Pristane

268.52

268.52

217-650-8

26HZV48DT1

114852

DTXSID70870919

C29850

Colorless, transparent; stable liquid|Mobile, transparent, stable liquid

29011000

0

9.38 (est)

Clear colorless liquid

0.7833 g/cm³ @ Temp: 20 °C

-99 °C

296 °C

110 °C

n 20/D 1.438(lit.)

soluble in carbon tetrachloride

Conditions for safe storage, including any incompatibilities: Keep container tightly closed in a dry and well-ventilated place. Containers which are opened must be carefully resealed and kept upright to prevent leakage.

0.0044 mm Hg at 25 deg C (est)

Henry's Law constant = 68 atm-cu m/mol at 25 °C (est)

Hydroxyl radical reaction rate constant = 2.44X10-11 cu cm/molecule-sec at 25 °C (est)

NONH for all modes of transport

3

36/38

26-36

RZ1880000

Xi

Stable. Combustible. Incompatible with strong oxidizing agents.

P305 + P351 + P338

H315-H319

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.

Incompatible materials: Strong oxidizing agents.

|Warning|H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]|P264, P280, P302+P352, P305+P351+P338, P321, P332+P313, P337+P313, and P362|Aggregated GHS information provided by 45 companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H315: Causes skin irritation [Warning Skin corrosion/irritation]

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).

Combustible.

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.

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.

A severe skin irritant.

Three waste water treatment plants and sewer sites in small rural areas in France were examined for pristane. Sewer sludge, sewer sediments and waste water in manholes had reported concentrations ranging from not detected to 20.8 ug/g(1).

SEDIMENT: Pristane was detected in surface, and 80 m and 140 m deep settling sediments from the southern basin of Lake Michigan, with the greatest concentrations found in the 140 m deep sediments(1).|SOIL: During the winter of 2002, soil and sand samples from six locations in the Riyadh metropolitan area of Saudi Arabia were examined for extractable organic matter. Pristane was detected at a relative concentration of 2.89% (of total extractable organic matter) at one of six locations(1).|SOIL: Two Antarctic expeditions (in 2009 and 2011) were carried out to assess the local and remote anthropogenic sources of aliphatic and aromatic hydrocarbons, as well as potential biogenic hydrocarbons. Polycyclic aromatic hydrocarbons (PAHs), n-alkanes, biomarkers such as phytane (Ph) and pristane (Pr), and the aliphatic unresolved complex mixture (UCM), were analysed in soil and vegetation samples collected at Deception, Livingston, Barrientos and Penguin Islands (South Shetland Islands, Antarctica). Overall, the patterns of n-alkanes in lichens, mosses and grass were dominated by odd-over-even carbon number alkanes. Mosses and vascular plants showed high abundances of n-C21 to n-C35, while lichens also showed high abundances of n-C17 and n-C19. The lipid content was an important factor controlling the concentrations of n-alkanes in Antarctic vegetation (r(2)=0.28-0.53, p-level<0.05). n-C12 to n-C35 n-alkanes were analysed in soils with a predominance of odd C number n-alkanes (n-C25, n-C27, n-C29, and n-C31), especially in the background soils not influenced by anthropogenic sources. The large values for the carbon predominance index (CPI) and the correlations between odd alkanes and some PAHs suggest the potential biogenic sources of these hydrocarbons in Antarctica. Unresolved complex mixture and CPI values approximately = 1 detected at soils collected at intertidal areas and within the perimeter of Juan Carlos research station, further supported the evidence that even a small settlement (20 persons during the austral summer) can affect the loading of aliphatic and aromatic hydrocarbons in nearby soils. Nevertheless, the assessment of Pr/n-C17 and Ph/n-C18 ratios showed that hydrocarbon degradation is occurring in these soils.

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).

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.

... 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.

/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.

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).

Branched alkanes such as pristane may be components in petroleum products(1) and may be released to the environment through the processing and combustion of petroleum products (SRC). Pristane's use in lubricants, transformer oils, as an anti-corrosion agent, biological marker and in experimental systems to induce plasmacytomas, and in production of monoclonal antibodies(2) 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 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).

The rate constant for the vapor-phase reaction of pristane with photochemically-produced hydroxyl radicals has been estimated as 2.4X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 16 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Pristane is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). Pristane does not contain chromophores that absorb at wavelengths >290 nm(3) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 230 was calculated in fish for pristane(SRC), using an estimated log Kow of 9.38(1) and a regression-derived equation(1). According to a classification scheme(2), this BCF suggests the potential for bioconcentration in aquatic organisms is high(SRC).

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).

The Henry's Law constant for pristane is estimated as 68 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that pristane is expected to volatilize rapidly 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)(3) is estimated as 1.6 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)(3) is estimated as 6.5 days(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 (4). Pristane's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). However, this process is expected to be attenuated by adsorption. Pristane is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 4.4X10-3 mm Hg(SRC), determined from a fragment constant method(3).

SURFACE WATER: Pristane was identified but not quantified in the waters of Besos and Llogregat Rivers, in the coasts of Barcelona and Vilanova-Sitges, and in La Pineda beach, Spain(1). Pristane concentrations ranged from 0.08 to 0.12 ug/L in six stations located in the Guanabara Bay Basin, Rio de Janeiro, Brazil, sampled from September 2011 to August 2012(2).|SEAWATER: Concentrations of biogenic pristane reported in seawater from the Laurentian Channel and Hibernia Stations, in 1981, were approximately 32 ng/L and 3.5 ng/L, respectively(1).|RAIN/SNOW/FOG: Pristane was detected in 2 out of 10 snow samples collected in March 1999 from rural and urban areas in Russia and Finland at concentrations of 1.76 and 2.10 ug/kg(1).

