Tumor model building and animal modeling are two applications for chyrene.

Absorption, Distribution and Excretion
Chrysene is absorbed via the oral and dermal routes; there is no direct evidence available for absorption via the lungs. Absorption through the lungs is inferred by the measurement of chrysene and its metabolites in groups exposed occupationally to polycyclic aromatic hydrocarbons and in cigarette smokers.
After oral administration in rats, chrysene was measured in peak concentrations within the hour in blood and liver. Chrysene has been found to concentrate in the adipose and mammary tissues after oral administration in rats; after oral administration, the majority of the chrysene is eliminated predominantly via the feces with up to 41%-79% intact and with complete recovery within 2 days.
Chrysene appeared to be absorbed and metabolized in both human and animal skin.

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Metabolism / Metabolites
Polycyclic aromatic hydrocarbon (PAH)-type compounds induce at least two rat UDP-glucuronosyltransferase isoforms, UGT1A6 and UGT1A7. Among the glucuronidation reactions of PAH metabolites studied, mono- and diglucuronide formation of benzo[a]pyrene and chrysene-3,6-diphenol showed the highest induction factors in rat liver microsomes. Availability of AHH-1 cells stably expressing UGT1A7 allowed us to study whether this PAH-inducible isoform could catalyze benzo[a]pyrene and chrysene-3,6-diphenol glucuronidation. It was found that UGT1A7 indeed catalyzed mono- and diglucuronide formation of both benzo[a]pyrene and chrysene 3,6-diphenols. V79 cell-expressed rat UGT1A6 also catalyzed these reactions, except for chrysene diphenol diglucuronide formation. Enzyme kinetic studies of the glucuronidation of 6-hydroxychrysene (used as a stable PAH phenol) indicated that UGT1A7 conjugated this compound with a lower apparent Km value (0.1 uM) than UGT1A6 (10 uM). The results suggest that the two PAH-inducible UGTs may cooperate in conjugating PAH metabolites, but that UGT1A7 is more efficient.
Six metabolites of polycyclic aromatic hydrocarbons (PAHs) were identified and quantified from the bile of 31 common eels (Anguilla anguilla), 29 European flounders (Pleuronectes flesus), and 15 conger eels (Conger conger) collected from the Severn Estuary and Bristol Channel during 1997. The bile metabolites were deconjugated by enzymatic hydrolysis and separated by reverse-phase HPLC with fluorescence detection. The major metabolite present in all fish was 1-hydroxy pyrene (75-94% of all metabolites detected) with lower proportions of 1-hydroxy chrysene (2-15%) and 1-hydroxy phenanthrene (2-8%), and small amounts of three benzo[a]pyrene derivatives (<3%). Metabolite concentrations (normalized to biliverdin content) were significantly higher in common eels than in the other two species and tended to be higher in all species at the beginning of the year than at the end. The data confirm the importance of 1-hydroxy pyrene as the key PAH metabolite in fish bile and suggest that the common eel is an ideal species for monitoring PAHs in estuarine environments.
We have investigated the regio- and stereoselective metabolism of chrysene, a four-ring symmetrical carcinogenic polycyclic aromatic hydrocarbon (PAH), by the liver microsomes of brown bullhead (Ameriurus nebulosus), a bottom-dwelling fish species. The liver microsomes from untreated and 3-methylcholanthrene (3-MC)-treated brown bullheads metabolized chrysene at the rate of 30.1 and 82.2 pmol/mg protein/min, respectively. Benzo-ring diols (1,2-diol and 3,4-diol) were the major chrysene metabolites formed by liver microsomes from control and 3-MC-treated fish. However, the control microsomes produced a considerably higher proportion of chrysene 1,2-diol (benzo-ring diol with a bay region double bond) plus 1-hydroxychrysene, than 3,4-diol plus 3-hydroxychrysene, indicating that these microsomes are selective in attacking the 1,2- position of the benzo-ring. On the other hand, 3-MC-induced microsomes did not show such a regioselectivity in the metabolism of chrysene. Control bullhead liver microsomes, compared to control rat liver microsomes, produced a considerably higher proportion of chrysene 1,2-diol, the putative proximate carcinogenic metabolite of chrysene. Like rat liver microsomes, bullhead liver microsomes produced only trace amounts of the K-region diol.Chrysene 1,2-diol and 3,4-diol formed by the liver microsomes from both control and 3-MC-treated bullheads consisted predominantly of their R,R-enantiomers. Chrysene is metabolized by bullhead liver microsomal enzymes to its benzo-ring diols with a relatively lower degree of stereoselectivity compared to benzo[a]pyrene (a five-ring PAH), but with a higher degree of stereoselectivity compared to phenanthrene (a three-ring PAH). The data of this study, together with those from our previous studies with phenanthrene, benzo[a]pyrene and dibenzo[a,l]pyrene (a six-ring PAH), indicate that the regioselectivity in the metabolism of PAHs by brown bullhead and rainbow trout liver microsomes does not vary greatly with the size and shape of the molecule, whereas the degree of stereoselectivity in the metabolism of PAHs to benzo-ring dihydrodiols does.
We have investigated the metabolism of chrysene (CHR) and 5-methychyrsene (5-MeCHR) by Shasta rainbow trout (Oncorhyncus mykiss) and Long Evans rat liver microsomes to assess the effect of a non-benzo ring methyl substituent on the reactions involved in the metabolism of polycyclic aromatic hydrocarbons (PAHs). Trout as well as rat liver microsomes metabolized both CHR and 5-MeCHR at essentially similar rates, indicating that the methyl substituent does not alter the substrate specificity of the cytochrome P450(s) involved in the metabolism of the two PAHs. Dihydrodiols were the major CHR metabolites formed by both trout and rat liver microsomes, whereas the trout liver microsomes formed a considerably higher proportion of 5-MeCHR phenols compared to diols, indicating that 5-methyl substitution alters the substrate specificity of trout microsomal epoxide hydrolase for 5-MeCHR epoxides. Unlike trout liver microsomes, rat liver microsomes formed a much greater proportion of 5-MeCHR diols compared to 5-MeCHR phenols, suggesting that 5-MeCHR epoxides are better substrates for the microsomal epoxide hydrolase present in rat liver than for the enzyme in trout liver. Both trout and rat liver microsomes are more efficient at attacking the bay-region bond versus the non-bay-region double bond in chrysene. In contrast the reverse is true in the case of 5-MeCHR, indicating that a non-benzo ring methyl substituent alters the regioselectivity of the enzymes involved in the oxidative metabolism of PAHs.
For more Metabolism/Metabolites (Complete) data for CHRYSENE (13 total), please visit the HSDB record page.
PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (L10)

