Studies on aromatic hydrocarbon quinone metabolism and DT-Diaphorase function in liver of fish species

Abstract Studies were carried out to examine the role of aromatic hydrocarbon (AH)-quinone metabolism and DT-diaphorase (quinone oxidoreductase; EC 1.6.99.2; DTD) function in pollution-caused oxidative damage in fish. Redox cycling of quinones to produce reactive oxygen species (ROS) was studied by oxygen consumption and oxidation of the hydroxyl radical scavenger 2-keto-4-methiolbutyric acid. NADH-dependent redox cycling by hepatic microsomes of flounder ( Platichthys flesus ) was seen for 1,4-benzoquinone, 1,2- and 1,4-naphthoquinones, phenanthroquinone and anthraquinone. Combined with previous similar results for duroquinone, menadione and benzo[a]pyrene (BaP) quinones (Lemaire et al., 1994), this demonstrates a general potential for AH-quinone-mediated ROS production. NADPH-dependent 3 H-BaP metabolism by hepatic microsomes of P. flesus produced 54% dials, 45% phenols and trace levels of quinones, whereas cumene hydroperoxide-dependent metabolism produced up to 67% quinones (metabolites resolved by HPLC). Exposure to AH-contaminated sediment can lead to enhanced hepatic lipid peroxidation (Livingstone et al., 1993) raising the possibility of an AH-mediated toxicity cycle of peroxidation leading to enhanced quinone and ROS production leading to more peroxidation and oxidative damage. Hepatic DTD purified almost to homogeneity from trout ( Oncorhynchus mykiss ); Sturve et al., in prep.) also catalysed NADH-dependent AH-quinone-mediated ROS production, indicating a possible function for this enzyme in quinone toxicity.