Group A-9 ‰»Šw\‘’@(Chemical Structure)  

œ Anthracene (ƒAƒ“ƒgƒ‰ƒZƒ“j (Paranaphthalene)
@  
CAS: 120-12-7 Industry @MW: 178.23
AM Sal./E.coli Min (?)

›w

1,2)

AM Sal. /E.coli Max (5.0 mg/plate, }S9)   3)
AM Sal. /E.coli Min (0.039 mg/ml, +HS9); Spa=5380 › 4)
CA CHL/IU Min (0.02 mg/ml, +S9), 6-18h; D20= 0.03;TR= 450

›

5)
CA CHL/IU Min (0.015 mg/ml, +S9), 6-18h; D20= 0.013; TR= 1500 › 4)
MLA L5178Y Min (?) › 6)
MLA L5178Y Min (?) › 7)
1) Dunkel VC., et al., Environ. Mutagen., 7 (Suppl. 5) 1-248 (1985)
2) Mortelmans, K., et al., Environ. Mutagen., 8 (Suppl. 7) 1-119 (1986)
3) Ministry of Labour: Mutagen. Test Data of Exist. Chem. Subst., JETOC (Ed.) (1996) (Tables in English)
4) Ministry of Labour: Mutagen. Test Data of Exist. Chem. Subst., JETOC (Ed.) (2008), p.123 (Tables in English
5) Sofuni T. (Ed.): Data Book of Chromosomal Aberration Test In Vitro, LIC, Tokyo
(1998j(Tables in English)
6) Mitchell AD., et al., Environ. Mol. Mutagen., 12 (Suppl.13) 37-102 (1988)
7) Myhr BC & Caspary WJ., Environ. Mol. Mutaagen., 12 (Suppl.13) 103-194 (1988)
IARC Carcinogenicity Criteria:
Group 3 (Inadequate evidence in human and experimental animals)

œ 9-Anthracenemethanol (9-ƒAƒ“ƒgƒ‰ƒZƒ“ƒƒ^ƒm[ƒ‹j
@
1468-95-7 Industry @208.26
AM Sal. /E.coli Min (0.078 mg/plate, +30%S9); Spa= 2070

›

1)

CA CHL/IU Min (0.1 mg/ml, +S9), D20= 0.073, TR= 290 › 2)
1) Ministry of Labour: Mutagen. Test Data of Exist. Chem. Subst., JETOC (Ed.), Suppl. 3, pp. 201 (2005) (Tables in English)
2) Ministry of Labour: Mutagen. Test Data of Exist. Chem. Subst., JETOC (Ed.), Suppl.4, pp.164 (2008) (Tables in English)

œ Anthraquinone iƒAƒ“ƒgƒ‰ƒLƒmƒ“j
@  
84-65-1 @Food@@208.22
AM Sal./E.coli Min (10.0 mg/plate+30%-S9); Spa= 12.8

›w

1)

1) Ministry of Labour: Mutagen. Test Data of Exist. Chem. Subst., JETOC (Ed.) (1996) (Tables in English)

œ Apocarotenal (10% aqueous solution)
@  
1107-26-2 Labouratory@@416.65
CA CHL/IU Max (1.0 mg/ml, -S9), 24-48h

 

1)

1) Sofuni T. (Ed.): Data Book of Chromosomal Aberration Test In Vitro, LIC, Tokyo (1998j (Tables in English)
œ L-Arginine L-gulutamate
@  
4320-30-3 @Food@@321.34
AM Sal./ E.coli Max (10.0 mg/plate}S9)

 

1)

CA CHL/IU Max (4.0 mg/ml, -S9), 24-48h

 

2)

1) Ishidate MJr (Ed): Data Book for Mutagenicity in Bacateria, LIC/Tokyo (1991) (Tables in English)
2) Sofuni T. (Ed.): Data Book of Chromosomal Aberration Test In Vitro, LIC, Tokyo (1998j(Tables in English)

