Malondialdehyde production (an index of lipid peroxidation), glutathione peroxidase activity and the concentrations of two antioxidants, glutathione and ascorbic acid, were measured in Atlantic croaker (Micropogonias undulatus) hepatic and ovarian tissues after exposure to representatives of two major classes of environmental contaminants, a polychlorinated biphenyl mixture (Aroclor 1254) or a metal (cadmium). One group of croaker was exposed to 5 mg Cd/l seawater for 6 days, followed by exposure to 1 mg Cd/l seawater for 33 days. Another group of croaker was fed 0.42 mg Aroclor 1254/100 g body wt./day for 17 days, followed by 7 days feeding with uncontaminated food. Both xenobiotics caused increased lipid peroxidation. Exposure to cadmium resulted in increased malondialdchyde production in incubates of homogenates and microsomes from both hepatic and ovarian tissues. Aroclor 1254 administration caused increased malondialdehyde production in croaker livers in vivo and in vitro and also in incubates of ovarian homogenates in vitro. Cadmium exposure also caused a decrease in glutathione peroxidase activity and the ascorbic acid content of both tissues. In contrast, glutathione peroxidase activity was increased in both tissues from Aroclor 1254-fed croaker. However, Aroclor 1254 administration did not affect the ascorbic acid content of the tissues. The glutathione status of the liver and ovary was not changed by either treatment, whereas both the gonadosomatic and hepatosomatic indices were altered after xenobiotic exposure. Thus, exposure of a marine fish to either a heavy metal or a polychlorinated biphenyl mixture by environmentally realistic routes of administration can result in increased lipid peroxidation, although these toxicants exert different effects on the activity of glutathione peroxidase, an important protective mechanism against oxidative damage.
