Proliferative response avoids mutagenic effects of titanium dioxide (TiO2) nanoparticles in a zebrafish hepatocyte cell line

Abstract

Titanium dioxide nanoparticles (TiO2NP) have been widely applied in numerous industrial products, and their discharge into wastewater continues to increase, representing a risk hazard for aquatic biota. In the aquatic environment, NP enter fish cells, accumulate in vesicles, and interact with organelles and DNA. This study evaluated the acute (24 h) toxic potential of TiO2NP in the emergent Neotropical model zebrafish liver (ZFL) cell lines at concentrations of 0, 250, 500, 750, and 1000 ng mL−1. The main aim was to determine if TiO2NP causes ROS production and affects cell function due to membrane damage, mitochondrial activity impairment, lysosome malfunction, and DNA damage, which may lead to cell death. High concentrations (750 and 1000 ng mL−1) of TiO2NP increased ROS production and caused cell membrane damage, cell proliferation, lysosome proliferation or swelling, DNA strand breaks, and a low frequency of micronucleus formation. Cytotoxicity and genotoxicity were likely related to ROS production and NP uptake, which impair cell function and integrity and activate necrosis and apoptosis. This study contributes to the understanding of TiO2NP cytotoxicity in fish cells and provides new insights into proliferative hepatocyte responses that allow ZFL cells to lower TiO2NP toxicity and avoid its mutagenic potential.