œ
Arsenic, elemental and inorganic compounds (Except Arsine)
@
(ƒq‘fA–³‹@ƒq‘f‰»‡•¨j
@ 
7440-38-2 (Elemental) @Industry@Atomic Wt: 74.92@@@@@@@@@@@@@@@@@@
AM E.coli Min (?) (Sodium arsenite)

›

1)

AM E.coli Max ( 3.25 mg/ml) (Sodium arsenite)

 

2)
YM Yeast Max (?) (Sodium arsenite) Gene Conversion Assay
Min (?) Reverse Mutation Assay

 
›

3)
SM CHO Max (?) (Sodium arsenite)

 

2)

SCE SH Embryo & Human LY Min (?) (Sodium arsenite & arsenate)

›

4), 15)

CA Human Leukocytes Na2HAsO4 @Min ( 72 x 10-7M)
H
3AsO4 @  Min ( 72 x 10-7M)
As
2O5@    Min ( 36 x 10-7M)
NaAsO
2@   Min ( 24 x 10-7M)
AsCl
3@@  Min (  6 x 10-7M)
As
2O3@    Min ( 12 x 10-7M)
›
›
›
›
›
›

5)

MLA L5178Y Min (?) (Sodium arsenite ), -S9
Min (?)(Sodium arsenate), +S9
›
›

6), 14)

CA CHO
Human LY
Min (5 ƒΚg/ml) (Sodium arsenite & arsenate)

›

7)

CT SH Embryo &
BALB/3T3
Min (?) (Sodium arsenite & arsenate)
Min (10 ƒΚM ) Sodium arsenite

›
›

8)
9, 23
)

SCG Human LY Min (?) ( 2 x 10-4 - 1.5 x 10-3M)

›

10)

UDS Human Fb Min (?) (Sodium arsenite) ( 1.5, 10ƒΚM)

›

11)

CA Human LY
CHO
Min (?) (Sodium arsenite )( 0.01ƒΚM), 24h, Poly(22.4%)
Min (?) (As
2O3 & As2O5)

›
›

12), 16)
13)

MNv Mouse BM Min ( 10 mgkg. ip, 24h) (NaAsO2), ip
Min ( 5 g/kg x 4, or) (Sodium arsenite)

›
›

17)
21)

SPMv Mouse Sperm Max (?) (NaAsO2), ip

 

17)

DLv Mice Max ( 5 mg/kg, ip ) (NaAsO2)

 

17)

SMv Drosophila Wing Max (?) (Sodium arsenite & arsenate)

 

18)

CAv Mice Min ( 0.1-2.5 mg/kg), po

›

19), 22)

SLRLv Drosophila Min ( 0.38-0.77 mM)

›

20)

1) Nishioka H: Mutation Res., 31, 185 (1975)
2) Rossman TG., et al.: Environ Mutagen 2, 371-379 (1980)
3) Kharab P & Singh I.: Mutation Res., 155, 117-120 (1985)
4) Larramandy ML., et al.:Environ Mutagen, 3, 597-606 (1981)
5) Nakamuro K. & Sayato Y: Mutation Res., 88, 73-80 (1981)
6) Oberly TJ., et al.: Toxicol Environ Health, 9, 367-376 (1982)
7) Wan B., et al.: Environ Mutagen 4, 493-498 (1982)
8) Lee TC., et al: Carcinogenesis, 6, 1421-1426 (1985)
9) Bertolero E.,et al.: Carcinogenesis, 8, 803-808 (1987)
10) Hartmann A & Speit G: Environ Mol Mutagen, 23, 299-305 (1994)
11) Dong JT & Luo XM,: Mutation Res., 315, 11-15 (1994)
12) Yega L., et al.: Mutation Res., 334, 365-378 (1995)
13) Kochhar YS., et al.: Toxicol Lett., 84, 37-42 (1996)
14) Moor MM., et al.: Mutation Res., 386, 279-290, (1997)
15) Ramussen RE & menzel DB.: Mutation Res., 386, 299-306 (1997)
16) Ramirez P., et al. Mutation Res., 386, 291-298 (1997)
17) Deknudt G., et al.: Mutagenesis, 1, 33-34 (1986)
18) Tripathy NK., et al.: Mutation Research, 242, 169-180 (1990)
19) Das T., et al.: Environ Mol Mutagen, 21, 383-388 (1993)
20) Romos-Morales P & Rodrinuez-Arnaiz R.: Environ Mol Mutagen, 25, 288-299 (1995)
21) Tice RR., et al.: Mutation Res., 386, 315-334 (1997)
22) Pddar S., et al.: Food Chem Toxicol, 38, 735-737 (2000)
23) Sabbioni E, et al., Carcinogenesis, 12, 1287-1291 (1991)

