2,6,10,14-テトラメチルペンタデカン

Colorless, transparent; stable liquid

Mobile, transparent, stable liquid

In water, 1.0X10-8 mg/L at 25 °C

Soluble in most organic solvents

Very soluble in benzene, ether, chloroform, petroleum ether

Soluble in carbon tetrachloride

296 °C

296.00 °C. @ 760.00 mm Hg

-60 °C /freezing point/

-100 °C

Transparent liquid; [Merck Index] Colorless liquid; [Sigma-Aldrich MSDS]

Liquid

1712；1708；1710；1709；1708；1709；1709；1712；1696；1710；1709；1709

1703.7；1703；1703；1702；1707；1681；1682；1684；1685；1685；1687；1687；1687；1687；1688；1692；1697；1681.9；1687；1687

1664；1655；1669；1671；1672；1670；1672；1668；1664；1675；1675

This chemical does not meet GHS hazard criteria for 2.2% (1 of 46) of reports.

Warning

H315 (97.8%): Causes skin irritation [Warning Skin corrosion/irritation]；H319 (95.7%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]

P264, P264+P265, P280, P302+P352, P305+P351+P338, P321, P332+P317, P337+P317, and P362+P364 (click each P-code to see the statement)

Aggregated GHS information provided per 46 reports by companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.；Reported as not meeting GHS hazard criteria per 1 of 46 reports by companies.；There are 2 notifications provided by 45 of 46 reports by companies with hazard statement code(s).；Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

Chemical: Pentadecane, 2,6,10,14-tetramethyl-

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

A severe skin irritant; Causes changes in liver and spleen weights, changes in blood serum composition, and inflammatory effects in acute intraperitoneal studies of mice; [RTECS] Causes burns; Inhalation may cause corrosive injuries to upper respiratory tract and lungs; [Sigma-Aldrich MSDS]

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Environmental precautions: Do not let product enter drains. Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal.

SRP: 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 air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material; Contaminated packaging: Dispose of as unused product.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Environmental precautions: Do not let product enter drains.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid inhalation of vapor or mist.

Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Eye/face protection: Safety glasses with side-shields conforming to EN166 Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

Skin protection: Handle with gloves.

Body Protection: Impervious clothing. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face respirator with multipurpose combination (US) or type ABEK (EN 14387) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

... We have investigated the effect of the potent bisphosphonate, zoledronic acid (ZOL), on the development of pristane (2,6,10,14-tetramethylpentadecane)-induced plasmacytoma (PCT) in six-week-old BALB/c mice. Different groups of pristane-treated mice also received ZOL (100 ug/kg) commencing after the development of PCT or ZOL (20 ug/kg) from the first day. Control groups received pristane alone, ZOL alone (20 ug/kg), or phosphate-buffered saline. The study was terminated on day 300, and the remaining mice were autopsied and abdominal tissues were examined histologically for PCT. Statistical analysis revealed a significant delay in PCT development in the group receiving pristane plus ZOL (20 ug/kg) from the first day compared to the groups receiving pristane alone and pristane combined with ZOL (100 ug/kg) after the appearance of PCT (Log-rank, p=0.0001 and 0.0001; respectively). Kaplan-Meier analysis revealed a significant difference in survival between the group treated with pristane alone and the groups receiving pristane plus ZOL (20 ug/kg) from the first day or ZOL (100 ug/kg) after the appearance of PCT (Log-rank, p=0.016 and 0.023; respectively). These results indicate a direct anti-tumor effect of ZOL in pristane-induced PCT development BALB/c mice, which may contribute to their significantly increased survival. This hypothesis should now be further investigated in clinical trials.

