Ricin liver damage

Ricin in the liver first targets the Kupffer cells which are heavily damaged as early as 4 h after the intravenous inoculation of 6 LDioo into mice (Bingen et al. 1987). Four hours after the inoculation of ricin every Kupffer cell bore several worm-Hke structures, which sometimes took a spindle-like aspect. About 14 % of the completely lysed cells (29 of 208) lay on the endothehal fining within the sinusoid. In vivo, Kupffer cells accumulated I-labelled ricin to a much greater extent than parenchymal cells (Skilleter et al. 1981). 

Abrin, a potent toxin, is extracted from the seeds of the rosary pea (Abrus precatorius). Due to its easy availability and preparation, this toxin is an attractive option for weap-onizing in poor countries, and thus has also been included in the Sch ule 1 of the CWC. The mechanism of action of abrin is very similar to that of ricin however, in mice, abrin is 75 times more toxic than that of ricin (0.04 pg/ kg for abrin is equivalent to 3pg/kg of ricin). Similar to ricin, inhalation of abrin is found to be more toxic than ingestion. However, abrin ingestion has reported to be toxic to the liver, unlike ricin. At the cellular level, abrin is a potent toxalbumin known to cause cell death by inhibiting protein synthesis (namely, type 2 ribosomal inhibitory protein). Further, abrin is also known to induce endothelial cell damage leading to an increase in cell permeability, fluid and protein leakage, and tissue edema. 

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