• Chlortetracycline genotoxicity;
  • Wheat bioassay;
  • Micronucleus;
  • Chomosomal aberration;
  • Sister chomatid exchange


Increasing attention is now being paid to antibiotic contamination as a serious environmental issue. Chlortetracycline has been widely used for decades as a human and veterinary medicine, which has resulted in environmental residues and damage to living organisms. In the present study, the physiological and potential genetic toxicity of chlortetracycline was investigated using a wheat (Triticum aestivum L.) bioassay at a concentration range of 0.0625 to 300 mg/L and an exposure time of 24, 48, and 72 h. The results indicated that chlortetracycline at the lower concentrations stimulated germination and cell mitotic division and growth, whereas higher concentrations significantly inhibited processes such as bud length (50–300 mg/L), percentage germination (25–300 mg/L), root length (25–300 mg/L), and mitotic index (MI) (25–300 mg/L). The lowest concentration of chlortetracycline slightly augmented the frequency of micronucleus (MN), chomosomal aberration (CA), and sister chomatid exchange (SCE) in the root tips; however, significant (p < 0.05 and 0.01) levels of augmentation were observed at higher concentrations in a concentration-dependent manner, including the frequencies of MN (25–200 mg/L), CA (10–200 mg/L), and SCE (5–200 mg/L), respectively. The inducement of MN, CA, and SCE decreased at 250 and 300 mg/L as a result of acute cell toxicity. In addition, all endpoints showed a time-dependent increase at 0.0625 to 200 mg/L. These results imply that chlortetracycline (≥5 mg/L) may be genotoxic to plant cells, and exposure to chlortetracycline may pose a potential genotoxic risk to living organisms. Comparatively, SCE was the most sensitive, followed by CA, and MN was the least sensitive to chlortetracycline genotoxicity in wheat. The results also suggest that the wheat bioassay is efficient, simple, and reproducible for monitoring the genotoxicity of chlortetracycline in the environment. Environ. Toxicol. Chem. 2010;29:922–928. © 2009 SETAC