Nomilin mitigates OBS-induced developmental cardiotoxicity via the Nrf2 pathway

Area of Science:

• Environmental toxicology
• Cardiovascular research
• Developmental biology

Background:

• Sodium p-perfluorous nonenoxybenzenesulfonate (OBS) is a PFOS replacement with environmental concerns.
• Limited data exists on OBS cardiotoxicity in aquatic organisms.

Purpose of the Study:

• To investigate OBS developmental and cardiac toxicity in zebrafish embryos.
• To explore the protective effects of nomilin (NOM) against OBS toxicity.
• To elucidate the underlying mechanisms of OBS cardiotoxicity, focusing on oxidative stress.

Main Methods:

• Zebrafish embryos were exposed to OBS (0.1 and 1 mg/L) for 96 hours.
• Developmental parameters (body length, hatching, survival) and cardiac function (heart rate, edema) were assessed.
• Gene expression analysis was performed for cardiac development and oxidative stress markers (Keap1/Nrf2 pathway).

Main Results:

• OBS exposure led to significant developmental abnormalities and cardiac dysfunction, including pericardial edema and reduced heart rate.
• OBS dysregulated cardiac gene expression and decreased transcript levels of oxidative stress genes, indicating oxidative stress induction.
• Nomilin (NOM) treatment attenuated OBS-induced cardiotoxicity, suggesting a protective role via Nrf2 activation.

Conclusions:

• Prenatal OBS exposure induces cardiac oxidative injury and developmental defects in zebrafish.
• The Keap1/Nrf2 pathway is implicated in OBS-induced cardiotoxicity.
• Nomilin shows potential as a protective agent against OBS-induced cardiac damage.