Stimulation of superoxide production by nitrofurantoin, p‐nitrobenzoic acid and m‐dinitrobenzene in hepatic microsomes of three species of freshwater fish

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Abstract
The importance of nitroaromatic compounds as aquatic contaminants and the association of superoxide (O−2) mediated toxicity with the mammalian metabolism of a number of these compounds has led our laboratory to conduct an in vitro investigation of nitroaromatic‐stimulated production by freshwater fish. Utilizing cytochrome c reduction and cyanide‐insensitive oxygen consumption assays for O−2, channel catfish (Ictalurus punctatus), largemouth bass (Micropterus salmoides) and rainbow trout (Salmo gairdneri) hepatic microsomes were exposed to nitrofurantoin (NF), p‐nitrobenzoic acid (PNBA) and m‐dinitrobenzene (MDNB). NF and PNBA were chosen for study as model nitroaromatic compounds, known to stimulate microsomal O−2 generation in mammals; MDNB was chosen because it frequently contaminates aquatic systems. The results demonstrated that each of the three nitroaromatics is capable of significantly enhancing superoxide dismutase (SOD) inhibitable cytochrome c reduction and oxygen consumption, providing specific evidence of stimulated microsomal production of O−2 by the fish species examined. The results also indicated chemical‐ and species‐specific differences in stimulated O−2 production. In both assay systems, enhancement by NF exceeded that produced by MDNB and, more pronouncedly, PNBA. Furthermore, although similar responses to all nitroaromatics were observed in microsomes isolated from catfish and bass, the assays employing trout microsomes demonstrated the greatest enhancement in NF and MDNB exposures. These findings suggest that the stimulation of O−2 production may be an important mode of action for these common aquatic pollutants that merits further ecotoxicological assessment.

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