Pyrene is a biochemical reagent that can be utilized in studies pertaining to life sciences as an organic compound or biological material.

Absorption, Distribution and Excretion
Rats were treated with benzo[a]pyrene (BaP) alone (150 μg/kg) or in combination with phenanthrene (PH) (4,300 μg/kg) and pyrene (PY) (2,700 μg/kg) (BPP group), once daily for 30 days. Increased 7-ethoxyhalothrin-O-deethylase activity in liver microsomal fractions was observed only in the BaP group. In rats treated with BaP alone, BaP concentration reached its peak at day 20 (34.5 ng/g); while in rats treated with BPP, BaP concentration was 23.6 ng/g at day 30. In the BPP group, the highest pH concentration was observed in muscle (47.1 ng/g) and in fat (118.8 ng/g); the PY concentration was 29.7 ng/g in muscle and 219.9 ng/g in fat. During treatment, urinary 3-OH-pH concentrations ranged from 114 to 161 ng/mL, and pH concentrations ranged from 41 to 69 ng/mL; urinary 1-OH-PY concentrations ranged from 201 to 263 ng/mL, and pH concentrations ranged from 9 to 17 ng/mL. After drug withdrawal, the levels of PY, pH, and their metabolites in urine rapidly decreased… This human controlled study investigated the excretion kinetics of 1-hydroxypyrene (1-OHP) in urine after consuming grilled meat. Two feeding experiments were conducted, with grilled meat doses of 15 g and 30 g per kilogram of body weight, respectively, in Experiment 1 and Experiment 2. All excreted urine was collected for 7 consecutive days, and the content of 1-hydroxypyrene (1-OHP) was analyzed. In both experiments, the excretion of 1-OHP in urine increased significantly 12 hours after exposure (P < 0.05), but no significant increase was observed 12–24 hours after exposure. In Experiment 1, the average percentage of 1-OHP excreted in urine at 0–12 hours and 12–24 hours after exposure was 3.80% and 0.61% of the administered dose, respectively; in Experiment 2, these figures were 1.66% and 0.38%, respectively. The excretion rate was negatively correlated with the dose. Furthermore, a diurnal variation in 1-OHP excretion was observed (P < 0.05), with lower excretion in the morning (~0:00–12:00) than in the afternoon (~12:00–24:00). This study indicates that even with high dietary intake, most urinary excretion of 1-hydroxypyrene (1-OHP) occurs within 12 hours. Therefore, participants in occupational or environmental studies can reduce the impact of dietary pyrene simply by recalling their diet on the current or previous day.
…Two groups of white oysters (Buccinum undatum) ingested equimolar amounts of pyrene and 1-hydroxypyrene via diet over 15 days. Extracts from muscle and visceral tissues were analyzed using liquid chromatography-fluorescence detection and mass spectrometry. Nine biotransformation products were detected in both groups, including two isomers each of 1-hydroxypyrene, pyrene-1-sulfate, pyrene-1-glucuronide, pyrene gluconate sulfate, pyrene glycol sulfate, and pyrene glycol disulfate, as well as one isomer of pyrene glycol glucuronide sulfate. These compounds indicate that the metabolic pathway of pyrene is more complex than typically reported. The importance of diconjugated metabolites was comparable in animals exposed to pyrene to that exposed to 1-hydroxypyrene. Biotransformation products accounted for more than 90% of the substances detected in the animals, highlighting the importance of analyzing metabolites when assessing exposure. The average content in muscle was only 2% to 3% of the body load compared to the visceral mass of both groups. The analytical methods were sensitive enough to detect biotransformation products in laboratory control snails and near-shore sampled snails. Furthermore, the tissue distribution of [(14)C]pyrene was investigated using autoradiography. The radioactive material was primarily found in the digestive and excretory systems of the snails, rather than in the gonads or muscle tissue. We investigated the transfer of 10 polycyclic aromatic hydrocarbons (PAHs) (pyrene, 3,4-benzophenanthrene, tribenzobenzene, chrysene, 1,2-benzanthracene, 1,1'-binaphthyl, 9-phenylanthracene, 2,2'-binaphthyl, m-tetraphenyl, and 1,3,5-triphenylbenzene) from phosphatidylcholine vesicles. The results showed that the molecular volume of PAHs was a determining factor in the transfer rate. Furthermore, high-performance liquid chromatography (HPLC) data confirmed the hypothesis that the transfer rate was related to molecular size and the partition coefficient of the molecule between the polar and hydrocarbon phases. The kinetics and characteristics of spontaneous transfer of carcinogens may have a significant impact on the competitive processes of intracellular PAH metabolism. For more complete data on the absorption, distribution, and excretion of pyrene (13 species), please visit the HSDB record page.

