TNF-α (pro-inflammatory cytokine), IL-6 (pro-inflammatory cytokine), TGF-β (anti-inflammatory cytokine), IL-10 (anti-inflammatory cytokine), and Foxp3 (specific biomarker of Treg cells).
No IC50/Ki/EC50/DC50 values were reported for these targets in this study.
Foxp3 is required for the development and function of Treg cells; Treg cells limit autoimmune responses and are involved in inflammation. [3]

In vitro study used pakchoi leaf discs (200 mg, 0.5 cm diameter) exposed to 5.61 μM phenanthrene for 72 h (leaf concentration 28.08 mg/kg). After washing, leaves were placed in phosphate buffer without phenanthrene and inoculated with 5% bacterial suspension of strain Ph6‑gfp (or non‑inoculated control) at 25 °C and 150 rpm. Phenanthrene removal followed first‑order exponential decay; the rate constant k for inoculated leaves was about 1.54 times higher than non‑inoculated, with half‑lives (T₁/₂) of 18.63 h and 28.52 h, respectively (R²>0.98). Inoculated leaves showed 31.36–61.78% lower phenanthrene content than controls after 24–72 h. Subcellular fractionation via differential centrifugation revealed that phenanthrene distributed into cell wall (CW), cell membrane (CM), cell organelles (CO), and cell solution (CS). Inoculation significantly (P<0.01) decreased phenanthrene content in CW and CO after 24 h (CM showed no significant difference). The bacterial cells colonized the intercellular space and cell wall region, increasing in number over time.[1]

In vivo hydroponic experiments: pakchoi seedlings were grown in 1/4‑strength Hoagland medium containing 5.61 μM phenanthrene for 3 days (resulting root and shoot concentrations of 61.61 and 9.67 mg/kg, respectively). Then roots were soaked in Ph6‑gfp suspension for 6 h, and leaves painted with the suspension three times (2 h each), followed by rinsing and transfer to phenanthrene‑free medium for 24‑day cultivation. Fluorescence microscopy confirmed internal colonization of roots, stems, and leaves. Compared to non‑inoculated controls, inoculated plants had 16.43–46.09% lower phenanthrene content in roots and 10.83–17.36% lower in shoots over 6–24 days; accumulation reductions were 16.56–44.67% in roots and 9.60–17.37% in shoots. Subcellular accumulation in inoculated roots: CW 37.45–28.73, CM 3.63–2.34, CO 26.28–18.35, CS 297.02–199.54 ng/plant (at 6–24 d), which were 12.13–27.51%, 7.70–16.68%, 13.37–30.70%, and 31.00–43.42% lower than non‑inoculated, respectively. In shoots, similar reductions were observed: CW 17.16–24.62%, CM 5.25–12.80%, CO 24.14–37.57%, CS 23.58–36.78% lower. The enhancement proportions (EP) of biodegradation were ordered CS > CO > CW > CM. Subcellular fraction normalized accumulation (A_FSF) decreased over time, with CO having higher values due to lipid content. Inoculation significantly (P<0.05) reduced A_FSF in most fractions.[1]

Suberin lamellae formation in exodermis and endodermis was assessed using Fluoro1 yellow 088 staining and fluorescence microscopy (FITC filter, λex: 465-495 nm). Root sections (200 µm thick) were obtained at 18 relative distances from the root apex (10% to 95% of total root length). The extent of suberization was quantified as the ratio of cells with developed suberin lamellae to total cells using digital image analysis. Effective distances for 10% (ED10) and 90% (ED90) suberization were estimated by nonlinear regression using the Hill model via REGTOX Excel macro, with 95% confidence intervals from bootstrap simulation.
Phenanthrene auto-fluorescence was directly observed using a UV-1A excitation filter (λex: 330-380 nm) and documented with a color camera. To discriminate phenanthrene from plant tissue auto-fluorescence, digital image analysis with a filter threshold was applied using images from control (non-exposed) roots. The same protocol was applied to sand grains as a control, with no difference observed between treated and non-treated images. ImageJ software with Bio-Formats and Biorad Reader plugins was used for image visualization, thresholding, and merging.

