Haloalkenes metabolism

In conclusion, this subsection has offered insights into the complex chemical and metabolic reactivity of haloalkene oxides. Contributing factors include ... 

An a priori classification of these various reactions as either toxification or detoxification is simply impossible, since each product from these various pathways may be toxic or not depending on its chemical properties and own products. Furthermore, the biological context plays a critical role [154], yet this role, best viewed as the influence of biological factors on the relative importance of competitive routes of metabolism, is often underplayed by those who venture to make predictions of metabolic outcome. Indeed, in the cascade of intertwined metabolic routes exemplified by haloalkenes, a small difference in pathway selectivity at an early metabolic crossroad may be amplified downstream, giving rise to major differences in relative levels of metabolites and overall toxicity. 

Compound A is a haloalkene degradation product of sevoflurane metabolism by carbon dioxide absorbers, and it has been suggested that prolonged low-flow closed-circuit anesthesia with sevoflurane may maximize exposure to the degradation product. Compound A can cause convulsions and neural damage in rats (1). It also causes nephrotoxicity and hepatotoxicity in rats, particularly if barium hydroxide Ume is used (2). 

Anders, M. W. Glutathione-dependent bioactivation of haloalkanes and haloalkenes. Drug Metabol. Rev. 2004, 36, 583-594. 

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