A further note on the utility of the excision repair-deficientmei-9a females of drosophila melanogaster in detecting chromosome breakage induced by procarbazine in male germ cells

1981 ◽  
Vol 3 (3) ◽  
pp. 293-295 ◽  
Author(s):  
S. Zimmering ◽  
N. Deitemeyer
1963 ◽  
Vol 4 (3) ◽  
pp. 446-456 ◽  
Author(s):  
H. Slizynska

1. Sensitivity of Drosophila melanogaster male germ-cells to chromosome breakage by X-rays has been measured by the structural changes found in the salivary gland chromosomes of larvae from irradiated fathers and untreated mothers. The genetical effectiveness of irradiation on the same males was measured by the frequency of sex-linked lethals.2. Assessed by the overall percentage of germ-cells carrying structural changes, sensitivity follows the well-known pattern: it is highest in spermatids and decreases over spermatozoa and spennatocytes to spermatogonia.3. This overall sensitivity has been analysed on three levels:(a) The proportion in successive broods of ‘positive’ males, i.e. males which respond to irradiation. The results indicate that spermatozoa and spermatids in most or all males are equally sensitive to X-rays, while in regard to spermatogonia the males represent a heterogeneous population consisting of positive and negative males. This is fully confirmed by statistical analysis which was carried out by Dr B. Woolf.(b) The proportion of ‘sensitive’ germ-cells per positive male, i.e. germ-cells carrying at least one structural change. While the proportion of sensitive cells per positive male is about 1:3 for spermatozoa, spermatocytes and spermatogonia, it is higher for spermatids. This is the main reason for the observed increase in overall sensitivity from spermatozoa to spermatids and for its subsequent drop in spermatocytes. On the contrary, the drastic drop in overall sensitivity from spermatocytes to spermatogonia results entirely from a drop in the proportion of positive males.(c) The distribution of breaks in sensitive cells. The clustering of breaks in sensitive cells is highest in spermatogonia, somewhat lower in spermatids, and lowest in spermatocytes and spermatozoa. It indicates that spermatogonial cells are a heterogeneous population, consisting of cells that are either highly sensitive to X-rays or not sensitive at all.4. The fact that the sensitivity of spermatogonia varies both between and within individual males is tentatively attributed to the presence or absence of spermatogonial mitoses.


1998 ◽  
Vol 45 (2) ◽  
pp. 545-559 ◽  
Author(s):  
M J Nivard ◽  
J Wijen ◽  
E W Vogel

Genotoxic carcinogens, able to damage DNA by alkylation reactions, represent a very diverse class of agents which are capable of producing a wide range of DNA modifications. The mechanisms leading to genetic changes as a result of exposure to alkylating agents (AAs) have been studied in male germ cells of Drosophila using a structure-activity relationship approach (SAR). The analytical tools available concern both genetic and molecular assays. The genetic tests enable to quantify excision repair and clastogenic potency of the AA after treatment of post-meiotic male germ cells and to determine the degree of germ-cell specificity, i.e., the mutagenic effectiveness in post- versus premeiotic cell stages. For a selected group of alkylating agents the molecular spectra have been studied in post-meiotic cell stages. On the basis of these descriptors clear SAR's between genotoxic activity in germ cells and physico-chemical parameters (s-values and O6/N7-alkylguanine adducts) and carcinogenic potency in rodents became apparent, resulting in five distinct classes of alkylating agents so far. These classes are: 1) SN2-type monofunctional AAs, 2) SN1-type monofunctional AAs, 3) polyfunctional AAs, 4) agents able to form etheno-DNA adducts, and 5) aflatoxin B1 (AFB1) a bulky-adduct forming agent. The recent finding that the molecular data obtained with Drosophila and data of the specific locus tests in male mice show remarkable similarities for most genotoxic agents supports the view that Drosophila is a useful model system for the study of transgenerational damage.


1995 ◽  
Vol 16 (11) ◽  
pp. 2679-2683 ◽  
Author(s):  
Ignacio Aguirrezabalaga ◽  
Madeleine J.M. Nivard ◽  
Miguel A. Comendador ◽  
Ekkehart W. Vogel

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