Penconazole is a systemic fungicide commonly used in agriculture as the commercial preparation Topas. Although triazole fungicides are widely found in the aquatic environment, little is known about their acute toxicity on fish. In this study we assessed the effects of short-term exposure to Topas on some parameters of homeostasis of reactive oxygen species (ROS), such as the levels of markers of oxidative stress and parameters of the antioxidant defense system of goldfish (Carassius auratus L.). Gills appeared to be the main target organ of Topas toxicity, showing the greatest number of parameters affected. Gills of Topas-treated fish showed a higher content of low (L-SH) and high (H-SH) molecular mass thiols and higher activities of superoxide dismutase (SOD), catalase, glutathione reductase (GR), glutathione-S-transferase (GST), and glucose-6-phosphate dehydrogenase (G6PDH) as well as reduced carbonyl protein content (CP), as compared with those in the control group. In the liver, goldfish exposure to 15ā€“25 mg Lāˆ’1 Topas resulted in a higher L-SH and H-SH content, but lower CP levels and activity of GST. In kidney, Topas exposure resulted in higher activities of glutathione peroxidase (GPx) and G6PDH, but lower L-SH content and activity of GST. The results of this study indicate that acute goldfish exposure to the triazole fungicide Topas increased efficiency of the antioxidant system in fish gills, liver, and kidney. This could indicate the development of low intensity oxidative stress which up-regulates defense mechanisms responsible for protection of goldfish against deleterious ROS effects.

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Keywords Antioxidant enzymes, Azole fungicides, Oxidative stress markers, Topaz, Triazole
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Journal Comparative Biochemistry and Physiology - C Toxicology and Pharmacology
Husak, V.V. (Viktor V.), Mosiichuk, N.M. (Nadia M.), Storey, J.M, Storey, K, & Lushchak, V.I. (Volodymyr I.). (2017). Acute exposure to the penconazole-containing fungicide Topas partially augments antioxidant potential in goldfish tissues. Comparative Biochemistry and Physiology - C Toxicology and Pharmacology, 193, 1ā€“8. doi:10.1016/j.cbpc.2016.12.003