Figure 1. A proposed pathway of compound A bioactivation and nephrotoxicity involving renal cysteine conjugate [small beta, Greek]-lyase. The first step of this mechanism involves the known dehydrofluorination of sevoflurane by carbon dioxide absorbents to form compound A. This product has been shown to form addition and addition-elimination conjugates with glutathione, in reactions catalyzed by glutathione-S-transferases. The glutathione conjugates are further metabolized to form cysteine conjugates, which are then acted on by renal cysteine conjugate [small beta, Greek]-lyase to form a thionoacyl halide reactive intermediate. The thionoacyl halide has been proposed to bind covalently to renal proteins and cause toxicity.