In vitro reactive oxygen species production by mitochondria from the rabbitfish Siganus fuscessens livers and the effects of Irgarol-1051

In this study, the mitochondria from the livers of Siganus fuscessens were exposed to the Irgarol-1051with or without respiratory chain inhibitors using succinate or malate as the substrate, and the effects on mitochondrial ROS production were tested. The mitochondrial ROS production was significantly enhanced by antimycin A with an increase of more than three folds but not by rotenone and NaN3, and this may suggest complex III is the major ROS-producing site. Irgarol-1051 treatments gave a somewhat contradictory result: this chemical can inhibit the mitochondrial ROS production but the inhibition decreased with the increase of doses. These contradictory data about Irgarol-1051 may be explained by the balance between the effects of inhibition through the opening of small-size pores and stimulation through blocking electron transfer, but the mechanism laid behind needs more evidence to support. As Irgarol-1051 was continuously used in antifouling and its bio-concentration factor is up to 160 in fish, the toxic effect of Irgarol-1051 on aquatic animals should be paid more attention to.

► The mitochondria from the liver of rabbitfish were exposed to the Irgarol-1051.
► Complex III is possibly the major ROS-producing site.
► Low concentration such as 0.004 mg/L inhibited the mitochondrial ROS production.
► The mitochondrial ROS production increased with the doses.
► Balance between inhibition and stimulation may determine the contradictory data.