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

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 10 min. Maximum TBARS levels (ca. 14 nmol 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 Fe(3+)/O(2)(-) redox system, and differed initiated by Fe(2+)/O(2). The effectiveness of FeAsS and FeSO(4) 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 Fe(3+)/O(2)(-), and differs from the mechanism characteristic of FeSO(4) initiated by the Fe(2+)/O(2) redox system. Proposedly, FeAsS surfaces contain a mixture of Fe(3+) and Fe(2+) that, along with O(2) and O(2)(-), 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.