Subcellular fractionation procedure: Pakchoi leaves were mixed with extraction buffer (pH adjusted to 7.5 with 1.0 M NaOH), ground, and passed through a 100‑μm nylon cloth. The filtrate was centrifuged at 500×g for 5 min to obtain cell wall (CW) pellet. The supernatant was centrifuged at 10,000×g for 30 min to obtain cell organelles (CO) pellet. The supernatant was further centrifuged at 100,000×g for 30 min to obtain cell membrane (CM) pellet, and the remaining supernatant was designated as cell solution (CS). All steps at 4 °C. Fraction fresh weights: CW 7.8%, CM 0.65%, CO 4.9%, remainder CS. Phenanthrene in each fraction was analyzed by HPLC. For in vivo, roots and shoots were processed similarly.
HRMS with isotope‑labeling: samples from medium containing phenanthrene and ¹³C₂‑phenanthrene (each 2.81 μM) for 24 d were analyzed by Triple TOF 5600⁺ mass spectrometer in full scan (m/z 50–1000) with ESI negative mode at ‑4.5 kV, ion transfer capillary 550 °C. Metabolite identification criteria: accurate mass (error <5 ppm), isotope mass difference (ΔMW=2.0067 for two ¹³C), intensity ratio ~1:1, and absence in control samples.[1]

Healthy female Wistar rats weighing 180-200 g were obtained and housed under controlled conditions (temperature 20 ± 2°C, relative humidity 60 ± 10%, 12-hour light/dark cycle) with standard chow diet and ad libitum tap water. After a 1-week acclimatization period, rats were randomly divided into three groups: control group, low-dose group, and high-dose group, with 6 rats per group.
Phenanthrene was dissolved in corn oil and administered orally on day 1 at doses of 180 mg/kg (10% of LD50) for low-dose and 900 mg/kg (50% of LD50) for high-dose groups. On the last 2 days, Phenanthrene was administered by intraperitoneal injection at 90 mg/kg (low-dose) and 450 mg/kg (high-dose). Control rats received the same volume of corn oil.
Body weights were measured daily. All rats were sacrificed after 72 hours by cervical decapitation under ether anesthesia. Blood samples were collected via cardiac puncture, and serum obtained by centrifugation at 1204 g for 10 minutes. Lung and liver tissues were collected: pieces were fixed in 4% paraformaldehyde in physiological saline for H&E staining, and remaining tissues were flash-frozen and stored at -80°C for further analysis.
All experiments and treatments were approved by the Institutional Animal Ethical Clearance of Lanzhou University (ethical clearance number: IRB181201-1). [3]