We investigated the protective role of chloroquine against pristane-induced macrophage activation, oxidative stress, and Th1/Th2 skewness in C57BL/6J mice. Those mice were treated with pristane alone or combined with chloroquine. Hematological and biochemical parameters, macrophage phagocytic function, the oxidant/antioxidant index, cytokine for IFN-gamma, TNF-alpha, IL-4, and IL-6, and the isotypes of IgG2a and IgG1 were determined. And the expression of T-bet/GATA-3 and IL-12/IL-10 mRNA in spleen were analyzed by real-time PCR. We found that pristane treatment for a period of 12 or 24 weeks triggered macrophage activation syndrome, characterized by hemophagocytosis in spleen and peripheral blood, enhanced lipid phagocytosis by peritoneal macrophages in vitro, erythropenia and leucopenia, increased anti-Smith, lactic dehydrogenase, triglyceride, and ferritin, as well as hypercytokinemia of IFN-gamma, TNF-alpha, IL-4, and IL-6. In parallel, a significant increase in lipid peroxidation and a decrease in superoxide dismutase, glutathione, and catalase activity, as well as a skewed Th1/Th2 balance in spleen, were observed. However, chloroquine supplementation showed a remarkable amelioration of these abnormalities. Our data indicate that pristane administration induces macrophage activation, oxidative stress, and Th1/Th2 skewness, which can be attenuated by chloroquine.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1.8X10+5(SRC), determined from a structure estimation method(2), indicates that pristane is expected to be immobile in soil(SRC). Volatilization of pristane from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 68 atm-cu m/mole(3). However, adsorption to soil is expected to attenuate volatilization(SRC). Pristane is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 4.4X10-3 mm Hg at 25 °C(SRC), determined from a fragment constant method(2). Pristane achieved 4 to 68% biodegradation in various sediment/marine water inoculums, indicating that biodegradation of pristane is an important environmental fate process in soil under certain environmental conditions(4).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1.8X10+5(SRC), determined from a structure estimation method(2), indicates that pristane 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 68 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 1.7 hours and 6.5 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 greater than 2 years if adsorption is considered(5). According to a classification scheme(6), an estimated BCF of 230(SRC), from an estimated log Kow of 9.38(2)and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is high(SRC). Pristane has a reported half-life of 4.3 days in unacclimated pond water and achieved 4 to 68% biodegradation in various sediment/marine water inoculums, indicating that biodegradation of pristane is an important environmental fate process in water under certain environmental conditions(7,8).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), pristane, which has an estimated vapor pressure of 4.4X10-3 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist almost entirely as a vapor in the ambient atmosphere. Vapor-phase pristane is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 16 hours(SRC), calculated from its rate constant of 2.4X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Pristane does not contain chromophores that absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

IDENTIFICATION AND USE: Pristane is a colorless, transparent liquid. It is used as lubricant, transformer oil and anti-corrosion agent. It is also used as biological marker and in experimental systems to induce plasmacytomas, in production of monoclonal antibodies. HUMAN EXPOSURE AND TOXICITY: Pristane induces cell death in human cells (monocytic cell line). ANIMAL STUDIES: Pristane induced arthritis and lupus in rodents sharing clinical and pathological features with the human diseases rheumatoid arthritis and systemic lupus erythematosus, respectively. Pristane, delivered in vitro as an inclusion complex with beta-cyclodextrin, resulted in 1.7-fold and 6.2-fold increases of mutant frequencies over controls in a cell line of rat fibroblasts and primary mouse B lymphocytes, respectively. Pristane treatment affects CYP isozyme expression in rat tissues.

/BIRDS and MAMMALS/ Whole body and liver analyses indicated that wintering redheads (Aythya americana; n = 70) in coastal Louisiana (one site) and Texas (two sites) were relatively free of contamination with common trace elements, organochlorines, and hydrocarbons. Most trace elements, including As, Cr, Hg, Mg, Mn, Ni, Pb, Se, Sr, and Zn, were within background concentrations in livers; levels of B, Cd, Cu, and Fe were elevated in some specimens. Only one organochlorine, DDE, was detected in redhead carcasses, but its concentration was below reported toxic levels in waterfowl. Body burdens of aliphatic and aromatic hydrocarbons were generally low, but levels of pristane, total hydrocarbons, and the ratios of phytane:n-octadecane and pristane:n-heptadecane were indicative of possible chronic exposure to petroleum. ...

