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Two lectins, called lanceolin and stenodactylin, were purified by affinity chromatography on CL Sepharose 6B from the caudices of the Passifloraceae Adenia lanceolata and Adenia stenodactyla, respectively. They are glycoproteins with Mw of 61,243 (lanceolin) and 63,131 daltons (stenodactylin), consisting of an enzymatic A chain linked to a larger B chain with lectin properties, with N-terminal amino acid sequences similar to that of volkensin, the toxic lectin from Adenia volkensii. These two lectins agglutinate red blood cells, inhibit protein synthesis in a cell-free system as well as in whole cells, and depurinate ribosomes and DNA, but not tRNA or poly(A). They are highly toxic to cells, in which they induce apoptosis and strongly inhibit protein synthesis, and to mice, with LD50s 8.16 mg/kg (lanceolin) and 2.76 mg/kg (stenodactylin) at 48 hours after administration. Thus, lanceolin and stenodactylin have all the properties of the toxic type 2 ribosomeinactivating proteins (RIPs). Further experiments were conducted in order to clarify the effects of these RIPs in cells. We investigated the cronological relationship between cytotoxic activity, indirectly evaluated as inhibition of protein synthesis, and loss of cell viability in NB100 cell line. The induction of apoptosis was assessed by determining caspases 3 and 7 levels, which increase 8-16 hours earlier than the beginning of protein synthesis inhibition. This suggest that the arrest of protein synthesis is not a central event in the pathway of cell poisoning by RIPs. The high toxicity and the induction of cell death only by apoptosis and not by necrosis in two muscular cell lines (TE671 and RD/18) suggest that lanceolin and stenodactylin may be potential candidates for experimental chemoablation in strabism and blepharospasm. These results show that lanceolin and stenodactylin are amongst the most potent toxins of plant origin.

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Background. Mesenchymal stem cells (MSC) may be of value in regeneration of renal tissue after damage, however lack of biological knowledge and variability of results in animal models limit their utilization. Methods. We studied the effects of MSC on podocytes ‘in vitro’ and ‘in vivo’ utilizing adriamycin (ADR) as a model of renal toxicity. The ‘in vivo’ experimental approach was carried out in male Sprague Dawley rats (overall 60 animals) treated with different ADR schemes to induce acute and chronic nephrosis. MSC were given a) concomitantly to ADR in tail vein or b) in aorta and c) in tail vein 60 days after ADR. Homing was assessed with PKH26-MSC. Results. MSC rescued podocytes from apoptosis induced by ADR ‘in vitro’. The maximal effect (80% rescue) was obtained with MSC/Podocytes co-culture ratio of 1:1 for 72 hours. All rats treated with ADR developed nephrosis. In no case MSC modified the clinical parameters (i.e. proteinuria, serum creatinine, lipids) but protected the kidney from severe glomerulosclerosis when given concomitantly to ADR. Rats given MSC 60 days after ADR developed the same severe renal damage. Only few MSC were found in renal tubule-interstitial areas after 1-24 hours from injection and no MSC was detected in glomeruli. Conclusions. MSC reduced apoptosis of podocytes treated with ADR ‘in vitro’. Early and repeated MSC infusion blunted glomerular damage in chronic ADR nephropathy. MSC did not modify proteinuria and progression to renal failure, that implies lack of regenerative potential in this model.

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