Absorption, Distribution and Excretion
Following oral administration of 15.8 μg of 14C-labeled phenanthrene to coalfish, the accumulation of radioactive material in the liver was higher than in the gallbladder or muscle. Maximum accumulation occurred 10–24 hours post-administration, with approximately 72% of the radioactive material remaining in the liver after 17 hours. The highest level of radioactive material in the gallbladder occurred 24–48 hours post-administration. In Norwegian lobster, oral administration of 14C-labeled phenanthrene resulted in the highest levels of radioactive material in the hepatopancreatic system and muscle. Except for the intestines, the highest levels of radioactive material in all tissues occurred 1 day post-administration, with only trace amounts remaining after 28 days. The low level of radioactive material in the gastrointestinal tract 1 day post-administration indicates that most of the radioactive material was absorbed by the intestines. Norwegian lobsters accumulate radioactive material rapidly, with most of the radioactive material being cleared within a few weeks after a single administration. To investigate the transfer of polycyclic aromatic hydrocarbons (PAHs) and 2,3,7,8-tetrachlorodibenzo-p-dioxins (TCDDs) in the food chain, researchers fed pigs milk supplemented with 14C-phenanthrene, 14C-benzo[a]pyrene, or 14C-TCDD, respectively. Radioactivity analysis of portal and arterial blood showed that both PAHs and TCDDs were absorbed, reaching peak concentrations 4–6 hours after milk ingestion. Subsequently, blood radioactivity decreased, returning to background levels 24 hours after milk ingestion. Furthermore, the radioactivity of phenanthrene in portal and arterial blood (even at the lowest injected dose) was higher than that of benzo[a]pyrene and TCDD, consistent with its differences in lipophilicity and water solubility. The major 14C absorption of phenanthrene occurs within 1–3 hours after ingestion, while the major 14C absorption of benzo[a]pyrene and TCDD occurs within 3–6 hours after ingestion. The portal vein absorption rate of phenanthrene is very high (95%), that of benzo[a]pyrene is close to 33%, and that of TCDD is very low (9%). These results indicate that these three molecules exhibit distinctly different behaviors during digestion and absorption. Phenanthrene has a high absorption rate, primarily through blood circulation; while benzo[a]pyrene and tetrachlorodibenzo-dioxin (TCDD) show partial and weak absorption, respectively. This study aimed to investigate the transport of two polycyclic aromatic hydrocarbons (PAHs) (benzo[a]pyrene and phenanthrene) and one dioxin (2,3,7,8-tetrachlorodibenzo-dioxin) across the intestinal barrier, as these three compounds have different physicochemical properties. This study conducted in vitro and in vivo experiments. In the in vitro experiments, Caco-2 cells cultured on permeable membranes were used to determine the transepithelial permeability of the studied 14C-labeled molecules. In the in vivo experiments, the portal vein absorption kinetics of pigs fed with toxic milk were assessed. The results showed that all molecules were absorbed, and the absorption of the studied molecules varied in the intestine. Phenanthrene appeared to be the fastest-absorbing and most readily absorbed compound, followed by benzo[a]pyrene, and lastly 2,3,7,8-tetrachlorodibenzo-p-dioxin. Their absorption rates were 9.5%, 5.2%, and 1.4% after 6 hours of in vitro exposure, respectively; and 86.1%, 30.5%, and 8.3% after 24 hours of in vivo ingestion, respectively. These results indicate that the physicochemical properties of exogenous substances and the intestinal epithelium play a crucial role in the selective permeability and bioavailability of the tested microcontaminants. For more complete data on the absorption, distribution, and excretion of phenanthrene (11 metabolites), please visit the HSDB record page. Metabolites/Metabolites In rats and rabbits, phenanthrene is converted to trans-9,10-dihydro-9,10-dihydroxyphenanthrene. In rabbits and rats, phenanthrene is converted to trans-1,2-dihydro-1,2-dihydroxyphenanthrene, trans-3,4-dihydro-3,4-dihydroxyphenanthrene, and s-(9,10-dihydro-9-hydroxyphenanthrene-10-yl)glutathione. Phenanthrene formations, including 1-hydroxyphenanthrene, 2-hydroxyphenanthrene, 3-hydroxyphenanthrene, and 4-hydroxyphenanthrene, were detected in rats and rabbits. Phenanthrene is metabolized in rats and rabbits to produce 9-hydroxyphenanthrene. For more complete data on the metabolism/metabolites of phenanthrene (13 metabolites), please visit the HSDB record page.
Known human metabolites of phenanthrene include 9,10-dihydroxyphenanthrene, phenanthrene-3,4-diol, and phenanthrene-1,2-diol.
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 produces reactive intermediates, including epoxide intermediates, dihydrodiols, phenols, quinones, and various combinations thereof. Phenolic, quinone, and dihydrodiol compounds can all bind to glucuronides and sulfates; quinone compounds can also form glutathione conjugates. (L10)

---

Phenanthrene is taken up by pakchoi roots and translocated to shoots, distributing into subcellular fractions: CW, CM, CO, and CS. The distribution proportion (DP) reached a relatively stable state after 3 days of contamination, with higher percentages in CW and CS due to their larger fresh weights. Inoculation with Ph6‑gfp altered the subcellular DP and reduced accumulation in all fractions, especially in CS and CO. Biotransformation products identified by HRMS included 1‑hydroxy‑phenanthrene (product of hydroxylation), 1‑hydroxy‑2‑naphthoic acid, and salicylic acid, indicating a salicylic acid pathway. Inoculation promoted further metabolism, as only 1‑hydroxy‑phenanthrene was detected in non‑inoculated plants. Additionally, 12 compounds (including conjugation products with endogenous plant compounds) were identified in inoculated plants, compared to only 3 in non‑inoculated. Conjugation products likely formed via covalent binding between phenanthrene metabolites and endogenous compounds (amino acids, fatty acids, carbohydrates, etc.) and were sequestered in vacuoles or cell walls. Removal kinetics gave half‑lives (18.63 h with inoculation, 28.52 h without) as degradation parameters, but no classical pharmacokinetic parameters (e.g., bioavailability, clearance) were quantified.[1]