yReviewsz
1) IARC Monographs 1-42, Supp. 6, Lyon, France (1987)
2) Leonard A & Lauwerys RR, Mutation Res., 75, 49-62 (1980)
3) Jacobson-Kram, Montalbano, 787 (1985))

US-NTP Genotoxicity ScreeningF
›@Ames Test: @
 

yNotez (Cited from IARC Monographs, Suppl. 6, 1987)@
@The genetic toxicology of arsenic has been reviewed (Jacobson-Kram, Montalbano, 787, 1985).
@In one study of people exposed to trivalent arsenic in drinking-water, no increase in the incidence of SCEs or CAs was observed (Vig, Figueroa, Cornforth, 325, 1984). A number of other studies (IARC, 23, 39; Nordenson, Beckman, 175, 1982) on people occupationally exposed to arsenic or patients treated with arsenic have shown increased levels of CAs or SCEs . The interpretation of these results remains uncertain because of methodological problems.
@Trivalent arsenic did not induce DL mutations in mice, but it produced a small increase in the incidence of CAs and MNs in bone-marrow cells of mice treated in vivo. It induced CAs and SCEs in human and rodent cells in vitro, and transformation of Sy. hamster embryo cells; it did not induce mutation in rodent cells in vitro. It induced gene conversion in Yeast but did not cause mutation or induce prophage in bacteria.
@Pentavalent arsenic induced CAs in human and rodent cells in vitro, equivocal results were obtained in assays for the induction of SCEs. It induced transformation in Sy. hamster embryo cells but did not induce mutation or DNA strand breaks in rodent cells in vitro. It induced gene conversion in yeast but did not induce mutation in bacteria. (IARC Monographs, 1, 41, 1972; 2, 48, 1973; 23, 39, 1980)@

@@@yNotez (Cited from ‚b‚h‚b‚`‚c‚“A‚h‚o‚b‚r@‚h‚m‚b‚g‚d‚l, WHO, 2002)

  No studies are available regarding the genotoxicity of arsine per se. Inorganic arsenic does not induce point mutations, but it does induce chromosomal abnormalities in vitro, including changes in structure and number of chromosomes, endoreduplication, and sister chromatid exchange, and it affects methylation and repair of DNA. Limited studies indicate that arsenite is also clastogenic in vivo (IPCS, 2001a).

œ Asbestos iƒAƒXƒxƒXƒgj
@  
1332-21-4 Natural/Fibrous mineral silicates@
AM Sal. Max (0.5 mg/plate}S9)

 

1)

AM E.coli Max (2.5 mg/plate}S9)   1)
SCE CH Min (0.01 mg/ml, -S9) › 2)
CA CH Min (0.005 mg/ml, -S9)

›

3)

CA Rat cells Min (0.002 mg/ml, -S9); Aneuploid › 4)
CT C3H10Ti/2 Max (0.01 mg/ml, -S9)   5)
CT Rat cells Min (0.002 mg/ml, -S9) › 6)
CA Hum Ly Min (0.01 mg/ml, -S9) › 7)
CAv Rat BM Max (0.5 mg/kg)   8)
MNv Mice Max (0.4 mg/kg)@

 

8)

