Developmental exposure of antibiotics shortens life span and induces teratogenicity in .

Antibiotics are the major therapeutic arsenal against bacterial infections. Yet, beneath this medical triumph lies an under investigated challenge of the potential teratological and toxicological impacts associated with the use of antibiotics. In the present study, we have explored the teratogenic potential of five commonly used antibiotics (streptomycin, metronidazole, tigecycline, doxycycline and norfloxacin) on Oregon-R strain. Except norfloxacin, all other tested antibiotics significantly delayed the onset of pupariation. Consistently, metronidazole, doxycycline and tigecycline resulted in statistically significant drops in egg-to-adult viability and adversely affected egg-to-pupa transition. In comparison, embryonic exposure of streptomycin impeded pupa-to-fly transition. All tested antibiotics induced morphological defects in antenna, wings, proboscis, eye, head, thorax, haltere and abdomen. Interestingly, developmental exposure of antibiotics resulted in statistically significant decrease in the lifespan of both male and female flies. This suggests an increased incidence of teratogenic faults at the systemic level, which are otherwise not manifested morphologically, due to the exposure of tested antibiotics during development. Taken together, our data show that developmental exposure of antibiotics may induce varying degrees of teratogenicity in . Given the genomic homology and conservation of major molecular pathways that underpin development in humans and , the findings do hold translational potential.