Toxicity Summary
Identification and Uses: Phenanthrene is a solid polycyclic aromatic hydrocarbon (PAH). It is used in dyes, explosives, pharmaceutical synthesis, biochemical research, and the production of phenanthrenequinone. Human Exposure and Toxicity: Exposure to phenanthrene in PAHs may be a risk factor for hyperuricemia. A metabolic activation assay in human lymphoblastic TK6 cells showed that 9 μg/mL of phenanthrene produced a positive mutagenic effect. Animal Studies: 24 hours after injection of 150 mg/kg phenanthrene into male rats, serum aspartate aminotransferase and gamma-glutamyl transferase levels were significantly elevated. No tumors were observed in 100 mice treated with phenanthrene for 9 months. Evidence from in vivo studies suggests that phenanthrene metabolites have relatively low tumorigenicity. The 1,2-, 3,4-, and 9,10-dihydrodiol metabolites of phenanthrene did not show tumor-initiating activity in mouse skin application assays. The mutagenicity of phenanthrene was assessed using genetic and cytogenetic mutagenicity assays (e.g., liver microsomal assay, host-mediated peritoneal assay, chromosomal aberration assay, sister chromatid exchange induction assay, etc.). The 3-methylcholanthrene-induced microsomal assay showed that phenanthrene was inactive in the gene conversion system, producing only a weak effect on the sister chromatid exchange system at high doses. Phenanthrene did not produce positive results in sister chromatid exchange and chromosomal aberration assays in mammalian cell cultures, nor in cell transformation assays in various mammalian cells (5–40 μg/mL). Phenanthrene induced cardiomyocyte hypertrophy in rats and H9C2 cells. This mechanism may involve reducing miR-133a expression through DNA methylation. Ecotoxicity studies: Phenanthrene is a major component of crude oil and one of the most abundant polycyclic aromatic hydrocarbons (PAHs) in aquatic ecosystems, and is readily absorbed and utilized by marine organisms. Phenanthrene may accumulate in fish, leading to altered antioxidant enzyme activity and the generation of reactive oxygen species (ROS) and oxidative stress. Phenanthrene can be passed from mother to embryo, affecting the health and viability of offspring. Phenanthrene may pose a risk to mussels and sea urchins. Polycyclic aromatic hydrocarbons (PAHs) can bind to blood proteins such as albumin, thereby facilitating their transport throughout 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 PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and various combinations thereof) covalently bind to DNA and other cellular macromolecules, inducing mutagenic and carcinogenic effects. (L10, L23, A27, A32)

---

Toxicity Data
LD50: 700 mg/kg (oral, mouse) (L907)
LD50: 700 mg/kg (intraperitoneal, mouse) (L907)
LD50: 56 mg/kg (intravenous, mouse) (L907)

