Toxicity of new emerging pollutant tris-(2,3-dibromopropyl) isocyanurate on BALB/c mice

摘要

The emerging heterocyclic brominated flame retardant tris-(2,3-dibromopropyl) isocyanurate (TBC), widely used in reinforced plastics, has demonstrated toxicity to fish. However, little is known about its toxicity in rodents. This study aims to determine the effect of TBC on growth, biochemical parameters in serum, organs and related gene expression of both male and female BALB/c mice after gastro-gavage administration of 0, 2, 10 and 50mgkg(-1) TBC for 28days. Results indicated that exposure to TBC had no effects on basic growth and food intake of mice, but significantly increased serum alanine aminotransferase levels in male mice. Histopathological analyses showed that focal necrosis (2, 10 and 50mgkg(-1) TBC-exposed groups) and ballooning degeneration (10 and 50mgkg(-1) TBC-exposed groups) were found in mouse liver, whereas transmission electron microscopy revealed dose-dependent hepatocyte apoptosis, mitochondrial degeneration and endoplasmic reticulum dilation. Histopathological and ultrastructural assessments in the lung showed dose-dependent hyperplasia of pulmonary alveolar epithelium, bronchial congestion, infiltration of inflammatory cells and mitochondrial swelling following TBC exposure. Our results also indicated that mitochondria are one of the major target cytoplasmic organelles for TBC, suggesting that damage in mitochondria is one of the pathways that led to toxic effects in the liver and lung of TBC-treated groups. Moreover, TBC effectively activated the gene expression of p53 in mice liver. Our findings provide strong evidence that TBC induces significant toxicity in mice organs, especially in liver and lung, which play vital roles in detoxification and gas exchange, respectively. This research will contribute to characterize the toxic effects of TBC, which was introduced as one of the candidates for brominated flame retardant replacement. Copyright (c) 2014 John Wiley & Sons, Ltd. Tris-(2,3-dibromopropyl) isocyanurate (TBC) exposure had no effects on basic growth or food intake of mice, whereas significantly increased alanine aminotransferase serum levels. TBC exposure induced p53 expression in mouse liver, and altered the ultrastructure in liver and lung. Results also indicated that mitochondria are one of the major target cytoplasmic organelles for TBC. These findings suggest that damage in mitochondria is one of the pathways that lead to toxic effects in the liver and lung of TBC-treated groups.