Abstract
Pyrrolizidine alkaloids (PAs) comprise a large group of plant toxins, characteristically producing veno-occlusive disease of the liver as a result of hepatic bioactivation to pyrrolic dehydroalkaloids4, 5 (Fig. 1). These pyrrolic metabolites are highly reactive alkylating agents, with aqueous half-lives of only a few seconds1. Dehydroalkaloids are detoxified in the liver by conjugation with glutathione (GSH) to yield 7-glutathionyl-6, 7-di-hydro-l-hydroxymethyl-5H-pyrrolizine (GSDHP; Fig. 1). Following exposure in vivo to a PA, or perfusion of an isolated liver in vitro, high levels of GSDHP are released into the bile11, 13.
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References
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Yan, C.C., Huxtable, R.J. (1996). Effect of the Pyrrolizidine Alkaloid Monocrotaline on Taurine and Sulfur Amino Acid Metabolism in the Rat Liver. In: Huxtable, R.J., Azuma, J., Kuriyama, K., Nakagawa, M., Baba, A. (eds) Taurine 2. Advances in Experimental Medicine and Biology, vol 403. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0182-8_16
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