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Metabolisms/Metabolites
Spotted trout (Salvelinus fontinalis) were orally exposed to monocyclic polycyclic aromatic hydrocarbons (PACs), including benzo[a]pyrene, carbazole, chloroquine, dibenzofuran, dibenzothiophene, fluorene, phenanthrene, and pyrene. Fish were euthanized 7 days after exposure, and the gallbladder was removed for bile analysis. The presence of PAC derivatives in bile was determined using high-performance liquid chromatography (HPLC) combined with fluorescence (F) and ultraviolet (UV) detection, without pretreatment. Glucuronide conjugates were predominant in all exposure groups, while the content of phenols and starting materials varied (0-53%). The compounds were identified by selective extraction of less polar unconjugated proanthocyanidins (PACs) and enzymatic hydrolysis of water-soluble substances. The generated phenolic compounds were subsequently characterized by high-performance liquid chromatography (HPLC) and/or gas chromatography-mass spectrometry (GC-MS). The total metabolite levels varied considerably among different compounds. The rat liver microsomal system metabolized pyrene to 1-hydroxypyrene and 4,5-dihydro-4,5-dihydroxypyrene, as well as 1,6-pyrenequinone and 1,8-pyrenequinone. In rats and rabbits, pyrene metabolites included trans-4,5-dihydro-4,5-dihydroxypyrene, s-(4,5-dihydro-4-hydroxypyrene-5-yl)glutathione, 1,6-dihydroxypyrene, 1,8-dihydroxypyrene, and 1-hydroxypyrene. No phenolic compounds were observed at the K-region (4,5 bond) of pyrene; a small amount of 4,5-dihydrodiol was detected, and no 4,5-dihydroxypyrene derivatives were found. The primary metabolite appears to be thiouric acid, namely N-acetyl-S-(4,5-dihydro-4-hydroxy-5-pyrene)L-cysteine. For more complete data on the metabolism/metabolites of pyrene (19 in total), please visit the HSDB record page. The metabolism of polycyclic aromatic hydrocarbons (PAHs) occurs in all tissues and is typically catalyzed by cytochrome P-450 and its associated enzymes. PAH metabolism results in reactive intermediates, including epoxide intermediates, dihydrodiols, phenols, quinones, and various combinations thereof. Phenols, quinones, and dihydrodiols can all bind to glucuronides and sulfates; quinones can also bind to glutathione. (L10)

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Biological half-life
……After 4.5 hours of exposure, the apparent elimination rate of (14)C-pyrene in the skin (23 hours) was similar to the apparent urinary excretion half-life of 1-hydroxypyrene (1-OHPy) (21 hours). These values are three times higher than the urinary excretion half-life of 1-OHPy after intravenous administration of pyrene (0.5 mg/kg). ... In two independent studies, two informed volunteers were exposed to 500 μg of pyrene, one orally and the other dermally. Urine samples were collected every 0.5–4 hours after administration for 48 hours, and urinary measurements of 1-hydroxypyrene (1-OHP) were performed. After the absorption period, 1-OHP was excreted with a first-order kinetic apparent half-life, approximately 12 hours for both volunteers and for both exposure routes. ... Urinary excretion curves following pyrene exposure were established in a psoriasis patient treated with coal tar shampoo and in two volunteers who received a single 100 μL creosote exposure. In another independent study, two volunteers applied 500 μg of pyrene to a 200 cm² area of the inner forearm skin for five consecutive days. Urine samples were collected at regular intervals up to 48 hours post-exposure. In psoriasis patients and volunteers exposed to creosote, peak excretion occurred between 10 and 15 hours post-administration, with the apparent first-order kinetic half-life of elimination calculated to be 11.5 to 15 hours. ...
This study conducted five experiments in male Sprague-Dawley rats to investigate the urinary excretion kinetics of 1-hydroxypyrene (1-OHP) following intravenous, oral, and dermal exposure to 0.5–50 μmol/kg pyrene (in the form of a single substance or a mixture of multiple polycyclic aromatic hydrocarbons (PAHs)). ...In all tissues examined, the half-lives of pyrene and 1-OHP ranged from 3.1 to 5.4 hours and 5.2 to 6.7 hours, respectively; therefore, based on these values, long-term accumulation in any tissue could not be predicted.