1) Chanberlain, M & Tarmy, EM, Mutation Res., 43, 159-164 (1977)
2) Livingston, GK, Rom, WN & Morris, MV, J. Environ. Pathol. Toxicol., 4, 373-382 (1980)
3) Kelsey, KT, Yano, E & Liber, HL,@Bri. J. Cancer, 54, 107-114 (1986)
4) Jaurand, MC, Kheuang, L Magne, L & Bignon, J, Mutation Res., 169, 141-148 (1986)
5) Brown, RC, Poole, A & , Fleming, GTA, Cancer Lett., 18, 221-227 (1983)
6) Patarour, MJ, Bignon, J & Jaurand, MC, Carcinogenesis, 6, 523-529 (1985)
7) Valerio, F, De Ferrari, M., et al., IARC Sci., Publ., 30, 485-489 (1980)
8) Lavappa, KS, Fu, MM & Epstein SS, Environ. Res., 10, 165-173 (1975)

yNotez (Cited from IARC Monographs, Suppl. 6, 1987)
@Insulation workers exposed to asbestos displayed a marginal increase in the incidence of SCEs in Ly in one study.
@Chrysotile did not induce micronuclei in bone-marrow cells of mice or CAs in bone-marrow cells of rhesus monkeys treated in vivo. In cultured human cells, conflicting results were reported for the induction CAs and negative results for the induction of SCEs by chrysotile and crocidolite; amosite and crocidolite did not induce DNA strand breaks, and croidolite was not mutagenic. Amosite, anthophylite, chrysotile andcrodidolite induced transformation of Sy. hamster embryo cells, chrysotile and crocidolite transformed BALB/c 3T3 mouse cells, and chrysotile transformed rat mesothelial cells. Neither amosite nor crocidolite transformed CH310T1/2 cells. In cultured rodent cells, amosite, anthophyllite, chrysotile and crocidolite induced CAs, and amosite, chrysotile and crocidolite induced SCE; chrysotile and crocidolite induced aneuploidy and mironuclei. Chrysotile did not induce UDS in rat hepatocytes. Amosite, chrysotile and crocidolite were inactive or weakly active in inducing mutation in rodent cells in vitro; none was mutagenic to bacteria. (IARC, Monograph, 2, 17 , 1973)

œ L-Ascorbic acid @(Vitamin C) iƒrƒ^ƒ~ƒ“ ‚bj
@  
50-81-7@Food/Medicine@176.13

AM Sal./E.coli Max (5.0 mg/plate, }S9)

 

1)

CA CHL/IU Max (0.3 mg/ml, -S9), 48h

 

2)

MNv Mice Max (?)

 

3)

1) Ishidate MJr (Ed): Data Book for Mutagenicity in Bacateria, LIC/Tokyo (1991) (Tables in English)
2) Sofuni T. (Ed.): Data Book of Chromosomal Aberration Test In Vitro, LIC, Tokyo (1998j (Tables in English)
3) Ishidate, MJr, et al: Natl Inst. Hygien. Sci., Tokyo ?

     œ L-Ascorbyl stearate
@@@@
25395-66-8   Food     442.59

AM Sal./E.coli Max (10.0 mg/plate, }S9)

 

1)

CA CHL/IU Max (2.0 mg/ml, }S9), 6-18h

 

2)

1) Ishidate MJr (Ed): Data Book for Mutagenicity in Bacateria, LIC/Tokyo (1991) (Tables in English)
2) Sofuni T. (Ed.): Data Book of Chromosomal Aberration Test In Vitro, LIC, Tokyo (1998j (Tables in English)
œ L-Aspartic acid iƒAƒXƒpƒ‰ƒMƒ“Ž_j
@  
56-84-8 @Industry@@133.10
AM Sal./E.coli Max (5 mg/plate, }S9)

 

1)

