involved in ergosterol synthesis (ERG genes). ... A homologue in C. albicans of the S. cerevisiae UPC2/ECM22 genes ... named ... UPC2 /has been identified/. Deletion of this gene impaired growth under anaerobic conditions and rendered cells highly susceptible to the antifungal drugs ketoconazole and fluconazole. Conversely, overexpression of Upc2p increased resistance to ketoconazole, fluconazole, and fluphenazine. Azole-induced expression of the ERG genes was abolished in a Delta upc2 strain, while basal levels of these mRNAs remained unchanged. Importantly, the purified DNA binding domain of Upc2p bound in vitro to putative sterol response elements in the ERG2 promoter, suggesting that Upc2p increases the expression of the ERG genes by directly binding to their promoters. These results provide an important link between changes in the ergosterol biosynthetic pathway and azole resistance in this opportunistic fungal species.|Ergosterol, a typical fungal sterol, induced in tobacco (Nicotiana tabacum L. cv. Xanthi) suspension cells the synthesis of reactive oxygen species and alkalization of the external medium that are dependent on the mobilization of calcium from internal stores. ... Specific inhibitors /were used/ to elucidate the signal pathway triggered by ergosterol compared with cryptogein, a proteinaceous elicitor of Phytophthora cryptogea. Herbimycin A and genistein, inhibitors of tyrosine protein kinases, had no effect on the oxidative burst and pH changes induced by both elicitors. Similarly, H-89, an inhibitor of protein kinase A, had no effect on the induction of these defense reactions. However, the response to both elicitors was completely blocked by NPC-15437, a specific inhibitor of animal protein kinase C (PKC). The responses induced by cryptogein but not those induced by ergosterol were inhibited by U73122 and neomycin, inhibitors of phospholipase C (PLC). On the other hand, the activity of phospholipase A2 (PLA2) measured using a fluorogenic substrate was stimulated by ergosterol and not by cholesterol and cryptogein. A specific inhibitor of PLA2, arachidonic acid trifluoromethyl ketone (AACOCF3), inhibited the pathway stimulated by ergosterol but not that induced by cryptogein. These results suggest that the cryptogein-induced signal pathway leading to the oxidative burst and DeltapH changes includes PLC and PKC, whereas this response induced by ergosterol includes PLA2 and PKC.|For more Mechanism of Action (Complete) data for ERGOSTEROL (7 total), please visit the HSDB record page.
The best crystalline form contains 1 1/2 molecules of water ...
/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 if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the 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. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. 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 ... . Anticipate seizures 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 ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/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. 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 if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/|TREATMENT OF HYPERVITAMINOSIS D CONSISTS IN IMMEDIATE WITHDRAWAL OF VITAMIN, LOW-CALCIUM DIET, ADMIN OF GLUCOCORTICOIDS, & GENEROUS INTAKE OF FLUID. ... A CONSPICUOUS IMPROVEMENT IN RENAL FUNCTION IS OFTEN NOTED WITH RETURN OF PLASMA CALCIUM TO NORMAL, BUT THIS MAY NOT OCCUR IF RENAL DAMAGE HAS BEEN SEVERE. /VITAMIN D/
/SIGNS AND SYMPTOMS/ Initial...symptoms of vitamin D toxicity are...associated with hypercalcemia and consist in weakness, fatigue, lassitude, headache, nausea, vomiting, and diarrhea. Early impairment of renal function...manifest by polyuria, polydipsia, nocturia, decreased urinary concentrating ability and proteinuria. /Vitamin D/|/SIGNS AND SYMPTOMS/ With prolonged hypercalcemia there may be deposition of calcium salts in soft tissues, most significantly within kidney.../resulting/ in nephrolithiasis, diffuse nephrocalcinosis, or both. Other sites of calcification may include blood vessels, heart, lungs, and skin. /Vitamin D/|/SIGNS AND SYMPTOMS/ Some individuals exhibit hypertension. ...Changes in blood chemistry are elevated concentrations of plasma calcium and nonprotein nitrogen; phosphate concentrations are variable. Mobilization of calcium from bone contributes to hypercalcemia and is...responsible for...osteoporosis in...hypervitaminosis D. /Vitamin D/|/SIGNS AND SYMPTOMS/ Vitamin D toxicity may be manifested in fetus. There is...relationship between excess maternal vitamin D intake or extreme sensitivity to vitamin and nonfamilial congenital supravalvular aortic stenosis. In infants, this anomaly is often found...with other stigmata of hypercalcemia. /Vitamin D/|For more Human Toxicity Excerpts (Complete) data for ERGOSTEROL (12 total), please visit the HSDB record page.
D2, Pro-Vitamin
Ergosterol Use and Manufacturing
EXTRACTION OF TOTAL FAT FROM YEAST, SAPONIFICATION, REEXTRACTION OF THE UNSAPONIFIABLE PORTION WITH ETHER, FOLLOWED BY DRYING & RECRYSTALLIZATION|Usually obtained from yeast which synthesizes it from simple sugars such as glucose. Damp yeast yields about 2.5% ergosterol, the variety of yeast being very important.|Isoln procedure: Green et al, US pat 3,006932 (1961 to Vitamins Ltd.)|Synthesized by yeast from simple sugars, obtained from fungus ergot.
Chemical intermediate for vitamin d2.
(1972) PROBABLY GREATER THAN 4.54X10+5 GRAMS|(1975) GREATER THAN 4.54X10+5 GRAMS
ESSENTIALLY 100% AS A CHEM INT FOR VITAMIN D2 (1976)
Usually obtained from yeast which synthesizes it from simple sugars such as glucose. Damp yeast yields about 2.5% ergosterol, the variety of yeast being very important.
RATIONALIZATION OF THE CHROMATOGRAPHIC BEHAVIOR OF VITAMIN D2/D3 IN ADSORPTION HPLC IS DERIVED FROM CONSIDERATION OF THE RALATIVE PLANARITY OF THE MOLECULES & STEREOCHEMICAL CONFORMATIONS ADOPTED IN SOLN.|SIMULTANEOUS DETERMINATION OF 8 VITAMINS D2 ISOMERS BY PROTON MAGNETIC RESONANCE SPECTROSCOPY.|SPECTROPHOTOMETRIC ANALYSIS OF MULTICOMPONENT MIXTURES OF 3,5-DINITROBENZOATES IN THE PRODN OF VITAMIN D2 IS PRESENTED.|Method: EPA-OW/OST 1698; Procedure: high resolution gas chromatography combined with high resolution mass spectrometry; Analyte: ergosterol; Matrix: multi-media environmental samples; Detection Limit: 20 nanograms/L.
Lipids -> Sterol Lipids [ST] -> Sterols [ST01] -> Ergosterols and C24-methyl derivatives [ST0103]|Cosmetics -> Undefined function
Computed Properties
Molecular Weight:396.6
XLogP3:7.4
Hydrogen Bond Donor Count:1
Hydrogen Bond Acceptor Count:1
Rotatable Bond Count:4
Exact Mass:396.339216023
Monoisotopic Mass:396.339216023
Topological Polar Surface Area:20.2
Heavy Atom Count:29
Complexity:712
Defined Atom Stereocenter Count:8
Defined Bond Stereocenter Count:1
Covalently-Bonded Unit Count:1
Compound Is Canonicalized:Yes
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