Toxicity Summary
IDENTIFICATION AND USE: Chrysene forms colorless platelets with blue fluorescence. It is used only for research purposes. Polycyclic aromatic hydrocarbons are a group of chemicals that are formed during the incomplete burning of coal, oil, gas, wood, garbage, or other organic substances, such as tobacco and charbroiled meat. HUMAN EXPOSURE AND TOXICITY: Chrysene is able to induce aryl hydrocarbon hydroxylase (AHH) in cultured human lymphocytes. Probable human carcinogen. ANIMAL STUDIES: A single topical application of chrysene to neonatal rats at 1 mg/10 g body weight resulted in induction of skin and liver activity of enzymes. AHH activity was increased 251% in skin and 339% in liver; 7-ethoxycoumarin deethylase 133 and 208%, respectively. Among 20 female mice painted with 1% solution of chrysene, papillomas appeared in 9 animals and carcinomas in 8, the first tumor being observed after 8 months. There was an obvious shortening of the lifespan. Groups of 10 rats received repeated injections of 2-6 mg chrysene; four tumors were observed in treated animals, and sarcomas were found in controls. Several hydroxylated metabolites of chrysene were formed by rat liver microsomal cytochrome P450 activity, some of which had estrogenic activity. Chrysene has a "bay-region" in structure. It is metabolized by mixed function oxidases to reactive "bay-region" diol epoxides that are mutagenic in bacteria and tumorigenic in mouse skin painting assays and when injected into newborn mice. Mutagenicity tests were performed with chrysene in the Salmonella (TA98 and TA1535) microsome test, mice oocytes, bone-marrow cells and spermatogonia of Chinese hamsters. Using the Salmonella microsome test, no mutagenic activity was found when chrysene alone was tested. Chrysene, 450 mg/kg was given to Chinese hamsters by oral, gavage, or intraperitoneal administration and showed no mutagenic effects. In oocytes of mice, 8-12 weeks of age, a single application of 450 mg/kg chrysene resulted in a weak but significant chromosome aberration. In spermatogonia of Chinese hamsters a low but not significant increase in chromosomal aberrations, excluding gaps, was found. The chemical was positive in the Ames test with metabolic activation using strains TA100 and TA98. Chrysene may be phototoxic as well as photogenotoxic under UVB irradiation. ECOTOXICITY STUDIES: Biotransformation and detoxification responses of mature scallop Chlamys farreri were studied during the reproduction period. Overall, females accumulated more chrysene than males, while males were more sensitive than females to chrysene exposure in gene expressions and enzyme activities.
The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (L10, L23, A27, A32)