/AQUATIC SPECIES/ Embryonic inland silversides, Meinida beryllina, were exposed to neutral, water-soluble fractions (WSFs) resulting from microbial degradation of artificially weathered Alaska North Slope (ANS) crude oil. Three individual microbes obtained from Prince William Sound, Alaska, and designated Phe#6 (enriched on phenanthrene), Hexaco#2 (enriched on the straight-chain alkane, hexacosane), and EI2V (grown by enrichment on Bushnell-Haas medium containing 0.2% pristane, a branched alkane) were used to individually biodegrade weathered ANS crude oil for 14 days in darkness in 20-L glass carboys containing nutrient enriched, sterilized 20% salinity sea water at 20 +/- 1 degrees C. Neutral WSFs resulting from biodegradation of ANS (lot 521) by each microbe were recovered and weighted. Neutral WSFs recovered were: 1.76 mg/L for Phe#6, 1.85 mg/L for Hexaco#2, and 13.02 mg/L for the EI2V microbe. Embryo toxicity and teratogenicity tests revealed that exposure of embryos to the WSFs from the EI2V incubation (with a total recovered neutral fraction approximately seven times greater than the Phe#6 and Hexaco#2 incubations) resulted in the most severe responses in craniofacial, cardiovascular, and skeletal organ systems. The total neutral WSFs recovered from the EI2V biodegradation of weathered ANS 521 were subfractionated into saturated (eluted with hexane), aromatic (eluted with CH2Cl2), polar (eluted with ethyl ether), and recombined (saturated + aromatic + polar) fractions. Developing fish embryos were then exposed to each subfraction and the recombined subfractions. The polar subfraction and recombined subfractions proved to be the most embryo toxic and teratogenic. They resulted in statistically significant (p < or = 0.05) responses (compared to controls) for craniofacial, cardiovascular, skeletal, and total severity effects in one or both tests with these subfractions.

/AQUATIC SPECIES/ Pristane (2,6,10,14-tetramethylpentadecane) concentrations in mussels (Mytilus trossulus) increase abruptly during spring in Prince William Sound (PWS), Alaska. This increase is mainly due to ingestion by mussels of pristane-laden feces produced by near-shore zooplanktivores, especially juvenile pink salmon (Oncorhynchus gorbuscha). Examination of the trophic and temporal distribution of pristane found in 3,007 samples implicates Neocalanus copepods, which often dominate the zooplankton biomass in PWS during spring, as the source of pristane. Juvenile pink salmon, preying on Neocalanus, produce pristane-laden feces that are accumulated by mussels 52 times more efficiently than is dissolved pristane. Releases en masse of approx. 10(sup 8) juvenile pink salmon from a hatchery at the peak of the Neocalanus bloom were immediately followed by increases in pristane concentrations of nearby mussels monitored during 1996 and 1998. Accumulation of dissolved pristane, or of fecal pellets produced by Neocalanus copepods, were substantially less important pathways of pristane transfer to mussels. The transfer pathway to mussels via feces produced by zooplanktivores preying on Neocalanus is the basis for a potential linkage between pristane accumulation by mussels and survival of juvenile pink salmon, because it reflects indirectly the magnitude of Neocalanus prey consumed. Annual survival values of hatchery pink salmon were weakly correlated (P = 0.10) with pristane concentrations monitored in mussels at 25 stations distributed throughout PWS from 1995 through 2001.

/AQUATIC SPECIES/ ... The objective of this study was to emulate natural levels of pristane in the diet fed to juvenile pink salmon. The salmon were separated into two treatments. Half were fed a diet spiked with 0.001% pristane and the other half were offered the same diet with no pristane supplement. Food consumption was measured daily. Changes in fish mass, fish length, assimilation efficiency, and pristane ingestion in the salmon tissue were analyzed. Average instantaneous growth and assimilation efficiency were found to be lower in the pristane-fed group when compared to the control group, which was consistent with the previous study. Ingestion rates of the pristane group were higher than those of the control group. However, there was no statistical difference between the two groups.

/OTHER TERRESTRIAL SPECIES/ A study was conducted to determine the effect of nonaqueous-phase liquids (NAPLs) on the bioavailability of benzo[a]pyrene (BaP) in soil. Sentry 19 oil and pristane reduced the availability of BaP for assimilation by the earthworm Eisenia fetida and for mutagenicity in a rifampicin-sensitive strain of Pseudomonas putida. As much as 80% of the compound could be rendered unavailable to the worms or for genotoxicity. Tests with five alkanes and an oil showed that the extent of reduction in genotoxicity of BaP varied with the identity, viscosity, and hydrophobicity of the NAPL. The magnitude of the decline in availability for genotoxicity differed in tests of three soils. Because little or no BaP was lost from the soil, the diminished bioavailability was not the result of a diminished total concentration of the compound. These findings show that exposure to hydrophobic toxicants can be appreciably altered in soils containing NAPLs.

