Mediation of bisphenol analogs-exposed developmental toxicity and malformations with Procyanidin-C1 in zebrafish embryos

Recent research has raised concerns about widespread exposure to bisphenol analogues with structural or functional similarities to bisphenol A (BPA). Due to strict regulations on BPA production and use, various bisphenol analogues such as bisphenol S (BPS), bisphenol F (BPF), and bisphenol AF (BPAF) are increasingly being used to replace BPA in a wide range of applications and industries. Unfortunately, some analogues have similar disruptive physiological and endocrine effects on humans and animals, particularly during the embryonic period, due to their potential toxicity and endocrine disrupting properties. These persistent contaminant activities have the potential to disrupt normal biological functions, rattle developmental patterns, and influence hormonal activity, primarily by altering mechanisms and causing genome mutations. Little is known about its analogues and how they affect embryonic morphology, developmental defects, mitochondrial activity, and related genes. This study sought to determine the effects of Procyanidin-C1 (PCY1) intervention on developmental toxicity and cytoskeletal malformations in zebrafish embryos exposed to bisphenol analogues. Studies have shown that PCY1 neutralises free radicals, protects cells from DNA damage, and reduces the effects of environmental toxins. This study included 300 zebrafish embryos. The zebrafish embryo acute toxicity test (ZFET) was used to assess embryotoxicity. Toxicological endpoints were monitored every 24 hours until 120 hours of exposure. The embryos' heartbeats, morphologies, developmental defects, survivability, and hatchability were all studied. Heartbeats were detected as early as 48 hours after conception.