According to the 2012 TSCA Inventory Update Reporting data, there are 0 reporting facilities for pristane(1).|Occupational exposure to pristane may occur through inhalation and dermal contact with this compound at workplaces where pristane is produced or used. Monitoring and use data indicate that the general population may be exposed to pristane via inhalation of ambient air, ingestion of food and dermal contact with consumer products containing pristane. The greatest potential for dermal and inhalation exposure is expected during use of petroleum products containing pristane. (SRC)

/EXPL THER/ This study evaluates the effects of pristane and phytol, two mineral oils with pro-oxidative effects, on the course of experimental autoimmune uveitis. C57BL6 mice were immunized with IRBP1-20 peptide emulsified in CFA and treated five days prior to immunization with phytol or with pristane or with PBS as control. Administration of pristane reduces the incidence and severity of IRBP-induced uveitis as demonstrated by the decrease in vasculitis and inflammatory foci in fundus and by a reduction in histological damages and leukocyte infiltration compared to untreated or phytol-treated mice. The protective effect observed is associated with a decreased activation of peripheral CD4+ and CD8+ T lymphocytes and a decrease in the intensity of the Th1 and Th17 autoimmune response to IRBP in pristane-treated mice compared to control mice, as evidenced by the decreased production of IFNgamma and IL17 by IRBP-specific lymphocytes from lymph nodes draining the site of immunization and by the increased production of anti-IRBP IgG1 over IgG2a. In addition, HUVEC and ARPE-19 cells incubated with the sera of mice treated with pristane presented a reduced production of H(2)O(2). The benefit of lowering the systemic oxidative stress by pristane in the course of EAU was confirmed by injecting the antioxidant NAC in IRBP-immunized mice. As pristane, NAC decreased clinical and histological inflammation of the retina and preserved the integrity of the hemato-retinal barrier. Finally, the protective effect of pristane on the development of EAU suggests that some mineral oils may represent a new therapeutic strategy in human uveitis.

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. (See all compounds classified as Carcinogens.)|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. (See all compounds classified as Immunosuppressive Agents.)

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.

42.00 Days

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.

/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. /Aliphatic hydrocarbons and related compounds/|/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 necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema 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. Administer activated charcoal ... . Treat frostbite with rapid rewarming techniques ... ./Aliphatic hydrocarbons and related compounds/|/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 ... . 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 (LR) 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 (Valium) or lorazepam (Ativan) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Aliphatic hydrocarbons and related compounds/|Emergency and supportive measures. 1. General. Provide basic supportive care for all symptomatic patients. Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen. Monitor arterial blood gases or oximetry, chest radiographs, and ECG and admit symptomatic patients to an intensive care setting. Use epinephrine and other beta-adrenergic medications with caution in patients with significant hydrocarbon intoxication because arrhythmias may be induced. 2. Pulmonary aspiration. Patients who remain completely asymptomatic after 4-6 hours of observation may be discharged. In contrast, if the patient is coughing on arrival, aspiration probably has occurred. Administer supplemental oxygen and treat bronchospasm and hypoxia if they occur. Do not use steroids or prophylactic antibiotics. 3. Ingestion. In the vast majority of accidental childhood ingestions, less than 5-10 mL is actually swallowed and systemic toxicity is rare. Treatment is primarily supportive. Injection. For injections into the fingertip or hand, especially those involving a high-pressure paint gun, consult with a plastic or hand surgeon immediately, as prompt wide exposure, irrigation, and debridement are often required. /Hydrocarbons/|For more Antidote and Emergency Treatment (Complete) data for Pristane (7 total), please visit the HSDB record page.

/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.

2,6,10,14-tetramethyl-pentadecane

Grade: 90% purity.

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.

A method for separating n-paraffins from petroleum hydrocarbons in foods was developed. The method consists of 5 initial steps: digestion of sample with alkali, silica gel column chromatography, molecular sieve adsorption, destruction of the sieve with HCl, and oxidation with KMnO4. Recoveries of n-paraffins added to 55 g oyster at a level of 0.36 ppm ranged from 80% for normal pentadecane to 100% for n-paraffins over 18 carbon atoms. This method also facilitated the analysis of iso-paraffins such as pristane (2,6,10,14-tetramethylpentadecane) and phytane (2,6,10,14-tetramethylhexadecane), and other hydrocarbons ... .|This paper describes a new extraction method for the determination of aliphatic hydrocarbons (AHs) in soil and sediment samples, using continuous microwave-assisted extraction (MAE) combined with liquid-liquid extraction, for clean-up purposes. Analytical determinations were carried out by gas chromatography coupled with impact ionization mass spectrometry. The influence of the experimental conditions was tested using an agricultural soil spiked with standards (stored at 4 degrees C for 1 month) as reference soil. Maximum extraction efficiencies (80-90%) were achieved using 0.1-1.0 g of sample, 60microl of water and 3 mL of n-hexane (extractant) and 5 min of extraction time; less than 70% of the most volatile hydrocarbons (C(9)-C(12)) were recovered since many evaporated during the drying step of the sample. MAE was compared with a conventional extraction method such as Soxhlet and a good agreement in the results was obtained (average recovery percentage value of 105% by comparing MAE against Soxhlet). Quality parameters such as linear range (0.5-800 ug/g), limits of detection (LODs) (0.1-0.2 ug/g) and precision (RSD, 4-6%) were determined using spiked soil samples. This method was successfully applied to the analysis of aliphatic hydrocarbons (C(9)-C(27) including pristane and phytane) in contaminated real samples.

Cosmetics -> Emollient; Moisturising