The mutagenic activity of the pyrrolizidine alkaloid heliotrine in Drosophila melanogaster II. Chromosome rearrangements

Brink, N.G.

doi:10.1016/0027-5107(69)90148-1

Cited by 30 publications

(5 citation statements)

References 24 publications

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“…However, when breakage of both segments of the Y chromosome are included, breakage occurs in 0·32 % of these chromosomes (excluding the possibility of multiple hits). Assuming that a correlation exists between the production of breaks and lethal mutations, such an observation supports the suggestion by Brink (1969) that differential production of lethal mutations in the X and Y chromosomes may account for some shift in sex ratio. Whatever the explanation, it appears that DDT causes ring-X lethality in D. melanogaster.…”

Section: Discussionsupporting

confidence: 79%

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Mutagenicity of DDT in Mice, Drosophila melanogaster and Neurospora crassa

Clark¹

1974

Aust. Jnl. Of Bio. Sci.

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The pesticide DDT was examined for possible mutagenicity in mice, D. melanogaster and N. crassa. Through the use of the dominant-lethal assay it was found that acute oral doses of DDT (2 x 150 mg/kg body weight) in male mice induced dominant lethal mutations in early spermatid and spermatocyte stages. Chronic oral doses of DDT (2 x 100 mg/kg body weight per week for 10 weeks) in male mice caused a persistent increase in the number of dominant lethal mutations. Histological sections showed that chronic treatment of mice with DDT caused changes in seminiferous tubule morphology and degeneration of B-type spermatogonia. Acute treatment of mice with DDT caused an increase in spermatocyte chromosome breakage, stickiness and precocious separation of the X and Y bivalent.Oral treatment of male Canton-S D. melanogaster with DDT caused an increase in dominant lethality in early spermatid and spermatocyte stages. DDT also caused non-disjunction of the X and Y chromosomes at the spermatocyte stage in treated male y/R(1)2,vj/B s yy+ D. melanogaster. The shift in sex ratio is discussed in terms of breakage of the ring-X chromosome. Treatment of a population of Canton-S D. melanogaster with DDT for eight months did not cause any increase in frequency of second-chromosome recessive lethal mutations.In tests for the induction of recessive lethal mutations in the ad-3 region of an N. crassa heterokaryon the results were inconclusive. However, in the host-mediated assay with N. crassa and mice as the host, DDT did not appear to be mutagenic.The results show that DDT has a deleterious effect on reproduction in mice and is a weak mutagen in both mice and D. melanogaster.

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Section: Discussionsupporting

confidence: 79%

“…Canton-S male flies were treated with DDT and mated sequentially, with a brood interval of 3 days, to virgin Canton-S females according to the method described by Brink (1969).…”

Section: Systems For Detection Of Mutations In D Melanogastermentioning

confidence: 99%

Mutagenicity of DDT in Mice, Drosophila melanogaster and Neurospora crassa

Clark¹

1974

Aust. Jnl. Of Bio. Sci.

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“…Mutagenicity of plant extracts and pure pyrrolizidine alkaloids has been extensively studied in different systems, including Drosophila melanogaster, Salmonella typhimurium, and Escherichia coli (108)(109)(110)(111)(112)(113). The mutagenic potency of a series of pyrrolizidine alkaloids in Drosophila melanogaster was determined by Frei et al (114) as follows: senkirkine > monocrotaline > seneciphylline > senecionine > retrorsine > 7-acetyllycopsamine > symphytine > jacoline > symlandine > intermedine > indicine > lycopsamine > indicine N-oxide > supinine.…”

Section: (B) Genotoxicity Of Pyrrolizidine Alkaloidsmentioning

confidence: 99%

GENOTOXIC PYRROLIZIDINE ALKALOIDS AND PYRROLIZIDINE ALKALOIDN-OXIDES—MECHANISMS LEADING TO DNA ADDUCT FORMATION AND TUMORIGENICITY

Chou

Xia

et al. 2001

Journal of Environmental Science and Health, Part C

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Plants that contain pyrrolizidine alkaloids and pyrrolizidine alkaloid N-oxides are widely distributed in the world. These plants are probably the most common poisonous plants affecting livestock, wildlife, and humans. Although pyrrolizidine alkaloids have been shown to be genotoxic, including tumorigenic in experimental animals, the mechanisms of tumor formation have not been fully understood. Our recent studies on riddelliine, riddelline N-oxide, and dehydroretronecine (DHR) provided evidence suggesting that pyrrolizidine alkaloids and pyrrolizidine alkaloid N-oxides induce tumors via a genotoxic mechanism, and that tumorigenicity is mediated by a set of eight DHR-derived DNA adducts. This mechanism may be general to other carcinogenic pyrrolizidine alkaloids and may also be responsible for the other genotoxicities of pyrrolizidine alkaloids, including mutagenicity and teratogenicity. It is hypothesized that these DHR-derived DNA adducts are potential biomarkers of pyrrolizidine alkaloid tumorigenicity. 353

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“…Heliotrine was a powerful mutagen in D. melanogaster (Brink, 1969;Clark, 1959;Sivlingham and Brink, 1988). Seneciphylline and senkirkine were found to produce sex-linked recessive lethal in males of D. melanogaster using the 3-day feeding method (Candrian et al, 1984).…”

Section: Mutations In Drosophilamentioning

confidence: 99%