1) Ministry of Labour: Mutagen. Test Data of Exist. Chem. Subst., JETOC (Ed.) Suppl. 2 (2000) (Tables in English)
œ Aspirin anhydride (–³…ƒAƒXƒsƒŠƒ“j
@ 
1466-82-6@ Medicine@@342.31
CA CHL/IU Min ( 0.25 mg/ml, -S9), D20= 0.31 (48h)

›

1)

1) Sofuni T. (Ed.): Data Book of Chromosomal Aberration Test In Vitro, LIC, Tokyo (1998j (Tables in English)
œ Asulam iƒAƒXƒ‰ƒ€j
@
 2302-17-2@@Pesticide@@@229.23
REC B.subtlis Max (2 mg/disk)

 

1)

AM Sal./ E.coli Max (?)

 

1)

HMA @? Max (?)

 

1)

CT @? Max (?)@

 

1)

DLv @? Max (?)@

 

1)

1) Japanese J, Agriculture, 15, 497-501 (1990) (Cited from Environ. Res., 21, 53-81, 1999)
œ Atrazine (and related symmetrical triazines) iƒAƒgƒ‰ƒWƒ“j
@ 
1912-24-9@@Herbicide@@216.06@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
AM Sal. Max (?)@

 

1), 2)

YM Yeast,
A. nidulans
Max (?) (Mitotic Gene Conversion Test)

 

3), 4)

PLN Maize Min (?) (Specific Local Mutation Assay)

›

5)

CA Barley(ƒIƒIƒ€ƒMj Min (500 ppm)

›

6)

CA CHL/IU Max (0.4 mg/ml, }S9), 6-18h

 

7)

SCE CHO Max (?)

 

8)

SLRLv Drosophila Max (?)@

 

8)

DLv Mice Min (1.5 g/kg)

›

8), 9)

CAv Mice Min (1.5 g/kg)

›

9)

1) Anderson KJ, et al.:J. Agr. food Chem., 20:649-656 (1972)
2) Shirasu Y, et al.: Mutation Res., 40, 19-30 (1976)
3) Siebert D & Lemperle E.: Mutation Res., 22, 111-120 (1974)
4) DeBertoldi M, et al.: Mutation Res.., 53, 174- 175 (1978)
5) Plewa MJ & Gentile JM: Mutation Res., 38, 287-292 (1976)
6) Wuu KD & Grant WF: Cytologia, 32, 31-41(1967)
7) Ishidate MJr(Ed.): Data Book, Chromosomal Aberration Test In Vitro, LIC, Tokyo/ Elsevier, Amsterdam (1988)
8) John GES, et al.: J. Dairy Sci., 47, 1267 (1964)@
9) Palmer JS & Radeleff RD: Ann. N.Y. Acad. Sci., 111, 729-736 (1964)
US-NTP Genotoxicity ScreeningF
›@Ames Test: @ 
œ Atropine sulfate (Atropisol)
   
55-48-1 @@Medicine@@@676.82
AM Sal./ E.coli Max (?)

 

1)

CA CHL/IU Max (0.25 mg/ml, -S9), 24-48h

 

2)

1) ?
2) Sofuni T. (Ed.): Data Book of Chromosomal Aberration Test ‚hn Vitro, LIC, Tokyo (1998j(Tables in English)
œ Auramine@iƒI[ƒ‰ƒ~ƒ“j
@
 492-80-8@@Industry/Dye@@267.41

CT Sy.ham Embryo Max (?)

 

1)

1) Pienta RJ, et al:: Intern. J. Cancer, 19, 642-655 (1977)

yNotez(Cited from IARC Monographs on the Evaluation of Carcinogenic Risk to Human (Suppl. 6, 1987)
@Auramine did not induce MNs in bone-marrow cells of mice treated in vivo. It transformed Syrian hamster embryo cells and induced SCEs and DNA strand breaks in rodent cells in culture, It cause aneuploidy, mitotic recombination and DNA damage in yeast. It was mutagenic to bacteria and induced prophage. (IARC Monographs, I, 69, 1972)

   @œ 10-Azabenzo(a)pyrene  (10-Aza B(a)P)
       @
189-92-4@ Laboratory@ 253.31

AM Sal/ TA100 Min (1.0 nmolg/plate, +HS9)

›

1)

1) Yamada K., et al., Mutation Res., 557, 159-165 (2004)
œ Azaserin (ƒAƒUƒ[ƒŠƒ“j@(o-diazoacetyl-L-serine)
   
115-02-6@ Industry@@173.13
BM E.coli Min (?)

