4.7 Article

Ammonia in the presence of nano titanium dioxide (nano-TiO2) induces greater oxidative damage in the gill and liver of female zebrafish

Journal

ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
Volume 236, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2022.113458

Keywords

Ammonia; n-TiO2; Oxidative; antioxidant responses; Nrf2-Keap1 signaling; Zebrafish

Funding

  1. National Key Research and Development Program of China [2019YFD0900303]
  2. China Agri-culture Research System of MOF and MARA [CAS-45-24]
  3. Na-tional Natural Science Foundation of China [32071621]

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Water pollution caused by ammonia and nano titanium dioxide (n-TiO2) has attracted extensive concern. This study reveals the oxidative stress and antioxidative imbalance caused by ammonia and n-TiO2 in the gill and liver of fish, posing a synergistic toxic risk to fish health.
Water pollution caused by a highly hazardous chemical ammonia and a widespread application nanomaterialsnano titanium dioxide (n-TiO2) in nature water has attracted extensive concern of the world. However, the potential joint effects of the two factors are unknown. Aim to investigate the potential interactive effects of ammonia and n-TiO2 and the behind mechanisms, adult female zebrafish (Danio rerio) were co-exposed for 8 weeks by total ammonia nitrogen (TAN; 0, 3, 30 mg/L) and n-TiO2 (0, 0.1, 1 mg/L) in different combination conditions based on a full-factorial design. The analysis of absorption kinetics confirmed that n-TiO2 could absorb free ammonia (NH3) in aqueous solution and the loss rate of free NH3 increased with the rise of n-TiO2 concentration. Consistent with this, free NH3 concentrations in the gill and liver were higher in the presence of n-TiO2 compared to TAN exposure alone. The increases of MDA and PC concentrations in the gill and liver of fish indicated that TAN and n-TiO2 alone or in combination caused oxidative stress. Simultaneously, the activity and transcription of antioxidant enzymes (T-SOD, CuZn-SOD, Mn-SOD, CAT, GPx and GST) as well as antioxidant GSH contents were extensively inhibited by TAN and n-TiO2 via Nrf2-Keap1 signaling. The significant interactive effects of TAN and n-TiO2 were detected on levels of GSH, GST and gstr1 mRNA in the gill, and on levels of GSH, T-SOD, Mn-SOD, CAT levels as well as gpx1a and keap1 mRNAs in the liver, implying synergistic toxic risk of TAN and n-TiO2. The more severe histopathological alterations and higher IBR analysis in co-treatment groups further proved that the existence of n-TiO2 excavated ammonia-induced toxicity in the gill and liver, especially in liver. In conclusion, ammonia and n-TiO2 have a synergistic toxic risk of fish health because ammonia and n-TiO2 cause oxidative-antioxidative imbalance by inducing ROS overproduction.

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