Hepatotoxic impact of diphenyl ether on zebrafish: DNA damage, oxidative stress, and histopathological insights after acute and subchronic exposure

Polybrominated diphenyl ethers have emerged as a major environmental pollutant, being used as an additive flame retardant in various kinds of products including electronic devices (computers and television sets), upholstery, carpets, plastics, textiles, and building materials. They can undergo the degradation process to form less brominated or low brominated diphenyl ethers in the environment. In the current study, genotoxic, biochemical, histopathological, and ultrastructural scanning electron microscopy (SEM) changes in liver tissue of zebrafish were studied after acute and subchronic exposure of diphenyl ether (DE). The zebrafish were exposed to 2.13 mg/L DE (¼ median lethal concentration [LC50]) and 4.25 mg/L DE (½ LC50) for the acute toxicity assessment and to 425 μg/L DE (1/20th LC50) and 850 μg/L DE (1/10th LC50) for the subchronic toxicity study. After acute and subchronic exposure of DE, % tail intensity in liver tissue was found to be significantly increased in a concentration and duration-dependent manner. The malondialdehyde content, glutathione-S-transferase, and acetylcholinesterase activity in liver tissue were found to be significantly elevated after acute and subchronic exposure of DE, whereas the activity of superoxide dismutase enzyme was found to be depleted in the liver tissue of zebrafish. The histological observations revealed various types of alterations including aggregation of hepatocytic nuclei, necrosis, vacuolization, sinusoidal dilation, disintegrated hepatocytes, and erythrocytic infiltration in liver tissue of zebrafish after DE exposure. The SEM analysis showed changes in the surface of liver tissue such as multiple pore formation, swelling in hepatocytes, necrosis, and degeneration of hepatocytes after acute and subchronic exposure of DE.