---

Interactions
The toxicity of polycyclic aromatic hydrocarbons (PAHs) was determined using embryo-larval bioassays in mussels, sea urchins, and sea squirts. Fluorescent illumination enhanced the toxicity of phenanthrene, fluoranthene, pyrene, and hydroxypyrene compared to dark conditions, but did not enhance the toxicity of naphthalene and fluorene.
This study evaluated the acute toxicity of mixtures of metal-PAHs (e.g., cadmium, mercury, lead, fluoranthene, and phenanthrene) in sediments to two benthic copepod species. Exposure of slit-mouth copepods (Schizopera knabeni) to sediments containing single contaminants and mixtures revealed high tolerance in adults to single contaminant exposures to phenanthrene, cadmium, mercury, and lead, as well as to mixtures of cadmium, mercury, and lead. Binary experiments showed that while phenanthrene exhibited synergistic effects with cadmium and mercury, the synergistic effect with cadmium was stronger (2.8 times the predicted mortality). A synergistic effect was observed when a mixture of cadmium, mercury, and lead was mixed with phenanthrene, with a mortality rate 1.5 times higher than expected. A cadmium-phenanthrene synergistic effect was also observed in S. knabeni in water exposure experiments, indicating that this interaction is related to pharmacological damage rather than sediment-related exposure effects. Antagonistic effects exist among cadmium, mercury, and lead, which may attenuate the cadmium-phenanthrene synergistic effect in mixtures containing cadmium, mercury, lead, and phenanthrene. Experiments on Amphiascoides atopus showed that phenanthrene and fluoranthene both exhibited synergistic effects with cadmium in water exposure experiments. Our study suggests that cross-toxicity between metal-PAH mixtures may be common in benthic copepods, and the strong synergistic effects observed in binary mixtures may be attenuated in more diverse pollutant mixtures. However, the observed strength of the synergistic effect is concerning, indicating that existing sediment quality standards may not protect organisms simultaneously exposed to PAHs and metals (especially cadmium-PAH mixtures). The PAHs phenanthrene and perylene (7-isopropyl-1-methylphenanthrene) are lethal to juvenile rainbow trout (Oncorhynchus mykiss) under long-term exposure. Phenanthrene is a low-toxicity, non-cytochrome P4501A (CYP1A) inducer compound that accumulates in fish tissues upon exposure to lethal concentrations in water. Perylene is a highly toxic CYP1A inducer that is undetectable in tissues at lethal exposure concentrations. This study investigated the metabolism, excretion, and toxicity of perylene and phenanthrene in juvenile and early-maturing rainbow trout under co-exposure to the model CYP1A inducer β-naphthylflavonoid (βNF) or the inducer-inhibitor piperonyl butyl ether to determine whether modulation of CYP1A activity affects the metabolism and toxicity of polycyclic aromatic hydrocarbons (PAHs). Results showed that co-exposure to βNF increased phenanthrene metabolism, excretion rate, and toxicity. Piperonyl butyl ether inhibited phenanthrene metabolism and reduced the excretion of all phenanthrene metabolites. Consequently, embryonic mortality was increased, but the incidence of sublethal effects was not increased. Co-exposure of rainbow trout to perylene and βNF did not alter perylene metabolism and excretion, but increased perylene toxicity, likely due to an additive effect. Piperyl butyl ether inhibited perylene metabolism, reduced the excretion of some perylene metabolites, increased the excretion of others, and enhanced perylene toxicity. These results support the role of CYP1A activity in the metabolism and excretion of polycyclic aromatic hydrocarbons (PAHs) and the role of PAH metabolites generated by CYP1A in the chronic toxicity of juvenile fish. This study used Daphnia magna to determine the toxicity of phenanthrene (PHE) and 9,10-phenanthrenequinone (PHQ) in the presence or absence of copper. Of the three chemicals tested, copper was the most toxic, followed by PHQ, and then PHE, with 48-hour half-maximal effective concentrations (EC50) of 0.96, 1.72, and 5.33 μM, respectively. A concentration of 0.31 μM copper (approximately 5% effective concentration) reduced the EC50 of PHQ from 1.72 μM to 0.28 μM. Similarly, PHQ at a concentration of 1.2 μM (approximately 10% of the effective concentration) significantly reduced the EC50 value of copper from 0.96 μM to 0.30 μM. However, based on an additive response model, this synergistic effect was not observed in the mixture of copper and phenanthrene. With increasing external copper concentration, the amount of copper absorbed remained similar regardless of the presence of PHQ, indicating that the increased toxicity of the mixture is based on a physiological mechanism. Furthermore, the ability of copper and PHQ to generate reactive oxygen species (ROS) was determined. With copper alone, even a low concentration (0.63 μM) led to increased ROS levels. However, in the presence of PHQ, even at lower copper concentrations (0.31 μM), ROS levels increased. The potential attenuating effect of ascorbic acid (vitamin C) on the toxicity induced by copper, phenanthrenequinone, and their mixtures, and on the generation of reactive oxygen species (ROS) was subsequently investigated. Ascorbic acid protected the body from the toxicity mediated by copper and copper plus phenanthrenequinone mixtures, but had no effect on the toxicity of phenanthrenequinone alone. Ascorbic acid can also reduce ROS levels in the presence of copper and copper garphenanthrenequinone. ...
For more complete data on interactions of phenanthrene compounds (17 in total), please visit the HSDB record page.

---

Non-human toxicity values
Oral LD50 in mice: 700 mg/kg
Intravenous LD50 in mice: 56 mg/kg

---

Phenanthrene is recognized as a mutagenic and carcinogenic compound, but no specific toxicity data (e.g., LD₅₀, organ toxicity) are provided in this study. The study focuses on its biodegradation and detoxification via plant and endophytic metabolism, which reduces its biotoxicity to plant cells. No toxicokinetic parameters (e.g., plasma protein binding) are reported.[1]

[1]. Subcellular distribution and biotransformation of phenanthrene in pakchoi after inoculation with endophytic Pseudomonas sp. as probed using HRMS coupled with isotope-labeling. Environ Pollut. 2018 Jun;237:858-867.

[2]. Effect and localization of phenanthrene in maize roots. Chemosphere. 2016 Apr;149:130-6.

[3]. Effects of phenanthrene on oxidative stress and inflammation in lung and liver of female rats. Environ Toxicol. 2020 Jan;35(1):37-46.

[4]. Phenanthrene-Induced Apoptosis and Its Underlying Mechanism. Environ Sci Technol. 2017 Dec 19;51(24):14397-14405.

