In ovo exposure to triphenyltin hydroxide induces genotoxicity, cytotoxicity and developmental toxicity in chick embryos, Gallus gallus domesticus

Triphenyltin hydroxide (TPTH) is a widely used agricultural fungicide and environmental pollutant well known for its potent toxicological potential. Despite this, its embryotoxic effects remain unexplored in avian models. This study presents a novel evaluation of TPTH’s acute toxicity, genotoxicity, cytotoxicity, teratogenic potential, and enzymatic and tissue architectural potential using the in ovo chick embryo model. Fertilized chicken eggs were exposed to varying TPTH concentrations that further revealed a time-dependent median lethal dose (LD50) decline from 547.37 µg/egg at 24 h to 395.74 µg/egg at 96 h. Later, evaluations using 1%, 5%, and 10% of the 96 h LD50 demonstrated profound subcellular damage. The Hen’s egg test for micronucleus (HET-MN) assay showed a significant dose-dependent induction of micronuclei, confirming genomic instability. Additionally, a reduced polychromatic to normochromatic erythrocyte (PCE/NCE) ratio indicated severe cytotoxicity and suppressed erythropoiesis. Morphometric assessments revealed teratogenic alterations, including heart tube failure, microcephaly, cranial edema, microphthalmia, localized hemorrhaging, and concentration-dependent growth retardation in body length, eye diameter, and limb elongation. Biochemical assessments revealed that TPTH triggers severe oxidative stress. This was supported by significant dose-dependent reductions in superoxide dismutase, catalase, and glutathione across major organs, alongside increased lipid peroxidation in the brain. Histopathological analysis also revealed severe toxicity. These findings validated that TPTH induces potent developmental toxicity through a cascade of genotoxic, cellular, enzymatic damage, and structural alterations, highlighting its extreme embryotoxic risks to avian populations and associated ecosystems.