Group A-2 ‰»Šw\‘’@(Chemical Structure)  
œ@2-Acetylaminofluorene (2-AAF)i‚Q|ƒAƒZƒ`ƒ‹ƒAƒ~ƒmƒtƒ[ƒŒƒ“j
@@
53-96-3@Laboratory/Carcinogen @MW: 223.27
AM Sal & E. col. Min ( 10ƒΚg/plate, +S9)  1)
CA CHL/IU Min ( 0.5 mg/ml, +S9), 3-18h: D20= 0.48; TR= 40) › 2)
MLA L5178Y Min ( 40ƒΚg/ml, +S9) › 3, 6)
CA Sy. Ham. Min ( 5ƒΚg/ml) › 4)
SOS E. coli Min ( 0.3 mM, +S9) › 5)
1) Ames BN, et al. : Mutation Res., 31, 347-364 (1971)
2) Sofuni T. (Ed.): Data Book of Chromosome Aberration Test In Vitro, LIC/Tokyo (1998) (Tables in English)
3) Clive D, et al.: Mutation Res., 59, 61-108 (1979)@@@@@@@@@@@@@
4) DiPaolo JA, et al.: Nature, 235, 278-280 (1979)

5) von der Hude W. et al., Mutation Res., 203, 81-94 (1983)     
6) Oberly TJ., et al., Mutation Res., 125, 291-306 (1984)
œ Acetylarsan
@@
534-33-6@Medicine@348.21
CA Human LY Max (?)   1j
1) Paton GR & Allison AC: Mutation Res., 16, 332-336 (1972)@@@

œ Acetylene tetrabromide i
ƒAƒZƒ`ƒŒƒ“@ƒeƒgƒ‰ƒuƒƒ}ƒCƒhj
@@
79-27-6@ Industry @@345.70

AM Sal. Max ( 17ƒΚmol/plate)   1)
AM Sal. Max (?)   2)
1) Brem H, et al.: Cancer Res., 34, 2576-2579 (1974)
2) Rosenkrantz HS, et al: Mutation Res., 41, 61-70 (1976)

œ N-Acetylglucosamine@iN-
ƒAƒZƒ`ƒ‹ƒOƒ‹ƒRƒTƒ~ƒ“j
@@
7512-17-6@ Food@@221.21
CA CHL/IU Max ( 5.0mg/ml, }S‚Xj   1)
1) Sofuni T. (Ed.): Data Book of Chromosome Aberration Test In Vitro, LIC/Tokyo (1998)@(Tables in English)@@@@
@@    œ 1-Acetyl-1-methyl-2-nitroso-2-phenylhydrazine@@@@@@@@@@@
         
76186-63-5   Industry @193.21
CA CHL/IU Min ( 0.25 mg/ml, -‚r9j, 48h, D20= 0.45CTR= 2.0@@@ › 1)
1) Sofuni T. (Ed.): Data Book of Chromosome Aberration Test In Vitro, LIC/Tokyo (1998) (Tables in English)
œ 1-Acetyl-1-methyl-2-phenylhydrazine
@@
38604-70-5@@Industry@164.21

CA CHL/IU Min ( 0.5 mg/ml, -S9j,@24h;@D20= 0.65C@TR= 8.0 › 1)
1) Sofuni T. (Ed.): Data Book of Chromosome Aberration Test In Vitro, LIC/Tokyo (1998) (Tables in English)

œ 1-Acetyl-5-nitroindoline
@
33632-27-8@ Industry@@206.2
CA CHL/IU Min ( 3.0 mg/ml, -S9), 6h: Poly., PD20= 3.4 ›w 1)
1) Ministry of Labor: Mutagen. Test Data of Exist. Chem. Subst, JETOC (Ed.), Suppl. 2 (2000) (Tables in English)

