AM	Sal & E. col.	Min ( 10μg/plate, +S9)	◎	1)
CA	CHL/IU	Min ( 0.5 mg/ml, +S9), 3-18h: D20= 0.48; TR= 40)	○	2)
MLA	L5178Y	Min ( 40μg/ml, +S9)	○	3, 6)
CA	Sy. Ham.	Min ( 5μg/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)

● Acetylarsan
　　534-33-6　Medicine　348.21

CA

Human LY

Max (?)

□

1）

1) Paton GR & Allison AC: Mutation Res., 16, 332-336 (1972)　　　

● Acetylene tetrabromide （アセチレン　テトラブロマイド）
　　79-27-6　 Industry 　　345.70

AM	Sal.	Max ( 17μmol/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)

● N-Acetylglucosamine　（N-アセチルグルコサミン）
　　7512-17-6　 Food　　221.21

CA

CHL/IU

Max ( 5.0mg/ml, ±S９）

□

1)

1) Sofuni T. (Ed.): Data Book of Chromosome Aberration Test In Vitro, LIC/Tokyo (1998)　(Tables in English)　　　　

● 1-Acetyl-1-methyl-2-phenylhydrazine
　　38604-70-5　　Industry　164.21

CA

CHL/IU

Min ( 0.5 mg/ml, -S9）,　24h;　D20= 0.65，　TR= 8.0

○

1)

1) Sofuni T. (Ed.): Data Book of Chromosome Aberration Test In Vitro, LIC/Tokyo (1998) (Tables in English)

● 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)

● Acetylsalicylic acid　(Aspirin)（アスピリン)　
　 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)
　　　　　
【Review】　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　
1) Brem H, et al.: Cancer Res., 34, 2576-2579 (1974)　　　　　　　　　　　　　　

US-NTP Genotoxicity Screening：
○Ames test: □

● Acridine （アクリジン）
　 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

【Review】
1) Kodolfo C, et al: Mutation Res., 171 (2), 179 (1992)

● Acrolein （アクロレイン）（Acrylaldehyde；　プロベナール；　プロパンアルデヒド）
　 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 ( 0.4μmol/plate, -S9)	○	5)
AM	Sal.	Max ( 5mM,/plate,　±S9)	□	6)
AM	Sal.	Max ( 2mM/plate, ±S9)	□	7)
AM	Sal.	Min ( 75 μM/plate, ±S9)	○	8)
AM	Sal.	Max ( 0.1 μg/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 μM, -S9)	○	12)
SM	CHO	Max ( 6.7 μg/ml, -S9)	□	13)
SM	CHO	Max ( 5.6 μg/ml, -S9)	□	14)
CA	CHO	Max ( 1μg/ml, ±S9)	□	15)
CA	CHO	Min ( 40 μM, +S9)	○	16)
SCE	Hum. lym.	Min ( 20μM, -S9)	○	17)
SCE	CHO	Min ( 18μM, -S9)	○	15)
DNA	Hum. fibroblasts	Min ( 300μM)	○	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：
○ Ames test: 　○
○ CA test: 　□
○ SCE test: 　○
○ Drosophila (SLRL) Test:　□　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　　

【Note】 (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.　Ｉｔ was mutanenic to bacteria . (IARC Monograph, 19. 479, 36, 133, 1979)

【Note】 (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.

● Acrylamide　(Acrylic amide) （アクリルアマイド）
　   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)

【Review】　
1) Kodolfo C, et al Mutation Res., 171 (2), 179 (1992)
2) Dearfield et al. ; Mutation Res., 195, 45-77 (1988)

IARC Carcinogenicity Criteria：  Group 2B

●Top Page　（トップページ）

●Abbreviation 　（省略記号）

●Mutagenicity (変異原性）

●Test Systems　(試験法の種類）

●Technical Problems　（技術的問題点）

●List of　Compounds（化合物リスト）

●Evaluation of Results（試験結果の評価）

●Information （その他の情報）