Phenanthrene is a colorless monoclinic crystal with a slightly aromatic odor. Solutions exhibit blue fluorescence. (NTP, 1992)
Phenanthrene is a polycyclic aromatic hydrocarbon (PAH) composed of three fused benzene rings, its name derived from the roots "phenyl" and "anthracene." It is an environmental pollutant and a metabolic product of mice. Phenanthrene is an ortho-fused PAH, an ortho-fused tricyclic hydrocarbon, belonging to the phenanthrene class of compounds.
Phenanthrene has been reported to exist in tobacco (Nicotiana tabacum), Buddleja lindleyana, and other organisms with relevant data.
Ravatite is a mineral with the molecular formula C14H10. Its corresponding International Mineralogical Association (IMA) number is IMA1992-019. The IMA symbol is Rav.
Phenanthrene is one of more than 100 PAHs. PAHs are chemical substances formed during the incomplete combustion of organic matter (such as fossil fuels). They usually exist in mixtures of two or more of these compounds. (L10)

---

Mechanism of Action
Increasing evidence suggests a link between environmental pollution and cardiac hypertrophy, but the mechanism remains unclear. This study aims to investigate whether phenanthrene (Phe) causes cardiac hypertrophy and to elucidate its molecular mechanism. We found that: 1) Phenanthrene exposure increased heart weight and cardiomyocyte volume in rats; 2) Phenanthrene exposure led to increased H9C2 cell volume and increased protein synthesis; 3) Phenylalanine exposure induced the expression of important markers of myocardial hypertrophy in H9C2 cells and rat hearts, such as atrial natriuretic peptide, B-type natriuretic peptide, and c-Myc; 4) Phenylalanine exposure disrupted the expression of key regulators of myocardial hypertrophy, miR-133a, CdC42, and RhoA, in H9C2 cells and rat hearts; 5) Phenylalanine exposure induced the expression of DNA methyltransferases (DNMTs) in H9C2 cells and rat hearts; 6) Phenylalanine exposure led to methylation of the CpG site at the miR-133a locus in H9C2 cells and reduced miR-133a expression; 7) Both DNMT inhibition and miR-133a overexpression alleviated the cell volume increase and CdC42 and RhoA expression disturbances induced by phenylalanine exposure. These results indicate that phenylalanine (Phe) can induce cardiomyocyte hypertrophy in rats and H9C2 cells. The mechanism may involve reducing miR-133a expression through DNA methylation.

---

Therapeutic Use
/Clinical Trials/ ClinicalTrials.gov is a registry and results 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 of the study; contact information for the study location; and links to relevant information from other health websites, such as the NLM's MedlinePlus (for providing patient health information) and PubMed (for providing citations and abstracts of academic articles in the medical field). The database includes [the following].

---

The study proposes three biotransformation mechanisms for phenanthrene in pakchoi with Ph6‑gfp inoculation: (1) plant metabolism via enzyme systems (polyphenol oxidase, peroxidase) that hydroxylate phenanthrene; (2) endophytic degradation by strain Ph6‑gfp, which mineralizes phenanthrene via the salicylic acid pathway to CO₂ and H₂O; (3) conjugation reactions where phenanthrene metabolites covalently bind to endogenous plant compounds to form less toxic conjugates. The inoculation hindered subcellular distribution from intercellular space to fractions by intercepting and biodegrading phenanthrene between cell wall and intercellular space. This is the first observation of endophyte‑enhanced biotransformation and conjugation at the subcellular level in a food crop. The strategy offers a low‑cost, environmentally friendly approach to reduce PAH contamination in crops. Future challenges include detection and risk assessment of conjugation products.[1]

C14H10

178.23

178.078

85-01-8

Phenanthrene-d10;1517-22-2;Phenanthrene-13C6;1189955-53-0

995

Monoclinic plates from alcohol
Colorless, shining crystals
Leaves (sublimes)

1.1±0.1 g/cm3

337.4±9.0 °C at 760 mmHg

98-100 °C(lit.)

146.6±12.8 °C

0.0±0.3 mmHg at 25°C

1.715

4.68

0

0

0

14

174

0

C1C=C2C=CC3C(C2=CC=1)=CC=CC=3

YNPNZTXNASCQKK-UHFFFAOYSA-N

InChI=1S/C14H10/c1-3-7-13-11(5-1)9-10-12-6-2-4-8-14(12)13/h1-10H

Phenanthrene

Phenanthrene Ravatite NSC 26256 NSC26256 NSC-26256[3] Helicene[3]Helicene [3]-Helicene

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 : ~250 mg/mL (~1402.68 mM)

Solubility in Formulation 1: ≥ 2.08 mg/mL (11.67 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

---

Solubility in Formulation 2: ≥ 2.08 mg/mL (11.67 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

---

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