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Updated: Jan 30, 2026

Flow Cytometric Measurement Of ROS Production In Macrophages In Response To FcγR Cross-linking
Published on: March 7, 2019
ROS changes are responsible for tributyl phosphate (TBP)-induced toxicity in the alga Phaeodactylum tricornutum
Qian Liu1, Xuexi Tang2, You Wang2
1Department of Marine Ecology, College of Marine Life Science, Ocean University of China, Qingdao, 266003, China.
Abstract:
As a newly emerging environmental contaminant, tributyl phosphate (TBP) is an additive flame retardant of high production volume that is frequently detected in biota and the environment. Despite evidence that TBP is a potential threat to marine organisms, ecotoxicology data for TBP in marine organisms at low trophic levels are scarce. In this study, the acute toxicological effect of TBP on the marine phytoplankton Phaeodactylum tricornutum was thoroughly investigated, and the possible mechanism was explored. The results showed that TBP at concentrations ≥0.2 mg L-1 significantly inhibited P. tricornutum growth in a clear dose-response manner, with 72-h EC10, EC20, EC50 and EC90 values of 0.067, 0.101, 0.219 and 0.716 mg L-1, respectively. Algal cells treated with TBP exhibited distorted shapes, ruptured cell membranes and damaged organelles, especially mitochondria. Additionally, apoptosis was triggered, followed by a decrease in mitochondrial membrane potential, indicating that cellular damage occurred during exposure. Although the activities of two antioxidant enzymes, superoxide peroxidase and catalase, were upregulated by TBP at 1.2 mg L-1, excess reactive oxygen species (ROS) and malondialdehyde still accumulated in algal cells after exposure, suggesting that the cells experienced oxidative stress. Moreover, both growth inhibition and apoptosis were positively correlated with ROS levels and were ameliorated by pretreatment with the ROS scavenger N-acetyl-l-cysteine. Taken together, the results indicate that TBP exposure leads to growth inhibition and cellular damage in P. tricornutum, and a ROS-mediated pathway might contribute to these observed toxicological effects.
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