Metabolism / Metabolites
Lipids from the Gram-negative marine bacterium Marinobacter hydrocarbonoclasticus, cultured in synthetic seawater with acetate or n-eicosane as the sole carbon source, were isolated, purified, and their structures determined. Based on the sequence of steps employed, three distinct lipids were isolated: solvent-extractable “free” lipids, lipids released under alkaline conditions (“ester-bound” lipids), and lipids released through acid hydrolysis (“amide-bound” lipids). Even-numbered n-form fatty acids were identified in the “free” lipids from both acetate and n-eicosane cultures. In addition to these compounds, n-eicosane induced the formation of n-eicosane-1-ol and n-eicosane-11-en-1-ol, as well as a series of β-hydroxy acids with C12 to C20 carbon atoms. In the “ester-bound” lipids from both cultures, short-chain and long-chain fatty acids were identified, in addition to β-hydroxy C12:0 acids. These hydroxy acids were the major compounds identified in the "amide-bound" lipids of both cultures. Comparison of the analytical data from the two cultures, and the resulting differences in the composition of the "unbound" lipid pools, revealed the following metabolic pathway for n-eicosane: hydroxylation to a C20 primary alcohol, conversion to a C20 β-hydroxy acid, and subsequent degradation to lower homologues. In stark contrast, lipids in both the "ester-bound" and "amide-bound" lipid pools were almost unaffected by changes in nutrients. Lipids in E. coli were also detected in the same manner. This paper discusses the geochemical implications of these results, particularly the presence of "unbound" β-hydroxy acids in particulate matter and sediments.

Interactions
Long-chain fatty acids and alcohols, including 1-eicosanol, inhibited the specific binding of (3)H-labeled ouabain to canine cardiac granule components. The degree of inhibition increased with increasing chain length, reaching its maximum in saturated fatty acids, unsaturated fatty acids, and alcohols with lauric acid, myristoleic acid, and decanol, respectively, and then decreased with increasing homologue chain length. These alcohols, when used alone, did not significantly increase plasma alanine aminotransferase (ALT) or aspartate aminotransferase (AST) levels, but administration of carbon tetrachloride (CCl4) or chloroform (CHCl3) to animals that had already been treated with alcohol resulted in a significant increase in plasma transaminases. Eicosanol (a 20-carbon alcohol) did not enhance the toxicity of any halomethane. Methanol, ethanol, isopropanol, and decanol, when used in combination with carbon tetrachloride, caused severe liver damage but did not enhance the lethality of carbon tetrachloride. Tert-butanol, pentanol, hexanol, and octanol significantly reduced the median lethal dose (LD50) of carbon tetrachloride (CCl4). All alcohols enhanced the hepatotoxicity of chloroform (CHCl3) and significantly reduced its LD50. The alcohol-enhanced chloroform toxicity was greater than that of carbon tetrachloride. This study aimed to investigate: (i) whether a single subtoxic dose of alcohols could enhance the hepatotoxicity of carbon tetrachloride (CCl4) and chloroform (CHCl3); and (ii) whether this enhancement would lead to higher animal mortality. A series of homologous straight-chain alcohols were selected for this study. Equimolar doses (10 mmol/kg) of methanol, ethanol, isopropanol, tert-butanol, pentanol, hexanol, octanol, decanol, and eicosanol were tested. Male Sprague-Dawley rats (175 to 250 g) were orally administered various alcohols 18 hours before a single oral administration of carbon tetrachloride (CCl4) or chloroform (CHCl3). Liver injury was assessed 24 hours after treatment with halomethanes by plasma transaminase (alanine aminotransferase, ALT; aspartate aminotransferase, AST) and liver histopathological examination. Neither alcohol alone significantly increased plasma ALT or AST levels, while administration of CCl4 or CHCl3 to animals already treated with alcohols resulted in a significant increase in plasma transaminase levels. Eicosanol (a 20-carbon alcohol) did not enhance the toxicity of either halomethane. Methanol, ethanol, isopropanol, and decanol, when used in combination with CCl4, caused severe liver injury but did not enhance the lethality of CCl4. Tert-butanol, pentanol, hexanol, and octanol significantly reduced the LD50 of CCl4… In contrast, the alcohol-enhanced toxicity of CHCl3 was greater than that of CCl4.

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Non-Human Toxicity Values
Oral LD50 in rats > 10,000 mg/kg
Oral LD50 in rats > 64 mL/kg /Data from table/ /Mixed eicosanol isomers/
Skin LD50 in rabbits > 20 mL/kg /Data from table/ /Mixed eicosanol isomers/

[1]. Benzophenones from Hypericum carinatum. Journal of Natural Products, 01 May 2005, 68(5):784-786.

Eicosanol (1-eicosanol) is a long-chain primary fatty alcohol formed by replacing a terminal methyl hydrogen atom in an eicosanol molecule with a hydroxyl group. It is a plant metabolite, a volatile oil component, and a human metabolite. It is both a long-chain primary fatty alcohol and an eicosanol. It has been reported that 1-eicosanol is found in Pyracantha angustifolia, Plumeria rubra, and several other organisms with relevant data.

C20H42O

298.55

298.323

629-96-9

1-Eicosanol-d41; 349553-89-5

12404

White to off-white solid

0.8±0.1 g/cm3

309.0±0.0 °C at 760 mmHg

66.1 °C ; 66.1 °C

141.6±5.2 °C

0.0±1.4 mmHg at 25°C

1.453

9.38

1

1

18

21

167

0

O([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])C([H])([H])[H]

BTFJIXJJCSYFAL-UHFFFAOYSA-N

InChI=1S/C20H42O/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-18-19-20-21/h21H,2-20H2,1H3

icosan-1-ol

Arachidyl alcohol; 1-Eicosanol; Icosyl Alcohol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: 2 mg/mL (6.70 mM)
H2O: < 0.1 mg/mL

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)