Using a structure estimation method based on molecular connectivity indices(1), the Koc of pristane can be estimated to be 1.8X10+5(SRC). According to a classification scheme(2), this estimated Koc value suggests that pristane is expected to be immobile in soil(SRC).

Pristane is found in 2.5-3 billion year old rock specimens; this chemical is known only to be produced by living organisms(1). Pristane is obtained from the unsaponifiable fraction of shark liver oil(2). Pristane is a component of crude petroleum oil, often present at high concentrations(3). Pristane is reportedly found in bacteria, algae, various plants, coal and mineral oil(4,5).

URBAN/SUBURBAN: A mean ambient air concentration of 97.2 ng/cubic m was reported for pristane from monitoring data measured on September 9, 1993 at Central Los Angeles, Azusa, and Claremont(1).

RURAL/REMOTE: Pristane was detected in 28% of 25 organic aerosol samples from tropical trade wind samples collected from a lighthouse at Fajardo in the Caribbean(1).

SOURCE DOMINATED: Pristane was detected in the tailpipe emissions of catalyst equipped and non-catalyst equipped gasoline powered motor vehicles at concentrations of 7.8 and 225 ug/km, respectively; it was also detected in the gasoline at 12.1 ug/g(1).

/HUMAN EXPOSURE STUDIES/ The irritant effects of 19 oils and 20 synthetic perfumes used in cosmetics were tested on the skin of animals and 50 male volunteers. ...Of the 20 oils tested, 2 hydrocarbons (hexadecane and pristane) proved to be severely irritating to human skin... .

/EPIDEMIOLOGY STUDIES/ This is a community comparison study that examines persons living in a subdivision exposed to petroleum products and mercury. ...Their health status and questionnaire responses /were compared/ to those living in another community with no known exposures of this type. Pristane house dust among the exposed homes was higher than in the comparison communities. The exposed subdivision has higher ambient air mercury levels compared to the control community. The prevalence of rheumatic diseases (OR = 10.78; CI = 4.14, 28.12) and lupus (OR = 19.33; CI = 1.96, 190.72) was greater in the exposed population compared to the unexposed. A higher prevalence of neurological symptoms, respiratory symptoms and several cardiovascular problems including stroke (OR = 15.41; CI = 0.78, 304.68) and angina (OR = 5.72; CI = 1.68, 19.43) was seen. There were statistically significant differences in B cells, Natural Killer Cells, gamma glutamyl transferase, globulin and serum calcium levels between control and exposed subjects.

/ALTERNATIVE and IN VITRO TESTS/ ... In this study, we show that activated CD4+ alphabetaT cells, which target peripheral joints, transfer pristane-induced arthritis (PIA). The pristane-primed T cells are of oligo or polyclonal origin as determined by their arthritogenicity after stimulation with several mitogenic anti-TCRVbeta and anti-TCRValpha mAbs. Arthritogenic cells secreted IFN-gamma and TNF-alpha (but not IL-4) when stimulated with Con A in vitro, and pretreatments of recipient rats with either anti-IFN-gamma or a recombinant TNF-alpha receptor before transfer ameliorated arthritis development. Most importantly, we show that these T cells are MHC class II restricted, because treatment with Abs against either DQ or DR molecules ameliorates arthritis development. The MHC class II restriction was confirmed by transferring donor T cells to irradiated recipients that were syngenic, semiallogenic, or allogenic to MHC class II molecules, in which only syngenic and semiallogenic recipients developed arthritis. These data suggest that the in vivo administration of a non-antigenic adjuvant, like pristane, activates CD4+ alphabetaT cells that are MHC class II restricted and arthritogenic.

