[Technology of medicinal castor oil].
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Castor Oil↗
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Effect of hydroxypropyl methylcellulose and hydrogenated castor oil on naproxen release from sustained-release tablets.
The effect of the concentration of hydrophilic (hydroxypropyl methylcellulose [HPMC]) and hydrophobic (hydrogenated castor oil [HCO]) products, fillers (lactose and dibasic calcium phosphate), and buffers (sodium bicarbonate, calcium carbonate, and sodium citrate) on naproxen release rate was studied. Matrix tablets were prepared by double compression, and in vitro dissolution tests were performed. The dissolution results showed that an increased amount of HPMC or hydrogenated castor oil resulted in reduced drug release. The inclusion of buffers in the HPMC matrix tablets enhanced naproxen release. For HCO tablets, only sodium bicarbonate enhanced naproxen release. The presence of lactose on HPMC matrix tablets did not show a significantly different result from that obtained with the formulation containing dibasic calcium phosphate as a filler. However, for the tablets containing HCO, the presence of lactose significantly enhanced the naproxen release rate. The matrix-forming materials in this study were suitable for use in sustained-release tablets containing naproxen. The drug release can be modulated by adding suitable amounts of diluents and buffers.
Castor Oil↗
Involvement of nitric oxide from nerves on diarrhea induced by castor oil in rats.
Nitric oxide (NO) is involved in the mechanism of castor oil-induced diarrhea. This study was performed to elucidate the source of NO. Diarrhea was induced by oral administration of castor oil in rats. Diarrhea was significantly inhibited by the pre-treatment with a relatively selective nerve NO synthase inhibitor, 7-nitroindazole. This effect was attenuated by the treatment with L-arginine. Capsaicin-sensitive afferent nerve degeneration did not affect the diarrhea. N(G)-Nitro-L-arginine methylester significantly inhibited diarrhea even in capsaicin-pretreated rats. These data suggest, at least in part, the involvement of NO from nerves on the diarrhea induced by castor oil in rats.
Animals↗
A fluorescence study of ligand-induced conformational changes in cytosolic fructose-1,6-bisphosphatase from germinating castor oil seeds.
The intrinsic fluorescence of homogeneous castor oil seed cytosolic fructose-1,6-bisphosphatase (FBPasec) was used as an indicator of conformational changes due to ligand binding. Binding of the substrate and the inhibitor fructose-2,6-bisphosphate (F-2,6-P2) was quantitatively compared to their respective kinetic effects on enzymatic activity. There are two distinct types of substrate interaction with FBPasec, corresponding to catalytic and inhibitory binding, respectively. Inhibitory substrate binding shares several characteristics with F-2,6-P2 binding which indicates that both ligands bind at the same site. However, F-2,6-P2 does not prevent fluorescence transitions attributed to catalytic substrate binding. The marked synergistic inhibition of FBPasec by AMP and F-2,6-P2 appears to arise via AMP's promotion of F-2,6-P2 binding. Based on the X-ray crystal structure of porcine kidney FBPase our modelling studies suggest the existence of a distinct F-1,6-P2/F-2,6-P2 inhibitory binding site which partially overlaps with the enzyme's catalytic site. We propose that a pronounced allosteric transition mediated by AMP binding increases access of F-1,6-P2 and F-2,6-P2 to this common inhibitory binding site.
Adenosine Monophosphate↗
Study of antidiarrhoeal activity of four medicinal plants in castor-oil induced diarrhoea.
A study was undertaken to evaluate the effect of aqueous and methanolic plant extracts of Acorus calamus rhizome, Pongamia glabra leaves, Aegle marmelos unripe fruit and Strychnos nux-vomica root bark for their antidiarrhoeal potential against castor-oil induced diarrhoea in mice. The methanolic plant extracts were more effective than aqueous plant extracts against castor-oil induced diarrhoea. The methanolic plant extracts significantly reduced induction time of diarrhoea and total weight of the faeces. The result obtained establish the efficacy of these plant extracts as antidiarrhoeal agents.
Animals↗
Ricinoleic acid (castor oil) alters intestinal surface structure. A scanning electronmiscroscopic study.
To determine if sodium ricinoleate, the active principle of castor oil, alters mucosal surface structure of the small intestine, rabbit ileum was perfused with isotonic buffer or buffer containing 10 mM of sodium ricinoleate. Mucosal biopsies were examined by scanning electron microscopy. Sodium ricinoleate produced deep clefts or holes at the tips of villi, and at the bases of these clefts unusual cells could be resolved. The microvillus surface of the intestine was also altered at the tips and sides of villi. Microvilli were clumped into "tufts" with numerous intervening "cracks" appearing on the surface. These changes may relate to the well-documented capacity of ricinoleate and dietary long-chain fatty acids to evoke fluid secretion in the intestine. The findings thus pertain to the pharmacology of castor oil and the pathophysiology of steatorrheal disease.