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Toxicity Data
LD50: >320 mg/kg (Intraperitoneal, Mouse) (T35)

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Interactions
Chrysene is one of the basic polycyclic aromatic hydrocarbons (PAHs) which is a toxic environmental pollutant and consistently exposed to sunlight. However, little information is available on its photogenotoxicity. The objective of the present study was to analyze the effects of chrysene, under environmental intensity of UVB (0.6 mW/sq cm) in human skin epidermal cell line (HaCaT). Kinetic of chrysene showed that the highest intracellular uptake of chrysene occurred after 24 hr of incubation. The intracellular reactive oxygen species (ROS) was increased in a concentration dependent manner in chrysene treated cells under UVB irradiation. It was observed that UVB-irradiated chrysene induced apoptosis through activation of caspases-3 and phosphatidylserine translocation. Glutathione reduced (GSH) and catalase activity were decreased while apoptosis and DNA damage were induced significantly (p>0.01) as concentration of chrysene increased. Thus our results suggest that chrysene may be phototoxic as well as photogenotoxic under UVB irradiation.
This study evaluates the toxic effects of chrysene (a component from cigarette smoke) on Muller cells (MIO-M1) in vitro and investigates whether the inhibitor lipoic acid can reverse the chrysene-induced toxic effects. MIO-M1 cells were exposed to varying concentrations of chrysene with or without lipoic acid. Cell viability was measured by a trypan blue dye exclusion assay. Caspase-3/7 activity was measured by a fluorochrome assay. Lactate dehydrogenase (LDH) release was quantified by an LDH assay. The production of reactive oxygen/nitrogen species (ROS/RNS) was measured with a 2',7'-dichlorodihydrofluorescein diacetate dye assay. Mitochondrial membrane potential was measured using the JC-1 assay. Intracellular ATP content was determined by the ATPLite kit. MIO-M1 cells showed significantly decreased cell viability, increased caspase-3/7 activity, LDH release at the highest chrysene concentration, elevated ROS/RNS levels, decreased mitochondrial membrane potential value, and decreased intracellular ATP content after exposure to 300, 500, and 1,000 uM chrysene compared with the control. Pretreatment with 80 uM lipoic acid reversed loss of cell viability in 500-uM-chrysene-treated cultures (24.7%, p<0.001). Similarly, pretreatment with 80 uM lipoic acid before chrysene resulted in decreased caspase-3/7 activities (75.7%, p<0.001), decreased ROS/RNS levels (80.02%, p<0.001), increased mitochondrial membrane potential values (86%, p<0.001), and increased ATP levels (40.5%, p<0.001) compared to 500-uM-chrysene-treated cultures. Chrysene, a component of cigarette smoke, can diminish cell viability in MIO-M1 cells in vitro by apoptosis at the lower concentrations of Chrysene (300 and 500 uM) and necrosis at the highest concentration. Moreover, mitochondrial function was particularly altered. However, lipoic acid can partially reverse the cytotoxic effect of chrysene. Lipoic acid administration may reduce or prevent Muller cell degeneration in retinal degenerative disorders.
Ferulic, caffeic, chlorogenic, and ellagic acids, four naturally occurring plant phenols, inhibit the mutagenicity and cytotoxicity of (+/-)-7beta,8alpha-dihydroxy-9alpha, 10alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (B[a]P 7,8-diol-9,10-epoxide-2), the only known ultimate carcinogenic metabolite of benzo[a]pyrene. The mutagenicity of 0.05 nmol of B[a]P 7,8-diol-9,10-epoxide-2 in strain TA100 of Salmonella typhimurium is inhibited 50% by incubation of the bacteria and the diol epoxide with 150 nmol of ferulic acid, 75 nmol of caffeic acid, 50 nmol of chlorogenic acid or, most strikingly, 1 nmol of ellagic acid in the 0.5-ml incubation mixture. A 3-nmol dose of ellagic acid inhibits mutation induction by 90%. Ellagic acid is also a potent antagonist of B[a]P 7,8-diol-9,10-epoxide-2 in Chinese hamster V79 cells. Mutations to 8-azaguanine resistance induced by 0.2 uM diol epoxide are reduced by 50% when tissue culture media also contains 2 uM ellagic acid. Similar to results obtained with the bacteria, ferulic, caffeic, and chlorogenic acids are approximately two orders of magnitude less active than ellagic acid in the mammalian cell assay. The antimutagenic effects of the plant phenols result from their direct interaction with B[a]P 7,8-diol-9,10-epoxide-2, because a concentration-dependent increase in the rate of diol epoxide disappearance in cell-free solutions of 1:9 dioxane/water, pH 7.0, is observed with all four phenols. In parallel with the mutagenicity studies, ellagic acid is 80-300 times more effective than the other phenols in accelerating the disappearance of B[a]P 7,8-diol-9,10-epoxide-2. Ellagic acid at 10 uM increases the disappearance of B[a]P 7,8-diol-9,10-epoxide-2 by approximately 20-fold relative to the spontaneous and hydronium ion-catalyzed hydrolysis of the diol epoxide at pH 7.0. Ellagic acid is a highly potent inhibitor of the mutagenic activity of bay-region diol epoxides of benzo[a]pyrene, dibenzo[a,h]pyrene, and dibenzo[a,i]pyrene, but higher concentrations of ellagic acid are needed to inhibit the mutagenic activity of the chemically less reactive bay-region diol epoxides of benz[a]anthracene, chrysene, and benzo[c]phenanthrene. These studies demonstrate that ellagic acid is a potent antagonist of the adverse biological effects of the ultimate carcinogenic metabolites of several polycyclic aromatic hydrocarbons and suggest that this naturally occurring plant phenol, normally ingested by humans, may inhibit the carcinogenicity of polycyclic aromatic hydrocarbons.
The influence of some compounds belonging to the group of polycyclic aromatic hydrocarbons (eg, ... chrysene, ... on the pharmacokinetics of theophylline in rats is described. ... /Chrysene/ significantly accelerated the elimination of the drug. ...
The potencies of various xenobiotics for induction of monooxygenases and their influence on the rat liver microsomal metabolite profile of the environmentally relevant weak carcinogen, chrysene, was determined. Among the widely distributed chemicals, polychlorinated biphenyls (PCB) and preferentially 3,3,'4,4'-tetrachlorobiphenyl as well as polycyclic aromatic hydrocarbons (PAHs) and their heterocyclic analogues such as benzo[a]pyrene, benzo[b]- and -[j]fluoranthene, indeno[1,2,3-cd]pyrene, dibenz[a,h]acridine, benzo[b]naphtho-[2,1-d]thiophene, and 5,6-benzoflavone were found to be potent inducers stimulating the formation of the proximate, and some of them also the ultimate carcinogen of chrysene. Lindane, carbaryl, DDT, and pentachlorophenol were found to be inefficient or weak inducers. With the exception of phenobarbital no inducers were found among the pharmaceuticals investigated. Sex-dependent metabolism was found for Wistar-rats. No 1,2-oxidation was observed in females, and turnover rates were lower than in males. ...in most cases the same effective xenobiotic induces the bay-region diolepoxide in both chrysene and benz[a]anthracene.

