Genotoxicity of crotonaldehyde in the bone marrow and germ cells of laboratory mice

Abstract

Genotoxicity of crotonaldehyde was evaluated by employing bone marrow and spermatocyte chromosomal aberration and dominant lethal mutation assays in Swiss albino mice. For bone marrow chromosomal aberration assay, animals were treated with 0.2 ml olive oil containing 8, 16 and 32 μl kg b.w. of crotonaldehyde for 6, 12 and 24 h through single intraperitoneal injection. Treatment induced dose-dependent and statistically significant decrease in mitotic index and increase in chromosome aberrations per cell (CAs/cell excluding gaps and stickiness and pulverizations) and percent aberrant metaphase (excluding gaps) in the bone marrow cells at 6, 12 and 24 h after treatment. For spermatocyte chromosomal aberration assay, male mice were treated with 8, 16 and 32 μl/kg b.w. of crotonaldehyde for 24 h through single intraperitoneal injection. The percentage of the induced chromosome aberrations in diakinesis-metaphase-I cells showed dose-dependent increase. For dominant lethal mutation assay, adult male mice were injected intraperitoneally with 0.2 ml olive oil containing crotonaldehyde at the rate of 8, 16 and 32 μl/kg b.w. for 5 consecutive days. The negative control animals received 0.2 ml olive oil as above. In the dominant lethal mutation assay after the last dose, the treated males were allowed to mate with untreated virgin females. The mating continued for 5 consecutive weeks. At pregnancy days 14–16, the females were killed and uterine contents were examined for live and dead implants. Treatment of mice resulted in statistically significant decrease in the fertility indices and total number of implants per female. Statistically significant decrease in the number of live implants per female and increase in the number of dead implants per female were recorded in females mated with males during 8–14 and 15–21 and 22–28 days post-treatment mating. Crotonaldehyde treatment of males induced appreciably higher frequencies of dominant lethal mutation during 8–14, 15–21 and 22–28 days post-treatment mating periods. Percent dominant lethal mutation increased concomitantly with the dose. Dominant lethality was maximum in females mated with males treated with 5 × 32 μl/kg b.w. during the 15–21 days post-treatment mating. The overall result suggests a positive dose–response relationship between treatment and induction of chromosomal aberrations in the somatic and germ cells and dominant lethal mutation in the germ cells.