Parental Lifetime PBSA Exposure Induces Neurodevelopmental Toxicity in F1 Zebrafish

Area of Science:

• Environmental Toxicology
• Developmental Biology
• Neuroscience

Background:

• 2-phenylbenzimidazole-5-sulfonic acid (PBSA) is a common UV filter in aquatic environments.
• Concerns exist regarding its ecological health impacts, particularly intergenerational toxicity.
• Existing data on PBSA's developmental and neurotoxic risks across generations is limited.

Purpose of the Study:

• To investigate the intergenerational developmental and neurotoxic effects of environmentally relevant PBSA concentrations.
• To establish a zebrafish life-cycle exposure model for assessing PBSA's transgenerational impact.
• To elucidate the mechanisms underlying PBSA-induced toxicity in offspring.

Main Methods:

• Zebrafish life-cycle exposure model with environmentally relevant PBSA concentrations (0.2, 2, 20 μg/L).
• Categorization of offspring into parental exposure only (F0+/F1-), continuous parental and F1 exposure (F0+/F1+), and F1 only exposure (F0-/F1+).
• Assessment of developmental endpoints, mortality, malformations, motor neuron axon length, gene expression (gap43, mbp, shha), oxidative stress markers (MDA, ROS, CAT).

Main Results:

• PBSA transferred from parental gonads to F1 embryos.
• Parental exposure significantly inhibited somitogenesis, increased mortality and malformations in F1 offspring.
• PBSA reduced F1 motor neuron axon length, downregulated neural development genes, and altered oxidative balance (ROS, CAT activity).
• Continuous F1 exposure aggravated developmental and neurotoxic effects.

Conclusions:

• Parental lifetime PBSA exposure induces significant intergenerational neurodevelopmental toxicity in zebrafish.
• Disruption of oxidative balance and neural gene expression are key mechanisms.
• Continuous offspring exposure exacerbates adverse effects, indicating cumulative risk.
• Traditional single-generation toxicity assessments underestimate the ecological risks of UV filters like PBSA.