Phenanthrene-Induced Apoptosis and Its Underlying Mechanism

Area of Science:

• Environmental Toxicology
• Molecular Biology
• Hepatotoxicity

Background:

• Phenanthrene (Phe) is a common low-molecular-weight polycyclic aromatic hydrocarbon (PAH).
• Human and aquatic organism exposure to Phe is widespread, but its toxic effects and mechanisms remain unclear.
• This study investigates the chronic hepatotoxicity of Phe in Chinese rare minnows (Gobiocypris rarus).

Purpose of the Study:

• To elucidate the chronic hepatotoxicity of Phenanthrene in Chinese rare minnows.
• To investigate the underlying molecular mechanisms of Phe-induced liver injury.
• To explore the role of microRNAs and protein interactions in Phe toxicity.

Main Methods:

• Adult Chinese rare minnows were exposed to varying concentrations of Phe (8.9, 82.3, 510.0 μg/L) for 30 days.
• Histopathological examination, TUNEL assays, caspase activity assays, and gene expression profiling were performed.
• Primary hepatocytes were used to assess mitochondrial membrane potential (MMP) and microRNA expression, with molecular docking used to predict interactions.

Main Results:

• Phe exposure increased liver lesion frequency and hepatocyte apoptosis.
• Caspase 9 and caspase 3 activity significantly increased in liver tissues.
• Mitochondrial membrane potential decreased in primary hepatocytes, and miR-18a expression was suppressed, potentially due to Phe interaction with hnRNP A1.

Conclusions:

• Phenanthrene induces liver damage and hepatocyte apoptosis via the intrinsic apoptosis pathway.
• Phe's interaction with hnRNP A1 contributes to the suppression of miR-18a expression.
• These findings provide insights into the molecular mechanisms of Phe hepatotoxicity in aquatic organisms.