ABSTRACT
Ricinus communis L. is of great economic importance due to the oil extracted from its seeds. Castor oil has been used for pharmaceutical and industrial applications, as a lubricant or coating agent, as a component of plastic products, as a fungicide or in the synthesis of biodiesel fuels. After oil extraction, a castor cake with a large amount of protein is obtained. However, this by-product cannot be used as animal feed due to the presence of toxic (ricin) and allergenic (2S albumin) proteins. Here, we propose two processes for detoxification and allergen inactivation of the castor cake. In addition, we establish a biological test to detect ricin and validate these detoxification processes. In this test, Vero cells were treated with ricin, and cell death was assessed by cell counting and measurement of lactate dehydrogenase activity. The limit of detection of the Vero cell assay was 10 ng/mL using a concentration of 1.6 x 10(5) cells/well. Solid-state fermentation (SSF) and treatment with calcium compounds were used as cake detoxification processes. For SSF, Aspergillus niger was grown using a castor cake as a substrate, and this cake was analyzed after 24, 48, 72, and 96 h of SSF. Ricin was eliminated after 24 h of SSF treatment. The cake was treated with 4 or 8% Ca(OH)2 or CaO, and both the toxicity and the allergenic properties were entirely abolished. A by-product free of toxicity and allergens was obtained.
Subject(s)
Animals , Allergens/drug effects , Aspergillus niger/growth & development , Calcium Compounds/pharmacology , Castor Bean/drug effects , Inactivation, Metabolic , Allergens/toxicity , Aspergillus niger/drug effects , Chlorocebus aethiops , Castor Bean/toxicity , Cell Death/drug effects , Cell Degranulation/drug effects , Enzyme Activation , Fermentation , L-Lactate Dehydrogenase/metabolism , Mast Cells/drug effects , Ricin/isolation & purification , Ricin/toxicity , Time Factors , Toxicity Tests , /isolation & purification , /toxicity , Vero CellsABSTRACT
Castor beans, sometimes used in traditional therapies, contain ricin one of the most toxic substances known. It may cause an acute and potentially fatal gastroenteritis in addition to neurological and ophthalmological lesions. Poisoning may also lead to delayed visceral damages; however, the latter is quite rare. The toxicity is dose related and depends on the amount of castor beans ingested. There is no specific treatment and symptomatic management to reduce the load of the toxin needs to be initiated quickly and early when a case of poisoning is suspected so that serious complications will be avoided. Increasing the awareness of the population to the dangers of ricin would be a way to avoid the utilisation of castor seeds in traditional therapies. Here we are reporting a case of mild poisoning after ingestion of a single castor bean. The patient, who presented at Nizwa Hospital, Oman, fortunately recovered completely as the ingested dose was quite small
Subject(s)
Humans , Male , Ricin/toxicity , AwarenessABSTRACT
Ricin, a glycoprotein from castor oil seeds, is specifically toxic to Kupffer cells and at low doses it leaves parenchymal cells comparatively unaffected. At a dose of approximately 1.5 microgram/100 g body weight, ricin significantly increases the hepatic antioxidant enzyme system in rats within 24 hr. Superoxide dismutase, catalase and glutathione peroxidase show an increase in liver tissue levels of 19-24%. However, hepatic lipid peroxidation is elevated by about 34% and non-protein sulphydryl is reduced by 26%. The enhanced levels of antioxidant enzymes appear to protect the hepatocytes from the toxin. The observed elevation of hepatic thiobarbituric acid-reactive substances appears to originate mainly from the damaged Kupffer cells.
Subject(s)
Animals , Antioxidants/metabolism , Liver/cytology , Male , Rats , Rats, Wistar , Ricin/toxicityABSTRACT
Effect of monensin, intercalated in liposomes on the cytotoxicities of ricin, Pseudomonas exotoxin A and diphtheria toxin in phagocytic and non-phagocytic cells as well as in mice has been studied. Intercalation does not disturb the integrity of the liposomal bilayer and substantially enhances the cytotoxicities of ricin and Pseudomonas exotoxin A in both phagocytic and non-phagocytic cells while it has no effect on diphtheria toxin. The observed effect is highly dependent on the liposomal lipid composition as well as cell types. The potentiating ability of monensin in neutral vesicle is 2.2-fold higher than in negatively charged vesicles in non-phagocytic cells while no difference was observed in phagocytic cells. Incorporation of stearylamine in liposomes reduces the potentiating effect of monensin. Liposomal monensin has also been found to enhance the cytotoxicity of ricin in mouse in vivo in a dose-dependent manner and is maximal when ricin is injected within 60 min of monensin injection. Liposomal monensin remains in circulation for 2 hr while free monensin remains only for 15 min. Tissue distribution studies reveal that liposomal monensin is present mainly in the liver and spleen which are also the major sites for ricin accumulation. Thus liposome is found to be an effective delivery vehicle for monensin to potentiate the cytotoxicity of immunotoxins or hormonotoxins and could prove useful for selective elimination of cancer cells.