/ALTERNATIVE and IN VITRO TESTS/ Hydrocarbon oils such as pristane or hexadecane induce arthritis and lupus in rodents sharing clinical and pathological features with the human diseases rheumatoid arthritis and systemic lupus erythematosus, respectively. In pristane-induced lupus in the mouse induction of apoptosis and augmentation of type-I Interferon signalling by pristane have been suggested to contribute to pathology, whereas in pristane-induced arthritis (PIA) in the rat the pathological mechanisms are still elusive. Here we show that pristane induces cell death in rat and human cells. Increased numbers of apoptotic cells were found in draining lymph nodes of pristane-injected rats and increased percentages of apoptotic and necrotic cells were observed in peripheral blood. In addition, neutrophil extracellular trap formation was triggered by pristane and hexadecane in neutrophils. Because levels of interleukin (IL)-1beta were elevated in sera of pristane-injected rats, with levels mirroring the course of PIA, we examined the effect of pristane at single cell level in vitro, using rat splenocytes and the human monocytic cell line THP-1. Pristane and other hydrocarbon oils induced IL-1beta secretion in THP-1 cells as well as in rat splenocytes. The potassium channel inhibitor glibenclamide partly inhibited IL-1beta induction, suggesting involvement of the inflammasome. Elevated levels of IL-1alpha were also found in supernatants of cells treated with pristane and hexadecane. In conclusion, autoimmunogenic hydrocarbon oils induce various forms of cell death in rat and human cells. The higher serum IL-1beta levels in pristane-injected animals might be caused by both inflammasome-dependent and -independent mechanisms, such as passive release from dying-cells and probably extracellular maturation of pro-IL-1beta.

Pristane has been reportedly found in various tissues of fish and mammals(1). Mean concentrations for pristane of 8710 and 7160 ng/g were determined in the volatile component of Korean salt-fermented fish and shrimp pastes from a Korean market that were made from hair tail viscera and shrimp, respectively(2). Barnacle samples collected from five locations in the Arabian Gulf had concentrations of pristane ranging from not detected to 1510 ng/g(3). Catfish samples collected from seven locations in the Arabian Gulf had concentrations of pristane ranging from not detected to 242 ng/g(4).

The content and distribution of n-alkane (C8-C35) and isoprenoid (pristane and phytane) hydrocarbons were investigated in two species of bivalve mollusk, mussel (Mytilus galloprovincialis) and cockle (Cerastoderma edule), collected at different points of the Galicia littoral zone during the period from December 2002 to February 2003 (after the Prestige oil spill). Samples were analyzed by high-resolution gas chromatography equipped with a flame ionization detector. The highest levels were found in mussels and cockles coming from two estuarine bays, Rias de Arousa and Vigo. Hydrocarbons with carbon chain length > 30 were detected and determined in all samples. The abundance of these hydrocarbons in biota could be interpreted with regard to the feeding and living habits. Chemometric techniques have been employed to analyze data and determine the potential source of hydrocarbon contamination. Differences between mussels and cockles were observed in relation to aliphatic content. According to the data analysis, the main source of hydrocarbon contamination of investigated samples seems to be more related to the intense traffic of vessels in these estuarine bays than to the Prestige oil spill.

Chemical: Pentadecane, 2,6,10,14-tetramethyl-

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

Diffuse pulmonary hemorrhage (DPH) is an uncommon but critical complication of systemic lupus erythematosus. Peritoneal administration of 2,6,10,14-tetramethylpentadecane (pristane) can recapitulate a lupus-like syndrome in mice, which can develop into DPH within a few weeks, especially in C57BL/6 mice. Mac-1 (CD11b/CD18), a leukocyte adhesion molecule, is known to play a role in inflammation by regulating migration of leukocytes into injured tissue. In this study, we aimed to clarify the role of Mac-1 in pristane-induced DPH, using Mac-1(-/-) and wild-type (WT) mice on a C57BL/6 background. After pristane injection, Mac-1(-/-) mice showed reduced prevalence of DPH and attenuated peritonitis compared with WT mice. Analysis of the peritoneal lavage on days 5 and 10 after pristane treatment revealed increased numbers of eosinophils and alternatively activated macrophages, but decreased numbers of neutrophils and classically activated macrophages in Mac-1(-/-) mice compared with WT. Enhanced production of IL-4 and IL-13, both key mediators of macrophage polarization toward the mannose receptor(+) (MMR(+)) phenotype, was observed in the peritoneal cavity of Mac-1(-/-) mice. Depletion of neutrophils and eosinophils or adoptive transfer of classically activated macrophages resulted in the exacerbation of pristane-mediated DPH in both WT and Mac-1(-/-) mice. Moreover, peritoneal transfer of F4/80(high)MMR(+) alternatively activated macrophages successfully reduced the prevalence of DPH in WT mice. Collectively, Mac-1 promoted acute inflammatory responses in the peritoneal cavity and the lungs by downregulating granulocyte migration and subsequent phenotypic conversion of macrophages in a pristane-induced systemic lupus erythematosus model.

Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included.

Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-CELLS or by inhibiting the activation of HELPER CELLS. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of INTERLEUKINS and other CYTOKINES are emerging.

Studies were conducted to assess the normal tissue-associated levels of pristane (2,6,10,14,-tetramethylpentadecane) in Copenhagen rats during ontogeny and adult life and to address whether or not dietary pristane can be adsorbed from the gut and disseminated throughout the body. During the course of this study the possible effects of dietary pristane on chromatin conformation of lymphoid cells were also examined by flow cytometry. The data indicated that 1) pristane crossed the placenta and accumulated in fetal tissues, 2) neonates were exposed to pristane via the colostrum, 3) there were significant increases in the amount of tissue-associated pristane in young adults and subsequent redistribution of the pristane to the muscle and adipose tissues in older rats and 4) after dietary exposure, significantly elevated levels of pristane were associated with the tissues and concomitant changes in chromatin conformation were observed. Collectively, these results suggest that pristane was adsorbed from dietary sources, disseminated to the tissues and exerted a transient, yet marked effect on chromatin of lymphoid cells in rats.

The fate of pristane (2,6,10,14-tetramethylpentadecane), a widespread isoprenoid hydrocarbon, has been studied in rats after a single /oral/ administration of 3H-labeled pristane. The balance study showed an extensive fecal excretion (66%) mainly as unchanged hydrocarbon, whereas about 14% of ingested pristane was excreted in urine as pristane metabolites and tritiated water. After one wk, 8.3% of the ingested 3H still was stored in the carcass, and radioactive distribution in tissues and organs showed a preferential incorporation into adipose tissue and liver. Over 75% of the radioactivity stored in the carcass was associated with pristane metabolites and tritiated water. Tissue metabolites were characterized by thin layer chromatography, gas chromatography and mass spectrometric analyses. Four metabolites were identified: pristan-1-ol, pristane-2-ol, pristanic acid and 4,8,12-trimethyltridecanoic acid. These demonstrate that this isoprenoid hydrocarbon undergoes subterminal hydroxylation or terminal oxidation followed by the classical beta-oxidation process. Incorporation of metabolites in phospholipids and more particularly in the phosphatidylserine fraction has been observed and is discussed.

Isoprenoid alkane found in shark liver oil; Used as a lubricant, transformer oil, corrosion inhibitor, and biological marker; [Merck Index]

Lubricant; transformer oil. Anti-corrosion agent. Biological marker. In experimental systems to induce plasmacytomas; in production of monoclonal antibodies.

Chromatographic oil

MEDICATION

Isoprenoid alkane obtained from the unsaponifiable fraction of shark liver oil where it occurs to an extent of 14%.

Isolation from petroleum crude oils; ... from wool wax. Synthesis from phytol.

Pentadecane, 2,6,10,14-tetramethyl-: ACTIVE

Found in rock specimens 2.5-3 billion years old. It is known to be synthesized only by living organisms and to withstand heat and pressure; thus it serves to date the existence of life on earth.

The distribution of pristane and phytane relative to the neighboring n-C17 and n-C18 peaks has been used to aid in the identification of crude oils and to detect the onset of biodegradation.

The ratio of dibenzothiophene to phenanthrene and the ratio of pristane to phytane, when coupled together, provide a ... way to infer crude oil source rock depositional environments and lithologies. Such knowledge can significantly assist in identifying the source formation(s) in a basin thereby providing valuable guidance for further exploration.