Oxidative stress induced by arsenopyrite and the role of desferrioxamine-B as radical scavenger

Abstract

Arsenopyrite (FeAsS) is one of the earth’s primary mineral sources of As, yet its effects on cell damage remain largely unknown. This paper addresses the question whether FeAsS induces lipid peroxidation (LP), a major indicator of oxidative stress. Screening and monitoring of LP was conducted using Thiobarbituric Acid Reactive Substances (TBARSs) assay. The lipid source was supernatant of rat brain homogenates. The formation of TBARS by FeAsS was rapid and took place just after 10min. Maximum TBARS levels (ca. 14nmol TBARS per mg of protein) were observed after 1h and remained constant thereafter. Suspension fraction separations showed that dissolved and structural components contributed to LP. The formation of TBARS by soluble As, As(III) or As(V), compared to basal levels. The initiation of LP by FeAsS was consistent with a mechanism initiated by the Fe3+/O2- redox system, and differed initiated by Fe2+/O2. The effectiveness of FeAsS and FeSO4 as inducer compared, and surpassed that of AAPH. On the other hand, the initiation of LP by FeAsS is consistent with a mechanism initiated by perferryl ion and Fe3+/O2-, and differs from the mechanism characteristic of FeSO4 initiated by the Fe2+/O2 redox system. Proposedly, FeAsS surfaces contain a mixture of Fe3+ and Fe2+ that, along with O2 and O2-, participate in multiple mechanisms of electron transfer. EPR determinations show decreases in DMPO-OH adduct signal in FeAsS suspensions after adding desferrioxamine-B (DFO-B), consistent with the idea that DFO-B serves as a radical scavenger.