›

1)

PLN soybeans Min ( 0.1 mg/ml)

›

2)

SM CH: V79 Min (?)

›

3)

CA Vicia Faba Min (?)

›

4)

UDS Mouse cells Max (?)

 

5)

SCE CHO Max (?)@

 

8)

1) Sedgwick B: Carcinogenesis, 18, 1561 (1995)
2) Katoh Y., et al.: Mutation Res., 342, 37-41 (1995)
3) Shaeffer BK., et al.,: Pancreas, 2, 518-522 (1987)
4) Kihlman BA & Sturelids S., Hereditas, 880, 35-41 (1978)
5) Brambilla G., et al.: J. Cancer Res. Clin. Oncol., 94, 7-20 (1979)
œ Azathioprine (ƒAƒUƒ`ƒIƒvƒŠƒ“jiAzothioprine; BW-57-322; Azanin; Imuranj
@
446-89-6@@Laboratory @@277.27
AM Sal. Min (?)@

›

1)

CA Human Ly Min (0.05 mg/ml, -S9), 24h

›

2, 3)

1) (?)
2) Obe G, et al: Arzneim-forsch., 21,504-505 (1971)
3) Van Zyl J & Wissmuller HF: Humangenetik, 21, 153-165 (1974)

yNotez (Cited from IARC Monographs, Suppl., 6, 1987)
@There are conflicting reports on the incidence of CAs in lymphocytes and bone-marrow cells of patients treated with azathioprine. In one study, the incidence of SCEs in lymphocytes of treated patients was not increased.
@In animals treated in vivo, it induced DL mutations in mice, CAs in rabbit lymphocytes and CH bone-marrow cells, and MNs in mice, rats and hamsters; it did not induce SCEs in CH mouse-marrow cells. It induced CAs but not SCEs in human lymphocytes in vitro. It induced CAs in Drosophila, was weakly mutagenic to fungi and was mutagenic to bacteria. (IARC Monographs, 26, 47, 1981)

œ Azinphos-Methyl@iƒAƒWƒ“ƒzƒX-ƒƒ`ƒ‹j
@
86-50-0 @Insecticide/Acaricide@317.34


 
US-NTP Genotoxicity ScreeningF
  ›@Ames Test: @
 
œ 2,2'-Azobis (2-mthylpropionitrile)@(ƒΏ,ƒΏ'-Azibis  isobutyronitrile; AIBN, ABN)
   
78-67-1@@Industry@@164.24
AM Sal. Max ( 5.0 mg/plate, }S9)

 

1-3)

CA CHL/IU Max ( 1.6 mg/ml, }S9)

 

1)

MNv Mice, BM Max (?), or x 2   3)
1) Ministry of Health & Welfare, Japan, Toxicity Testing Reports of Environ. Chem., Vol. 5 (1997) (Tables in English)
2) Ministry of Labour: Mutagen. Test Data of Exist. Chem. Subst., JETOC (Ed.) (1996) (Tables in English)
3) Takenaka SL, J Toxicol. Sci., 18, 418 (1993)
œTop Page@iƒgƒbƒvƒy[ƒWj
œAbbreviation @iΘ—ͺ‹L†j@
œMutagenicity i•ΟˆΩŒ΄«j
œTest Systems@(ŽŽŒ±–@‚ΜŽν—ށj
œTechnical Problems@i‹Zp“I–β‘θ“_j
œList of@Compoundsi‰»‡•¨ƒŠƒXƒgj
œEvaluation of Results@iŽŽŒ±Œ‹‰Κ‚Μ•]‰Ώj