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EC number: 205-711-1 | CAS number: 148-24-3
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Genetic toxicity: in vivo
Administrative data
- Endpoint:
- in vivo mammalian somatic cell study: cytogenicity / bone marrow chromosome aberration
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- study well documented, meets generally accepted scientific principles, acceptable for assessment
Data source
Reference
- Reference Type:
- publication
- Title:
- Genotoxic potency of three quinoline compounds evaluated in vivo in mouse marrow cells
- Author:
- McFee, A.F.
- Year:
- 1 989
- Bibliographic source:
- Environmental and Molecular Mutagenesis
Materials and methods
Test guideline
- Qualifier:
- equivalent or similar to guideline
- Guideline:
- OECD Guideline 475 (Mammalian Bone Marrow Chromosome Aberration Test)
- GLP compliance:
- not specified
- Type of assay:
- mammalian bone marrow chromosome aberration test
Test material
- Specific details on test material used for the study:
- 8-hydroxyquinoline. Purity and batch not reported.
Test animals
- Species:
- mouse
- Strain:
- B6C3F1
- Sex:
- female
- Details on test animals or test system and environmental conditions:
- Food and water were provided ad libitum. Mice were obtained from NTP contract supplier (Frederick Cancer Reseach Institute).
Administration / exposure
- Route of administration:
- intraperitoneal
- Vehicle:
- Corn oil
- Duration of treatment / exposure:
- 17 h and 36 h for chromosomal aberrations. 23 h and 42 h for SCE analyses.
- Frequency of treatment:
- Single doses
- Control animals:
- yes, concurrent vehicle
- Positive control(s):
- 7,12-dimethylbenz[a]anthracene (DMBA)
Examinations
- Tissues and cell types examined:
- Bone marrow cells
- Details of tissue and slide preparation:
- A single femur was removed, stripped of its adherent tissue, and the epiphyseal ends were snipped off. Cells were flushed into a centrifuge tube by approximately 6 ml of saline injected through a 25-gauge needle inserted into the marrow cavity. Tubes were centrifuged at 800g for 5 min, the saline was decanted, and cells were resuspended in 3 ml of hypotonic solution (0.01 M sodium citrate plus 0.05 M potassium chloride) and held at 37°C for 20 min. After centrifugation and decanting, cells were resuspended in 5 ml of 3: I methano1:acetic acid and washed through one additional change of 3:1 and one change of 2:l fixative before being resuspended in a small quantity (.25-.75 ml) of the 2:l fixative. Two drops of this cell suspension were dropped onto the flat surface of a clean microscope slide that had been freshly removed from cold,
distilled water, the fixative was ignited by touching the edge of the slide to an alcohol flame, and slides were placed on a warming plate (56°C) until completely dry. Slides were labeled with the animal number and stored for 24-96 h before being stained by the fluorescence-plus-Giemsa technique. - Evaluation criteria:
- CAs were quantitated among 50 metaphases known to be at their first post-treatment division by their uniformly darkstained chromosomes; one-half of the cells were scored by each of two observers. For aberration scoring, gaps were defined as achromatic regions fully traversing the chromatid, but having a length equal to or less than the diameter of the chromatid; open regions of a greater extent or with obvious displacement of the distal segment of the chromatid were considered to be deletions. All anomalies were tabulated, and separate statistical analyses were performed on the data including and excluding the values for gaps. Sister chromatid exchanges were counted in 25 second-division metaphases from each animal sacrificed 23 h post-treatment; approximately one-half were scored by each observer. The rate of cell division was estimated for mice killed at 23 h by tabulating the proportion of first, second, and third or later metaphases among the first 100 encountered in a random scan of slides from each animal.
- Statistics:
- Statistical analyses of the data employed the one-tailed trend test of Margolin et al. [1986], based on individual animal responses and utilizing an alpha level of 0.05. Separate analyses were performed to determine if treatmentrelated increases occurred for SCEdcell and for average generation time; aberration data were separately analyzed for both the percent cells with at least one aberration and for the aberration ratekell, both values being independently analyzed with and without the inclusion of data for gaps.
Results and discussion
Test results
- Key result
- Sex:
- female
- Genotoxicity:
- negative
- Toxicity:
- yes
- Remarks:
- at 70 and 100 mg/kg bw
- Vehicle controls validity:
- valid
- Negative controls validity:
- not examined
- Positive controls validity:
- valid
- Additional information on results:
- In first trial, 8-hydroxyquinoline was injected intraperitoneally at doses 25, 50 and 100 mg/kg bw. Due to lethality of high dose,doses were reduced to 17.5, 35 and 70 mg/kg bw in the second trial. High mortality was observed at the high dose level in the first and second trial, respectively.
Any other information on results incl. tables
Table 1. CAs and SCEs in marrow cells of mice injected with 8 -hydroxyquinoline. 17 h exposure.
Dose (mg/kg) | No. of mice | % aberrant cells (±SE) |
0 | 8 | 0.50±0.33 |
25 | 8 | 1.50±0.63 |
50 | 8 | 1.75±0.59 |
100 | 8 | 1.25±0.75 |
DMBA | 8 | 12.00±1.31 |
TrendPvalue | .2410 |
Table 2. CAs and SCEs in marrow cells of mice injected with 8 -hydroxyquinoline. 23 h exposure.
Dose (mg/kg) | No. of mice | % SCE/cell (±SE) |
0 | 4 | 5.49±0.40 |
25 | 4 | 3.60±0.53 |
50 | 4 | 4.55±0.68 |
100 | 4 | 4.60±1.25 |
DMBA | 4 | 9.31±0.53 |
TrendPvalue | .2578 |
Table 3. CAs and SCEs in marrow cells of mice injected with 8 -hydroxyquinoline. 36 h exposure.
Dose (mg/kg) | No. of mice | % aberrant cells (±SE) |
0 | 8 | 4.75±1.31 |
17.5 | 8 | 4.24±0.80 |
35 | 8 | 4.50±1.76 |
70 | 8 | 6.00±2.04 |
DMBA | 8 | 39.25±5.50 |
TrendPvalue | .2438 |
Table 4. CAs and SCEs in marrow cells of mice injected with 8 -hydroxyquinoline. 42 h exposure.
Dose (mg/kg) | No. of mice | % SCE cells (±SE) |
0 | 4 | 4.68±0.97 |
17.5 | 4 | 4.61±0.26 |
35 | 4 | 3.60±0.69 |
70 | 4 | 3.99±0.04 |
DMBA | 4 | 9.23±0.97 |
Trend P value | .1688 |
Applicant's summary and conclusion
- Conclusions:
- No induction of chromosomal aberrations in bone marrow cells was observed. Also, no increase in the rate of sister chromatid exchange was observed.
- Executive summary:
8-hydroxyquinoline was assayed for the potential to induce chromosomal aberrations in bone marrow cells of B6C3F1 mice by single dose levels ranged from 17.5 to 100 mg/kg bw
(McFee, 1989). Sister chromatid exchanges in the marrow cells were also quantified. The study was non-GLP compliant and pre-guideline. Purity and batch specifications of the test
compound were unknown. In a first trial, 8-hydroxyquinoline was injected intraperitoneally at doses of 25, 50 and 100 mg/kg bw. Due to lethality of the high dose, doses were reduced to 17.5, 35 and 70 mg/kg bw in the second trial. High mortality, 42 and 40%, was observed at the high dose level in the first and second trial, respectively.
Under the conditions of this study, 8-hydroxyquinoline did not induce chromosomal aberrations in bone marrow cells of mice. Besides, no increase in the rate of sister chromatid
exchange was observed.
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