Animals↗
Epoxydicarboxylic aciduria resulting from the ingestion of castor oil.
A woman who was investigated because of suspected malabsorption was found to excrete large amounts of 3,6-epoxyoctanedioic, 3,6-epoxydecanedioic and 3,6-epoxydodecanedioic acids. The origin of these compounds could be traced to the factitious ingestion of castor oil. Healthy subjects and conventional as well as germ-free rats also excrete these substances after ingestion of castor oil. The epoxydicarboxylic acids are thus endogenous metabolites from ricinoleic acid. The shortest of the three homologues is present in small amounts in normal urine. It may be formed by cyclization of a hydroxylated beta-oxidation intermediate.
Animals↗
Toxicity of polyoxyethylene hydrogenated castor oil 60 (HCO-60) in experimental animals.
HCO-60, a polyoxyethylene castor oil derivative, is used as a solubilizer in the injectable formulations of lipophilic agents. This study was performed to examine the toxicity of HCO-60 in various experimental animals including dogs, monkeys, rabbits, guinea pigs and rats. With 1.25 or 2.5 mg/kg of HCO-60 injected i.v. to dogs, blood pressure decreased, flush, swelling and itching appeared after injection, and with 10 mg/kg of HCO-60 there was additionally a decrease of spontaneous motility. In the two higher dose groups, these symptoms paralleled an increase of histamine levels. Since degranulation was observed after injection in the mast cells of the skin, but not in the liver of dogs, the histamine in the plasma was considered to be released from the mast cells of the skin. Pretreatment with diphenhydramine, a H1-receptor antagonist, suppressed the decrease of blood pressure induced by HCO-60. These findings show that the toxicity of HCO-60 is associated with histamine release from the mast cells. No symptoms occurred in monkeys, rabbits, guinea pigs or rats with 50 or 100 mg/kg of i.v. of HCO-60, and there was no change in plasma histamine levels. This study demonstrated that the toxicity of HCO-60 is species specific to dogs among the animals tested.
Animals↗
Saccharomyces boulardii inhibits water and electrolytes changes induced by castor oil in the rat colon.
The biotherapeutic agent Saccharomyces boulardii has been shown to inhibit castor oil-induced diarrhoea in rats. The present study investigated the mechanism(s) of this antidiarrhoeal effect in terms of water and electrolyte (sodium, potassium and chloride) changes using two rat models. A single oral dose of S. boulardii of up to 12 x 10(10) CFU/kg of viable cells did not inhibit castor oil-induced fluid secretion in the enteropooling model. However, the yeast dose dependently reduced castor oil induced fluid secretion into the colon, with a significant protection at 12 x 10(10) CFU/kg. In this model, castor oil reversed net sodium and chloride absorption into net secretion, and increased net potassium secretion into the lumen. Single pre-treatment with S. boulardii at 4 and 12 x 10(10) CFU/kg dose dependently decreased these electrolyte changes. In conclusion, S. boulardii possesses potent anti-secretory properties versus water and electrolyte secretion induced by castor oil in the rat colon.
Animals↗
Antimicrobial and toxicological studies on an antiseptic based on hexachlorophene and destructive distillate of castor oil.
Bactericidal, bacteriostatic, fungistatic and toxicological evaluaton of an emulsion containing 0.25% hexachlorophene (W/V), 9.5% terpineol (V/V), 1.5% oil of terpentine (V/V), 13% ethanol (V/V), 6% castor oil distillate 1201275 degrees C (V/V) and 6% sodium salt of the residue (W/V) in aqueous medium was performed. The bactericidal concentration for Salmonella typhi was found to be 1:400 which increased to 1:350 in the presence of 5% horse serum. The bacteriostatic concentration of the emulsion varied from organism to organism. A 4% solution of the emulsione was found to be most effective against Microsporum vanbreuseghemii showing an inhibition zone of 7.2 cm and was least effective on Aspergillus niger. 1 to 8% solution of the emulsion given orally or instilled into conjunctival sacs of albino mice indicated lethal and insignificant toxic manifestations respectively but a dose equivalent to 50 mg/Kg given subcutaneously was found to produce a subacute lethal effect in guinea pigs.
Animals↗
[An emulsion of castor oil].
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Castor Oil↗
Ingestion of castor oil plant seeds.
Ingestion of seeds of the castor oil plant is rare, and may cause toxicity but rarely death. The presumed toxic component is ricin, a highly potent cellular poison. We report the case of a young adult who ingested a large number of the seeds, causing initial toxicity, but with subsequent full recovery. The management of such ingestions and the apparent discrepancy between the extreme toxicity of ricin and the generally milder toxicity of ingested seeds are discussed.
Adult↗
Effects of castor oil on lipid metabolism in rats.
Weanling rats were given diets contained castor oil (CAO-diet), coconut oil (CO-diet), or high-oleic safflower oil (HO-diet) each 10% (wt). No growth retardations were observed on the CAO-diets. The CAO-diet group showed significantly lower serum cholesterol and hepatic triacylglycerols than the HO-diet group. Ricinoleic acid was found at an extremely low level in perirenal adipose tissue.