œ Acetylsalicylic acid@(Aspirin)i
ƒAƒXƒsƒŠƒ“)@
@
50-78-2 @Medicine@@180.15

REC B. subtilis Min ( 5 mg/disk) › 1)
AM Sal . Max ( 50 mg/plate,}S9)   2)
CA CHL/IU Min ( 0.03 mg/ml, +S9), 3-21h; D20= 0.037 TR= 500  3)
CA Human LY Min ( 0.075 mg/ml, -S9), 72h › 4)
CA ML Min (?) › 5)
CT C3H/10T1/2 Max ( 3.0 mg/ml), 24h   6)
1) Kuboyama N & Fujii A: J. Nihon Univ. Sch. Dent., 34, 183-195@(1992)
2) Ishidate M.Jr & Odashima S:@Mtution Res., 48, 377-354(1977)@@
3) Sofuni T. (Ed.): Data Book of Chromosome Aberration Test In Vitro, LIC/Tokyo (1998) (Tables in English)
4) Watanabe M., Jpn. J. Hyg., 37, 673-685 (1998)
5) Sanker DV, et al.: Res Comm. Chem. Pathol. Pharmacol., 2, 477-482 (1971)
6) Patierno SR, et al: Cancer Res., 49, 1038-1044 (1989)

@@@@@
yReviewz@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
1) Brem H, et al.: Cancer Res., 34, 2576-2579 (1974)@@@@@@@@@@@@@@

US-NTP Genotoxicity ScreeningF
›Ames test:  

œ Acridine
iƒAƒNƒŠƒWƒ“j
@
260-94-6@Industry@178.2
CA CHL/IU Min ( 0.03 mg/ml, -S9), 24h: D20= 0.041; TR= 500), Poly (48h) › 1)
1) Ishidate, M.Jr.. (Ed.): Data Book of Chromosomal Aberration Test in Vitro LIC/Tokyo, Elsevier/Amsterdam (1987

yReviewz
1) Kodolfo C, et al: Mutation Res., 171 (2), 179 (1992)

œ Acrolein iƒAƒNƒƒŒƒCƒ“jiAcrylaldehydeG@ƒvƒƒxƒi[ƒ‹G@ƒvƒƒpƒ“ƒAƒ‹ƒfƒqƒhj
@
107-02-8@Industry@56.06

AM Sal. Max ( 0.005 mg/plate, }S9)   1)
AM Sal. Min ( 0.05 mg/plate, +S9) ›w 2)
AM Sal. Min ( 0.0001 mg/plate, -S9) ›w 3)
AM Sal. Min ( 4 mM, -S9) › 4)
AM Sal. Min ( 0.4ƒΚmol/plate, -S9) › 5)
AM Sal. Max ( 5mM,/plate,@}S9)   6)
AM Sal. Max ( 2mM/plate, }S9)   7)
AM Sal. Min ( 75 ƒΚM/plate, }S9) › 8)
AM Sal. Max ( 0.1 ƒΚg/plate,}S9)   9)
AM E. coli Min ( 10 mM, -S9) ›w 10)
YM S. cerevisiae Max ( 640 mg/L, -S9)   11)
SM V79 Min ( 2 ƒΚM, -S9) › 12)
SM CHO Max ( 6.7 ƒΚg/ml, -S9)   13)
SM CHO Max ( 5.6 ƒΚg/ml, -S9)   14)
CA CHO Max ( 1ƒΚg/ml, }S9)   15)
CA CHO Min ( 40 ƒΚM, +S9) › 16)
SCE Hum. lym. Min ( 20ƒΚM, -S9) › 17)
SCE CHO Min ( 18ƒΚM, -S9) › 15)
DNA Hum. fibroblasts Min ( 300ƒΚM) › 18)
SLRLv Drosophila Max ( 3000 ppm, fed ), for 72h   19)
SM Drosophila Min ( 280 mg/kg, fed ) › 20)
DLv Mice Max ( 2 mg/kg , ip )   21)
1) Hales  BF, Cancer Res., 42, 3016-3021 (1982)
2) Haworth S., et al., Environ Mutagen., 5 (suppl 1), 3-142 (1983)
3) Lutz D., et al., Mutation Res., 93, 305-315 (1982)

4)Foiles PG, et al: Carcinogenesis, 10, 87-90 (1989)
5) Marnett LJ., Mutation Res., 148, 25-34 (1985)
6) Jung R., et al., Mutation Res., 278, 265-270 (1992)
7) Rosen JD., et al., Mutation Res., 78, 113-119 (1980)
8) Parent RG., et al., J. Appl. Toxicol., 16 (2) 103-108 (1996)
9) Lijinsky N & Andrews AW, Teratog. Carcinog. Mutagen., 1, 259-267 (1980)
10) Hemminki K., et al., Arch Toxicol., 46, 277-285 (1980)
11) I zard C, C.R. Acad. Sci.,, Paris, D276, 3037-3040 (1973)

