Tolfenpyrad-induced Embryotoxicity in Chick Embryos: Oxidative Stress–mediated Multi-organ Damage and Hematobiochemical Alterations
V. S. Diviyaanandhan
Department of Veterinary Pharmacology and Toxicology, College of Veterinary and Animal Sciences, Pookode, Wayanad, Kerala, India.
D. Ranjith *
Department of Veterinary Pharmacology and Toxicology, College of Veterinary and Animal Sciences, Mannuthy, Thrissur, Kerala, India.
Patil Arpita
Department of Veterinary Pharmacology and Toxicology, College of Veterinary and Animal Sciences, Pookode, Wayanad, Kerala, India.
Adheena Xavier
Department of Veterinary Pharmacology and Toxicology, College of Veterinary and Animal Sciences, Pookode, Wayanad, Kerala, India.
H. S. Patki
Department of Veterinary Anatomy, College of Veterinary and Animal Sciences, Pookode, Wayanad, Kerala, India.
K. P. Surjith
Department of Veterinary Anatomy, College of Veterinary and Animal Sciences, Pookode, Wayanad, Kerala, India.
P. Hamza
Department of Veterinary Pathology, College of Veterinary and Animal Sciences, Pookode, Wayanad, Kerala, India.
Sanis Juliet
Department of Veterinary Pharmacology and Toxicology, College of Veterinary and Animal Sciences, Pookode, Wayanad, Kerala, India.
*Author to whom correspondence should be addressed.
Abstract
Background: Tolfenpyrad is a mitochondrial electron transport inhibitor used for insect pest control, but information on its developmental toxicity in avian embryos remains limited.
Aim: This study aimed to evaluate the developmental and embryotoxic effects of tolfenpyrad, a pyrazole insecticide that targets mitochondrial Complex I, in a non-target vertebrate model, given the rising agricultural use of this insecticide against resistant pests and the limited understanding of its impact on avian development.
Study Design: The study used chick embryos as a sensitive, cost-effective model for developmental toxicity screening. Tolfenpyrad was administered via air-sac injection on day 12 of incubation to assess dose-dependent embryotoxicity and systemic physiological disturbances.
Methodology: Different doses of tolfenpyrad were injected into the air sac of chick eggs on day 12, and mortality was monitored to determine the median lethal dose. Surviving embryos were examined on day 20 for absolute and relative organ weights of the liver, heart, kidneys, and lungs. Haematological parameters, serum biochemical markers of hepatic, renal, cardiac, and metabolic function, and oxidative stress indicators, including lipid peroxidation and antioxidant enzyme activities, were analysed.
Results: The LD₅₀ was determined to be 361 ± 97.5 µg/egg, with dose-dependent mortality. Surviving embryos showed reduced organ weights, anaemia, thrombocytopenia, lymphopenia, and altered leukocyte counts. Serum biochemistry revealed elevated liver, kidney, and cardiac injury markers, inflammatory markers, glucose, and lipids, with decreased protein levels. Oxidative stress markers increased, while antioxidant enzyme activities declined, indicating mitochondrial dysfunction.
Conclusion: Tolfenpyrad induces dose-dependent, oxidative stress-driven multi-organ embryotoxicity and metabolic disruption, highlighting ecological risks to avian species and emphasising the need for thorough safety assessments before widespread agricultural application.
Keywords: Tolfenpyrad, chick embryo, embryotoxicity, oxidative stress, mitochondrial dysfunction, haematological alterations, serum biochemistry, organ toxicity, lipid peroxidation, developmental toxicity.