Toxicity Summary
Identification and Uses: Pyrene is a solid. It is used as an additive in electrical insulating oils and epoxy resins for electrical insulation. The complex of pyrene with cyanuric chloride and aluminum chloride can be used to synthesize optical brighteners. Pyrene itself can act as an electron donor, enhancing the blackness of pencil lead. It is also used in biochemical research. Human Exposure and Toxicity: Exposure to sunlight may cause skin irritation from pyrene and lead to chronic skin discoloration. Pyrene (not the associated polycyclic aromatic hydrocarbons) can enhance basal transcription of the IL-4 promoter in humans and mice. Animal Studies: Transdermal exposure to 10 g/kg of pyrene in mice was not fatal. Inhalation of pyrene caused pathological changes in the liver, lungs, and stomach tissues, and resulted in a decrease in the number of neutrophils, white blood cells, and red blood cells. No embryogenic or carcinogenic effects were observed, except for occasional papilloma. Some teratogenic effects were observed. In in vitro assays in some mammalian cells, pyrene induced mutagenic and unplanned DNA synthesis. Limited evidence of pyrene activity in short-term studies. Ecotoxicity studies: Pyrene interacts with the thyroid system of fish. In rockfish, pyrene exposure impairs skeletal development by disrupting chondrocyte proliferation. Zebrafish embryos exposed to low concentrations of environmental pyrene disrupt normal heart development and alter the expression of genes related to defective heart differentiation. Pyrene may be a contributing factor to behavioral and neurodevelopmental toxicity in pufferfish. In red earthworms (Lumbricus rubellus), pyrene was found to cause a dose-dependent decrease in the concentrations of lactic acid and saturated fatty acids myristanoic acid, hexadecanoic acid, and octadecanoic acid, while increasing the production of amino acids alanine, leucine, valine, isoleucine, lysine, tyrosine, and methionine. This is thought to indicate impaired glucose metabolism, accompanied by enhanced fatty acid metabolism and changes in tricarboxylic acid cycle intermediates. Polycyclic aromatic hydrocarbons (PAHs) can bind to blood proteins such as albumin, thereby being transported in the body. Many PAHs induce the expression of cytochrome P450 enzymes, particularly CYP1A1, CYP1A2, and CYP1B1, by binding to aryl hydrocarbon receptors or glycine N-methyltransferases. These enzymes metabolize PAHs into their toxic intermediates. The active metabolites of polycyclic aromatic hydrocarbons (epoxide intermediates, dihydrodiols, phenols, quinones, and various combinations thereof) covalently bind to DNA and other cellular macromolecules, inducing mutagenicity and carcinogenicity. (L10, L23, A27, A32)

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Toxicity Data
LC50 (rat) = 170 mg/m3
LD50: 2700 mg/kg (oral, rat) (L908)

