Worm Breeder's Gazette 14(5): 52 (February 1, 1997)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
Department of Biology, University of Houston, Houston, Texas, 77204-5513
In Drosophila, short term and chronic exposure of young females to ethanol causes an approximately 10 fold rise in chromosome nondisjunction (Rey et al., 1992). However, the question remains as to whether this effect is caused by ethanol or its primary metabolite, acetaldehyde (Rey et al., 1994). Caenorhabditis elegans provides a good model for studying this effect because X chromosome nondisjunction can be easily monitored by determination of the number of male progeny produced following acute chemical exposure. Ethanol, in optimal experimental conditions of 30 minute exposures of mid to late L4s to 7% ethanol in M9 salts, caused a greater than 10 fold increase in the production of male progeny (13.2 males/1000 worms compared to 1.03 males/1000 worms for M9 alone with approximately 10,000 F1 progeny counted for each class). Concentrations as low as 5% generated a five fold increase in nondisjunction than controls while 10% and 12.5% ethanol concentrations also resulted in a 10 fold increase in nondisjunction. Higher concentrations of ethanol proved too toxic as noted by egg laying defects and reduced brood sizes. Synchronous populations of N2 worms grown at 20 degrees were tested at different developmental stages (according to age and criteria described by Kimble and White, 1981) to determine the most sensitive stage to 30 minute exposures of 10% ethanol in M9 salts. When L1s, L2s and L3s were exposed to ethanol, only the normal background numbers of males were observed. Early L4s treated with ethanol showed a slight rise in number of males while mid to late L4s treated with ethanol produced significantly more males than the controls. However, young adults as well as older adults showed no increase in the number of male progeny when treated with ethanol. The stage most sensitive to short-term ethanol exposure correlates with the time when the majority of sperm are produced. This suggests that ethanol induces meiotic nondisjunction during spermatogenesis. Surprisingly, acute exposures of mid to late L4s to acetaldehyde concentrations ranging from 0.1% to 1.0% did not produce a higher rate of chromosome nondisjunction compared with M9 controls, approximately 12,600 F1 progeny of 0.1% acetaldehyde treated L4s were counted producing 1.11 males/1000 worms. Hermaphrodites treated with 0.5% acetaldehyde had similar numbers of male progeny while 1.0% treated hermaphrodites had such small brood sizes that no male progeny were observed. This study suggests that ethanol in Caenorhabditis elegans causes chromosome nondisjunction rather than its primary metabolite, acetaldehyde. Kimble, J.E. and White, J.G. (1981). On the Control of Germ Cell Development in Caenorhabditis elegans. Dev. Bio. 81, 208-219. Rey, M., Palermo, A.M. and Munoz, E.R. (1992). Nondisjunction induced by ethanol in Drosophila melanogaster females. Mutation Research. 268, 95-104. Rey, M., Palermo, A.M. and Munoz, E.R. (1994). Lack of effect of acute acetaldehyde treatment on X chromosome segregation in Drosophila melanogaster females. Mutation Research. 320, 1-7.