ascorbic-acid and 9-10-phenanthrenequinone

Polycyclic aromatic hydrocarbons and their derivatives are ubiquitous environmental contaminants. They are commonly present in complex mixtures with other contaminants, such as metals. The toxicities of phenanthrene (PHE) and 9,10-phenanthrenequinone (PHQ) with or without Cu were determined using Daphnia magna. Copper was the most toxic among the three chemicals tested, followed by PHQ and then PHE, with 48-h median effective concentrations (EC50s) of 0.96, 1.72, and 5.33 microM, respectively. Copper at 0.31 microM, or approximately the 5% effective concentration, decreased the EC50 of PHQ from 1.72 to 0.28 microM. Likewise, PHQ at 1.2 microM, or approximately the 10% effective concentration, significantly lowered the EC50 of Cu from 0.96 to 0.30 microM. This synergistic effect was not observed, however, in mixtures of Cu and PHE based on the response addition model. Assimilation of Cu wasfound to be similar with or without PHQ at increasing external concentrations of Cu, indicating that the increased toxicity of their mixtures is physiologically based. The ability of Cu plus PHQ to generate reactive oxygen species (ROS) was measured as well. Copper alone caused elevated ROS levels at a low concentration (0.63 microM). With PHQ present, however, this elevation in ROS occurred at an even lower Cu level (0.31 microM). Possible attenuation effects of ascorbic acid (vitamin C) on toxicity and ROS production induced by Cu, PHQ, and their mixtures were then examined. Ascorbic acid protected against Cu and Cu-plus-PHQ mixture-mediated toxicity but did not affect PHQ toxicity. Ascorbic acid also lowered ROS levels in the presence of Cu and Cu plus PHQ. We conclude that there exist potential toxic interactions between metals and modified PAHs and that these interactions can involve ROS formation.

Topics: Animals; Antioxidants; Ascorbic Acid; Copper; Daphnia; Drug Interactions; Mutagens; Phenanthrenes; Reactive Oxygen Species; Water Pollutants

When redox cycling of four polycyclic aromatic hydrocarbon o-quinones is catalyzed by the 17 beta-hydroxysteroid dehydrogenase, autooxidation of the hydroquinone is a free radical chain reaction in which superoxide anion is the propagating species. Superoxide dismutase inhibits the redox cycling of these quinones, and ascorbate reverses this inhibition. Studies of the mechanism, using 9,10-phenanthrenequinone, show that ascorbate competes with superoxide dismutase for the superoxide anion; the ascorbyl radical formed then oxidizes the hydroquinone. In this mechanism, ascorbyl radical participates in chain propagation. The reversal of superoxide dismutase inhibition by ascorbate is observed when other two-electron reductases catalyze the cycling, and it occurs in the absence of metal ions. Although ascorbate is generally thought to be an antioxidant, it behaves as a prooxidant in the experiments reported here.

Topics: 17-Hydroxysteroid Dehydrogenases; Animals; Ascorbic Acid; Cattle; Free Radicals; Oxidation-Reduction; Oxygen; Phenanthrenes; Polycyclic Aromatic Hydrocarbons; Quinones; Superoxide Dismutase