Superoxide Dismutase 3 Deficiency Disrupts the Regulation of Oxidative Stress Caused by Polystyrene Nanoplastics

TL;DR

This study shows that a deficiency in the SOD3 enzyme worsens the harmful effects of polystyrene nanoplastics in zebrafish, highlighting the enzyme's role in managing oxidative stress.

Contribution

The study reveals the novel role of SOD3 in mitigating oxidative stress caused by nanoplastics using a zebrafish model.

Findings

Sod3a mutant zebrafish showed increased accumulation of polystyrene nanoplastics in tissues.

Deficiency in SOD3 led to higher oxidative stress, cell death, and immune and intestinal dysfunction in zebrafish.

The study highlights the importance of extracellular antioxidant defenses in mitigating nanoplastic toxicity.

Abstract

Nanoplastics have been recognized as emerging pollutants posing potential risks to ecosystems and human health. They are now detected ubiquitously in the environment and even human tissues, where their small size allows for tissue accumulation and cellular penetration. Growing evidence links nanoplastics to oxidative stress, yet the specific contribution of extracellular accumulation to toxicity remains poorly understood. To address this, we used zebrafish, a transparent vertebrate model suitable for toxicological studies, to explore the role of extracellular antioxidant defenses in polystyrene nanoplastic (PSNP)-induced oxidative stress. In particular, we focused on superoxide dismutase 3 (SOD3), which is an enzyme that regulates extracellular reactive oxygen species by catalyzing the detoxification of superoxide radicals. Zebrafish Sod3a is a homolog of human SOD3, preserving conserved metal-binding sites critical for enzymatic function. We established sod3a mutant zebrafish and examined their responses following PSNP exposure. In sod3a mutant larvae, tissue accumulation of PSNPs was higher than in wild-type (WT), and this was associated with elevated oxidative stress, enhanced cell death, and abnormalities in intestinal function and immune responses. Collectively, these observations reveal the functional importance of SOD3 during PSNP-induced oxidative stress and provide new insight into extracellular antioxidant mechanisms that mitigate PSNP-induced toxicity.

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