Adipose Tissue↗
[Micellar formation and micellar structure of poly(oxyethylene)-hydrogenated castor oil].
The effects of the oxyethylene chain length of poly(oxyethylene) hydrogenated castor oil (HCOn) on the micellar formation and on the micellar structure were investigated. Some physicochemical properties of HCOn (critical micelle concentration cmc, surface tension at cmc, free energy of micellization, and surface excess) concerning surface-activity were measured. These physicochemical properties were little affected by the oxyethylene chain length of HCOn. In addition, several physical techniques have been used to study the micellar structure of HCOn. It was found that HCOn micelles were spherical or nearly spherical, and that an increase in the oxyethylene chain length led to an increase in the looseness of HCOn micelle.
Castor Oil↗
Bioreactor operated production of lipase: castor oil hydrolysis using partially-purified lipase.
A highly stable lipase from Pseudomonas aeruginosa KKA-5 was produced by batch cultivation technique employing shake flask and 5 L-bioreactor. The bioreactor was run at different airflow rates. Low airflow rates (1 and 3 L/min), did not lead to effective growth and lipase production. Growth increased by about one order and lipase production increased by about 6 times, at an airflow rate of 5 L/min. Lipase production occurred during decelerated cell growth. A highly stable lipase was produced which retained its activity in the running bioreactor, even after a period of one month. This stable lipase was partially-purified using ammonium sulphate precipitation technique. Castor oil was hydrolyzed using 300U crude and partially-purified lipase, each. Approximately 21-fold, partially-purified lipase could hydrolyze 81% castor oil within a period of 96 hr, where as only 63% hydrolysis was obtained, in 216 hour, when crude lipase was used.
Bioreactors↗
Differentiation of Malassezia species: selectivity of cremophor EL, castor oil and ricinoleic acid for M. furfur.
In recent years, the genus Malassezia has been reclassified based on molecular data. In addition to M. furfur, M. pachydermatis and M. sympodialis, four new species, M. globosa, M. obtusa, M. restricta and M. slooffiiae, have been described. However, apart from their lipid dependence, little is known about the metabolism and nutritional requirements of all the seven species. Further to recent studies, 10 hydrophilic emulsifiers (HLB > 10) were examined in an agar diffusion test to determine their growth-promoting effect on reference strains of the different Malassezia species. Polyethylene glycol (PEG) 7 glyceryl monoalcanoate (Cetiol HE). PEG-glyceryl stearate (Tagat S2) and macrogol-50 stearate (Myrj 53) were metabolized by all strains, while PEG-35 castor oil (Cremophor EL) was metabolized only by M. furfur. The latter observation is due to a different metabolism of castor oil and its main component, ricinoleic acid (12-hydroxy oleic acid), which may also give an insight into the pathogenesis of diseases that are associated with Malassezia spp. As hydroxy fatty acids are important in maintaining the epidermal structure and function, their metabolism specifically by M. furfur might clarify some clinical aspects of pityriasis versicolor. Apart from this speculation, use of Cremophor EL, with splitting of esculin as an additional key character, improves the distinction of the species M. furfur, M. slooffiae and M. sympodialis.
Castor Oil↗
Suborganellar Localization and Molecular Characterization of Nonproteolytic Degraded Leukoplast Pyruvate Kinase from Developing Castor Oil Seeds.
Plastid pyruvate kinase (PKp) activity and anti-(castor oil seed [COS] PKp) immunoglobulin G immunoreactive polypeptides were recovered in the stroma but not from envelope membranes of purified COS leukoplasts that had been subfractionated by sucrose density gradient centrifugation. The PKp was highly purified from isolated leukoplasts using anion-exchange and ADP-agarose chromatographies. Proteolysis of PKp was almost entirely eliminated by including 2,2[prime]-dipyridyl disulfide in purification buffers. The final preparation contained 63.5-kD ([alpha] subunit) and 54-kD ([beta] subunit) polypeptides that stained for protein and cross-reacted with anti-(COS PKp) immunoglobulin G with similar intensities. These two polypeptides co-eluted following gel-filtration chromatography and co-migrated during nondenaturing isoelectric focusing-polyacrylamide gel electrophoresis. The enzyme's native Mr was estimated to be 334,000. This PKp thus appears to exist as an [alpha]3[beta]3-heterohexamer. Comparison of the respective N-terminal sequences of the [alpha] and [beta] subunits with the deduced amino acid sequences for several PKp cDNAs indicated that (a) the [alpha] and [beta] subunits are encoded by COS genes previously designated as PKpA and PKpG, respectively, and (b) respective transit peptides of 4.8- and 5.5-kD are cleaved from the [alpha] and [beta] subunit preproteins following their translocation into the leukoplast.
Journal Article↗