Evaluating the Therapeutic Potential of BSA-Reduced Mussel-Derived Selenium Nanoparticles to Mitigate Copper Sulfate-Induced Hepatic Damage and Neurodegeneration in Zebrafish Model

Suganiya UmapathyIeshita Pan^*

• Saveetha School of Engineering, Saveetha University, Chennai, India

Liver fibrosis is the abnormal accumulation of extracellular matrix and eventual formation of fibrous scar in response to chronic liver injury, which can be triggered by increased levels of reactive oxygen species. The brain-liver axis is a crucial communication pathway that significantly influences the intricate interactions between hepatic function and brain health. Emerging evidence suggests that metabolic and inflammatory signals from the liver can impact brain function, leading to conditions such as Parkinson's disease, Alzheimer's disease, and other neurodegenerative disorders. Selenium, as a source of selenoproteins, plays a vital role in antioxidant defense systems, neutralizing reactive oxygen species and protecting cellular structures. Mussels are abundant sources of selenium. The extraction of selenium from mussels leverages their natural bioaccumulation, providing a biocompatible source. Selenium nanoparticles are known for their potential antioxidant activity and can be employed to regulate ROS levels to overcome hepatic damage. The present study explores the synthesis and characterization of mussel-extracted selenium nanoparticles reduced and stabilized with bovine serum albumin. It evaluates their potential role as antioxidants against hepatic damage induced by copper sulfate in vivo in the zebrafish model. The bovine serum albumin stabilized selenium nanoparticles reduced for 30 minutes and 1 hour were spherical with a size of 19 and 16 nm. The antioxidant properties of the stabilized selenium nanoparticles reduced for 30 minutes showed significant in vitro reactive oxygen species scavenging activity at 25µg/ml. Furthermore, it was confirmed that treatment with stabilized selenium nanoparticles reduced for 30 minutes at 25µg/ml concentration improved antioxidant enzyme levels while decreasing lipid peroxidation and nitric oxide levels in vivo in zebrafish larvae and adult zebrafish exposed to copper sulfate stress. Histopathological examination showed that stabilized selenium nanoparticles delayed the progression of copper sulfate-induced hepatic damage, and the expression of antioxidants was upregulated, while the hepatic and mitochondrial damage markers were downregulated. In conclusion, bovine serum albumin-reduced selenium nanoparticles can be a promising therapeutic antioxidant for protecting against reactive oxygen species-induced hepatic damage and neurodegeneration.