Anaphase aberrations: A measure of genotoxicity in mutagen‐treated fish cells

Abstract

Rainbow trout gonad cells (RTG-2) were cultured for various lengths of time in the presence of several classes of known mutagenic chemicals and several related compounds that possessed no known mutagenic/carcinogenic activity. During the course of exposure the cells were examined for the presence of abnormalities in the chromosome arrangement of anaphase figures during mitosis. Untreated and solvent-treated (dimethylsulfoxide-treated) cells exhibited a background abnormality rate of 12% with only minor chromosomal defects being observed. This was also true for those cells exposed to naphthol and anthracene, two chemicals with no proven mutagenic or carcinogenic activity. Conversely, significant increases in the frequency of anaphase aberrations were produced in cells treated with N-methyl-N'-nitro-N-nitrosoguanidine, benzo(a)pyrene, 9-aminoacridine and mitomycin-C. These abnormalities were also far more complex and extensive than those observed in the control and nonmutagen-treated cells. Many species of fish have extremely small and numerous chromosomes, making resolution of chromosome defects such as sister chromatid exchange and deletions more difficult than in most mammalian diploid cells, which generally have larger and fewer chromosomes. Examination of cells during anaphase eliminates the need to observe each chromosome separately as well as the need to produce well-spread metaphase chromosomes. Since the sensitivity of anaphase aberrations to known mutagenic/carcinogenic compounds appears to be quite high in trout cells and since hundreds of suitable cells are available for analysis, this may be an appropriate alternative or addition to some of the more standard chromosome macrolesion tests developed in mammalian systems.

Juvenile Sea Bass Liver P450, EROD Induction, and Erythrocytic Genotoxic Responses to PAH and PAH-like Compounds

“…Therefore, EMN and ENA must be a consequence of nonconjugated metabolites covalently bound to erythrocytic DNA. Furthermore, B(a)P induced DNA adduct formation (Venier and Canova, 1996;Canova et al, 1998) and DNA damage (Bihari et al, 1990;Canova et al, 1998) in mussels, and anaphase aberrations (Kocan et al, 1982), chromosome aberrations (Hooftman, 1981), and hepatocarcinogenicity (Hendricks et al, 1985) in "sh.…”

Alterations in patterns of excretion and other metabolic functions in developing fish embryos exposed to benzo(a)pyrene

“…From these studies we have shown that fish cells in vitro exhibit chromosomal damage (Kocan et al, 1982), as well as developing mutations (Kocan et al, 1981) much as mammalian cells do. The chromosome damage seen in vitro has also been verified in vivo in our laboratory by Liguori (Ph.d. Thesis, 1984) as well as being described under natural conditions (Longwell & Hughes, 1980).…”

Effects of Brayton Point Station's Thermal Discharge on Mount Hope Bay Winter Flounder

“…More subtle abnormalities are identified by irregular cleavages, blister-like outcrops from the body axis and failure of blastopore closure. Detection of cytogenetic defects follows a method determined by Kocan et al (1982), in which numbers of mitotic cells with aberrations at anaphase/telophase are scored to give a relative index. Common malformations include the occurrence of stray chromosomes, attached and free fragments and multi-polar spindles Klumpp and Westernhagen, 1995).…”