12) Smith RA,m et al., Carcinogenesis, 11, 497-498 (1990)
13) Parent RA., et al., J. Appl. Toxicol., 11 (2), 91-95 (1991)
14) Foiles PG, et al: Carcinogenesis, 2059-2061 (1990)
15) Galloway SM., et al., Environ. Mol., Mutagen., 10m 1-175 (
1987)
16) Au Wl, et al., , Cytogenet. Cell Genetics., 26, 108-116 (1980)
17) Wilmer JL., et al., Environ. Mol. Mutagen., 7 (Suppl. 3 ), 67 (1985)
18) Dypbukt JM., et al., Carcinogenesis, 14, 975-980 (1993)
19) Zimmering S., et al., Environ. Mutagen., 7, 87-100 (1985)
20) Sierra LM., et al., Mutation Res., 260, 247-250 (1991)
21) Epstein SS & Shafner H., Nature, 219, 285-387 (1968)
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@

US-NTP Genotoxicity ScreeningF
› Ames test: @›
› CA test: @ 
› SCE test: @›
› Drosophila (SLRL) Test:@ 
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@

yNotez (Sited from IARC Monograph, Suppl. 6 (1987)
@No data were available on the genetic and related effects of acorlein in humans. Acrolein did not induce DL mutation in mice. it induced SCE in CHO cells in vitro. In yeast, it did not cause DNA cross-links or strand breaks and was not mutagenic.@‚h‚” was mutanenic to bacteria . (IARC Monograph, 19. 479, 36, 133, 1979)

yNotez (Sited from CICADS Document, 43, 2002)

  In the absence of cytotoxicity, acrolein induces gene mutations in both bacteria (with or without metabolic activation) (Hemminki et al., 1980; Lijinsky & Andrews, 1980; Hales, 1982; Lutz et al., 1982; Haworth et al., 1983; Marnett et al., 1985; Foiles et al., 1989; Parent et al., 1996) and mammalian cells in culture (Smith et al., 1990), as well as structural chromosomal aberrations in Chinese hamster ovary (CHO) cells (Au et al., 1980) and sister chromatid exchanges in CHO cells (Au et al., 1980; Galloway et al., 1987) and cultured human lymphocytes (Wilmer et al., 1986). The mode of induction of the genotoxicity of acrolein appears to involve the induction of DNA damage. Acrolein binds to DNA, forms DNA-protein cross-links (Grafstrom et al., 1988), and induces DNA single strand breaks in human fibroblasts (Dypbukt et al., 1993) and bronchial epithelial cells (Grafstrom et al., 1988). In human fibroblasts, acrolein induces mutations at the HPRT locus in DNA repair-deficient cells from xeroderma pigmentosum patients but not in normal cells (Curren et al., 1988), supporting DNA damage as the primary mechanism for acrolein-induced mutagenesis. The results of in vitro studies suggest that intracellular glutathione (or other free sulfhydryl groups) may protect against the DNA-damaging effects of acrolein (Eisenbrand et al., 1995).

  Although the results of in vitro studies indicate that acrolein can react directly with DNA and proteins to form stable adducts, an increased formation of DNA-protein cross-links was not observed in the nasal mucosa of male F344 rats exposed in vivo (by inhalation) to 5 mg acrolein/m3 (2 ppm) for 6 h (Lam et al., 1985).

  Although less relevant to the assessment of genotoxicity at the site of initial contact (i.e., where critical effects occur), in vivo studies of the genotoxicity of acrolein at systemic sites are not extensive. In a dominant lethal study in male ICR/Ha Swiss mice, acrolein (administered by intraperitoneal injection) at doses up to 2.2 mg/kg body weight had no effect upon the numbers of pregnancies, implants, or fetal deaths (Epstein et al., 1972). Increases in the frequency of chromosomal aberrations in peripheral blood lymphocytes or bone marrow cells were not observed in studies in which F344 rats were exposed (by inhalation) to concentrations up to 9.2 mg acrolein/m3 (4.0 ppm) for 6 h/day, 5 days/week, for 62 days (Kutzman, 1981) or in which Sprague-Dawley rats were administered (by intraperitoneal injection) single doses of up to 4.1 mg acrolein/kg body weight (BSC, 1982b), respectively.