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Interactions
Benzo[a]pyrene (B(a)P) can inhibit the mutagenicity of 1-nitropyrene (1-NP) by reducing nitroreductase activity and forming adducts with DNA. This study evaluated the relationship between the chemical structures of L-nitropyrene and nine polycyclic aromatic hydrocarbons (PAHs) and their antagonistic effects on L-nitropyrene-induced mutagenesis using a binary mixture of L-nitropyrene and nine PAHs, without the presence of the S9 mixture. The results showed that these nine PAHs exhibited significantly different antagonistic effects on the mutagenicity of L-nitropyrene. Among the PAHs tested, crownenes showed the strongest antagonistic effect, followed by benzo[g,h,i]perylene (B(g,h,i)P), benzo[e]pyrene (B(e)P), dibenzo[a,h]pyrene (DB(a,h)P), benzo[a]pyrene, and pyrene. Naphthalene, anthracene, and chrysene had only slight inhibitory effects on the mutagenicity of L-nitropyrene. This study further investigated the effect of PAHs on the nitroreductase activity of strain TA98 in the presence of L-nitropyrene, using the production of L-AP as an indicator. Statistical analysis showed that the inhibitory effect of polycyclic aromatic hydrocarbons (PAHs) on the mutagenicity of L-nitropyrene was significantly correlated with their effect on nitroreductase activity (r = -0.69, p < 0.05). Furthermore, the formation of L-nitropyrene-DNA adducts in binary mixtures of L-nitropyrene and PAHs was determined using the 32P labeling method. The results indicated that the regulatory effect of PAHs on the formation of L-nitropyrene-DNA adducts was significantly negatively correlated with their antagonistic activity (r = -0.91, p < 0.011). Based on these results, the relationship between the chemical structure of PAHs and their antagonistic effect on the mutagenicity of L-nitropyrene was revealed by analyzing the surface area and electronic parameters of PAHs. The correlation between the planar molecular area of polycyclic aromatic hydrocarbons (PAHs) and the antagonistic effect of L-nitropyrene mutagenicity (r = -0.81, p < 0.01) was stronger than the energy difference ΔE between their EHOMO and ELUMO (r = 0.69, p < 0.05). In summary, the interaction of binary mixtures may involve two mechanisms: (1) PAHs with larger planar surface areas have higher binding affinity to nitroreductases; (2) the high-energy interaction between L-nitropyrene with low ΔE values and PAHs may reduce their nitroreduction capacity.
Co-carcinogenicity studies were conducted on mouse skin (50 female ICR/HA mice per group). 5 μg of benzo[a]pyrene and pyrene (0.004 mg and 0.012 mg) were dissolved in the same solution and applied to the skin three times a week with 0.1 mL of acetone each time. Squamous cell carcinoma was observed in 6/50 and 20/50 mice, respectively. No tumors were observed in mice treated with pyrene alone. /Excerpt from Table/
Sunlight exposure may trigger pyrene irritation of the skin and lead to chronic skin discoloration.
Chemical pollution in aquatic environments is almost always the result of the combined effects of multiple rather than single toxic compounds. The possibility of distinguishing the effects of critical risk chemicals from the effects of other chemicals (including their combined effects) is obvious. This has significant theoretical and technical value. …This study used multi-gene expression profiling to investigate the livers of juvenile brown trout (Salmo trutta lacustris) exposed to three model chemicals (cadmium, carbon tetrachloride, and pyrene) to achieve the above objectives. These chemicals were administered alone at low acute sublethal concentrations, in binary and ternary combinations, and in a partially dose-responsive manner. Differentially expressed genes were grouped based on the correlation of their expression profiles, and their dose dependence was analyzed using multivariate regression. Responses to cadmium and carbon tetrachloride were largely similar, with no interaction observed (i.e., in the binary combination, the effect was the same as that produced by the more toxic compound cadmium). The presence of pyrene made the combined effect more pronounced, leading to significantly different alterations in gene expression. Comparison with results from 118 previous experiments revealed… a group of 23 genes showed significantly higher probabilities of response to chemical toxicity (cadmium, carbon tetrachloride, pyrene, and resin acids). The expression levels of this group of genes were significantly elevated compared to other stressors (such as transport or viral and bacterial infections). This group of genes included genes associated with immune and stress responses, which were significantly enriched in extracellular proteins. In summary, the study demonstrates that characteristic genomic endpoints often persist when chemicals are present in binary or ternary mixtures. Despite differing chemical properties and cellular targets, the responsiveness of the cadmium and carbon tetrachloride combination appears to be less than an additive effect. Chemical interactions or non-additive effects occur when a compound with a significantly different mechanism of action (pyrene) is added to the mixture. For more complete data on pyrene interactions (6 in total), please visit the HSDB record page.

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Non-human toxicity values
Oral LD50 in rats: 2700 mg/kg
LD50 in mice: 800 mg/kg
LD50 in mice via intraperitoneal injection: 514 mg/kg

Pyrene is a colorless solid with weak blue fluorescence in both solid and solution. It is commonly used in biochemical research. (EPA, 1998)
Pyrene is a peri- and ortho-fused polycyclic aromatic hydrocarbon (PAH) composed of four fused benzene rings forming a planar aromatic system. It can be used as a fluorescent probe and is also a persistent organic pollutant.
Pyrene is the parent compound of PAHs containing four fused rings. (IUPAC 1998)
Pyrene is a PAH composed of four fused benzene rings forming a planar aromatic system. Its chemical formula is C16H10. This colorless solid is the smallest peri-fused PAH (rings fused on multiple faces). Pyrene is formed during the incomplete combustion of organic compounds. Although pyrene is not as toxic as benzo[a]pyrene, animal studies have shown that pyrene is also toxic to the kidneys and liver.

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Therapeutic Use
/Clinical Trials/ ClinicalTrials.gov is a registry and outcomes database that lists human clinical studies funded by public and private institutions worldwide. The website is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each record on ClinicalTrials.gov includes a summary of the study protocol, including: the disease or condition; the intervention (e.g., the medical product, behavior, or procedure under investigation); the title, description, and design of the study; participation requirements (eligibility criteria); the location where the study was conducted; contact information for the study location; and links to relevant information from other health websites, such as the NLM's MedlinePlus (for patient health information) and PubMed (for citations and abstracts of academic articles in the medical field). Information about pyrene is included in this database.

C16H10

202.25

202.078

129-00-0

41496-25-7;17441-16-6

31423

Light yellow to yellow solid powder

1.2±0.1 g/cm3

404.0±0.0 °C at 760 mmHg

145-148ºC

168.8±12.8 °C

0.0±0.4 mmHg at 25°C

1.852

5.17

0

0

0

16

217

0

BBEAQIROQSPTKN-UHFFFAOYSA-N

InChI=1S/C16H10/c1-3-11-7-9-13-5-2-6-14-10-8-12(4-1)15(11)16(13)14/h1-10H

pyrene

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

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

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.)