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Non-Human Toxicity Values
LD50 Mouse ip >320 mg/kg bw

[1]. Degradation of Chrysene by Enriched Bacterial Consortium. Front Microbiol. 2018 Jun 26;9:1333.

Chrysene can cause cancer according to The Environmental Protection Agency (EPA).
Chrysene appears as a crystalline solid. Denser than water and insoluble in water. The primary hazard is the threat to the environment. Immediate steps should be taken to limit spread to the environment. Toxic by ingestion. Used to make other chemicals.
Chrysene is an ortho-fused polycyclic arene found commonly in the coal tar. It has a role as a plant metabolite.
Chrysene has been reported in Camellia sinensis with data available.
Chrysene is an aromatic hydrocarbon in coal tar, allied to naphthalene and anthracene. It is a white crystalline substance, C18H12, of strong blue fluorescence, but generally colored yellow by impurities.
Chrysene is one of over 100 different polycyclic aromatic hydrocarbons (PAHs). PAHs are chemicals that are formed during the incomplete burning of organic substances, such as fossil fuels. They are usually found as a mixture containing two or more of these compounds. (L10)

C18H12

228.29

228.093

218-01-9

Chrysene-d12;1719-03-5

9171

White to off-white solid powder

1.2±0.1 g/cm3

448.0±0.0 °C at 760 mmHg

246-256ºC

209.1±13.7 °C

0.0±0.5 mmHg at 25°C

1.771

5.91

0

0

0

18

264

0

WDECIBYCCFPHNR-UHFFFAOYSA-N

InChI=1S/C18H12/c1-3-7-15-13(5-1)9-11-18-16-8-4-2-6-14(16)10-12-17(15)18/h1-12H

chrysene

NSC6175; NSC-6175; ChryseneNSC 6175

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

DMSO : ~3.03 mg/mL (~13.27 mM)

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.)