œ
Acrylamide@(Acrylic amide) iƒAƒNƒŠƒ‹ƒAƒ}ƒCƒhj
@
  79-06-1@@Industry @71.08@@@@@@@@@@@@@@@@@@@@@@
AM Sal Max ( 30 mg/plate, }S9)   1-3)
CA CHL/IU Min ( 0.15 mg/ml, -S9): D20= 0.14,TR= 60 › 4)
SM CHO, (HGPRT) Max ( 1.2 mg/ml)
  5)
MLA L5178Y Min ( 0.85 mg/ml) › 6)
UDS Rat hepatocytes Max@(?)   7)
UDS Rat hepatocytes Max ( 10-2 M)   8)
SCE CHO Max (?)   9)
CT C3H /10T1/2 Min ( 0.2 mg/ml) › 10)
CT BALB/c3T3 Min ( 0.15 mg/ml) › 11)
MN Ch, Fb Max ( 10-3 M, 3h)   12)
MNv Mice, BM Max ( 100 mg/kg x 2, ip)   13)
MNv Mice Max ( 75 mg/kg /day x 2, or)   14)
CAv Mice, BM Max ( 100 mg/kg@ip)   15)
CAv Mice, Germ Cells Min  ( 100 mg/kg@ip) › 15)
DL Mice Min  ( 50 mg/kg/d x 5, ip) › 16)
DL Rats Min  ( 5.8 mg/kg/d, or) › 17)
SLRLv Drosophila Max ( 100 ppm)   18)
CAv Mice, testis Min  (?) › 19)
DNAv Mice Min  (?), derm › 20)
1) Lijinsky W & Andrews AW: Teratogen. Carcinogen. Mutagen., 1, 259-267 (1980)
2)  Hashimoto K. & Tani H., Mutation Res., 158, 129-133 (1985)
3)  NTP Publication NTP-85-055 (1985)
4)  Sofuni T. (Ed.): Data Book of Chromosome Aberration Test In Vitro, LIC/ Tokyo (1998) (Tables in English)
5)  Bull RJ, et al.: Cancer Res., 44, 107-111 (1976)

6) Moore MM, et al: Environ. Mutagen., 9, 261-267 (1987)
7) Butterworth BE, et al.: Environ. Mutagen., 8, 99-108 (1986)
8)  Miller MJ. & McQueen C., Environ. Mutagen., 8, 99-108 (1986)
9) Abe S. & Sasaki M: Prog Top. Cytogenet. 2, 461-514 (1982)
10) Banerjee S, & Segal A., Cancer Lett., 32, 293-304 (1986)
11) Tsuda H., et al. : Mutagenesis, 8, 23-29 (1993)
12) Zaichkina S. & Ganassi Y., Stud. Biophys, 99, 203-210 (1984)
13)@Morita T, et al : Mutation Res., 389, 3-122 (1997)
14)  American Cyanamid Co., EPA Doc. Cntract. No. 878211681 (1983)
15)  Shiraishi Y: Mutation Res., 57, 313-324 (1978)
16)  Shelby MD., et al., Mutation Res., 173, 35-40 (1986)
17)  Smith MK, et al., Mutation Res., 173, 273-278 (1986)
18) American Cyanamid Co., EPA Doc. Cntract. No. 878216235 (1985)
19) Adler, ID et al.: Mutation Res., 309, 285-291 (1994)
20) Carlson and Weaver, Toxicol. Appl. Pharmacol., 79, 307-313, 1985)

(Additional Ref.)
1) IPCS/WHO, Environ. Health Criteria, 49 (1985)
2)ACGIH, Documentation of the Threshold Limit Values and Biollogical Exposure Indicies (1991)
3) IARC,  Monog. on the Evaluation of the Carcinogenic Risk of Chemicals to Human, 60 (1994)
4) IARC,  Monog. on the Evaluation of the Carcinogenic Risk of Chemicals to Human, 39 (1986)

yReviewz@
1) Kodolfo C, et al Mutation Res., 171 (2), 179 (1992)
2) Dearfield et al. ; Mutation Res., 195, 45-77 (1988)

IARC Carcinogenicity CriteriaF  Group 2B
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œAbbreviation @iΘ—ͺ‹L†j@
œMutagenicity (•ΟˆΩŒ΄«j
œTest Systems@(ŽŽŒ±–@‚ΜŽν—ށj
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