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At least 19 recordsLinked to original sources
PubMed1992

Time course of PAF formation by gastrointestinal tissue in rats after castor oil challenge.

When castor oil was administered by gavage to rats, the duodenum and jejunum, but not the stomach, produced large amounts of platelet activating factor 3-7 h after oil challenge with a peak at 3 h. Intraluminal release of acid phosphatase was also markedly increased in the duodenum and jejunum of castor oil-treated rats, especially 3-5 h after oil challenge. No increase was observed in the stomach. There was a correlation between elevated release of acid phosphatase and intestinal hyperaemia.

Acid Phosphatase↗
PubMed1976

The reduction of coma time in lipophilic drug overdose using castor oil.

A clinical trial of castor oil in overdoses of lipophilic drugs gave a strong clinical impression that it was effective in speeding up recovery. Therefore, animal experiments were undertaken to confirm that castor oil acts as a ligand in Ethchlorvynol poisoning and that its use reduces coma time. Serial serum levels of Ethchlorvynol were obtained from dogs given Ethchlorvynol 150 mg/kg alone, and the same dose dissolved in castor oil 15 ml/kg in a crossover fashion. The result was a reduction of peak serum levels and of the half-life of the drug when the castor oil solution was used. In order to mimic the clinical situation more closely, a further crossover study was undertaken using Ethchlorvynol 300 mg/kg alone and the same dose followed by castor oil 15 ml/kg repeated q12h. This showed no delay in reaching peak serum concentration and no reduction of peak levels. However, it did show a 31 per cent reduction in the half-life of the drug. This change is statistically significant, and supports the continued use of castor oil in lipophilic drug overdose.

Animals↗
PubMed1995

Haematopoietic radioprotection by Cremophor EL: a polyethoxylated castor oil.

The polyethoxylated castor oil, Cremophor EL (Cremophor) is approved for human use as a vehicle for oral and intravenous administration of water-insoluble compounds. Cremophor has also previously been shown to reverse the multidrug resistance phenotype at clinically acceptable doses. This study demonstrates that doses of Cremophor in the range of 25-50 microliters/kg intravenously (i.v.) administered 1 day prior to near-lethal irradiation protected the regenerative capacity of the marrow, resulting in haematopoietic radioprotection and long-term survival of near-lethally-irradiated mice. In normal mice, Cremophor administration (1) markedly reduced the level of serum haematopoietic inhibitory activity 4-8 h following injection; (2) resulted in a transient decrease in femoral bone marrow cellularity and upregulated B220 (B cells), and 7/4 (neutrophils and activated macrophages), but not Thy-1 (T-cells) surface antigen expression in bone marrow cells within 24 h of injection; and (3) transiently elevated the incidence of both primitive and committed haematopoietic progenitor cells detected in clonal agar culture within 48 h of injection. Bone marrow progenitor cell content, and peripheral blood white cell, platelet and reticulocyte counts were unaffected. This suggests that the haematopoietic radioprotection and recovery observed in irradiated mice pretreated with Cremophor may be the result of accessory cell activation and/or modulation of accessory factors regulating haematopoietic progenitor cells. Our data suggest a potential clinical use of Cremophor as an adjunct to, or as a substitute for, cytokines to minimize myelosuppression following cytotoxic therapy.

Animals↗
PubMed1993

Inhibitors of nitric oxide synthetase prevent castor-oil-induced diarrhoea in the rat.

1. Castor oil (2 ml orally) produced copious diarrhoea in rats 3 h after its administration. 2. Pretreatment (intraperitoneal, i.p.) of rats with the NO synthesis inhibitors NG-nitro-L-arginine methyl ester (L-NAME, 1-25 mg kg-1) and NG-monomethyl-L-arginine (L-NMMA, 2.5-100 mg kg-1) inhibited or prevented castor-oil-induced diarrhoea. L-Arginine (150-600 mg kg-1, i.p.) administered to rats pretreated with L-NAME 10 mg kg-1, drastically reduced the antidiarrhoeal activity of L-NAME in a dose-related manner. D-Arginine (900 mg kg-1) did not modify the protection by L-NAME. 3. Pretreatment (i.p.) of rats with L-NAME (2.5-25 mg kg-1) decreased the intestinal fluid accumulation and Na+ secretion induced by castor oil. L-Arginine (600 mg kg-1) but not D-arginine (900 mg kg-1) counteracted the inhibitory effect of L-NAME (10 mg kg-1). 4. L-NAME (10 and 25 mg kg-1) had no significant effect on the intestinal transit in normal rats or those given castor oil. 5. These results provide evidence that nitric oxide (NO) could play an important role in castor-oil-induced diarrhoea.

Amino Acid Oxidoreductases↗
PubMed1982

The effect of oral castor oil on the disposition of methyprylon in intoxicated dogs.

Clinical observations indicate that large oral doses of castor oil are effective in reducing the time of coma resulting from acute intoxication with lipophilic drugs. It has been further suggested that the rate of removal of these drugs from the body is increased by castor oil. In order to investigate the effect of castor oil on the disposition of lipophilic drugs, five dogs were given toxic doses of methyprylon by intravenous infusion. Each dog was treated with a large oral dose of castor oil in a cross-over fashion. No significant difference was observed in the sleep times of the dogs treated with castor oil, or in the methyprylon pharmacokinetics compared to controls. It was concluded that castor oil does not affect the disposition of methyprylon.

Animals↗
PubMed1993

A comparison of the effectiveness and patient tolerance of oral sodium phosphate, castor oil, and standard electrolyte lavage for colonoscopy or sigmoidoscopy preparation.

One hundred thirteen patients were randomized to receive either oral sodium phosphate (Fleet Phospho-Soda), lemon-flavored castor oil (Purge), or standard polyethylene glycol-based lavage solution (GoLYTELY) before elective colonoscopy. The study purpose was to confirm the efficacy of oral sodium phosphate and extend observations to include castor oil. Overall, patients reported that sodium phosphate and castor oil were easier to complete (p < 0.05). Scores for cleansing the entire colon as determined by endoscopists who were blinded to the cathartic agent were highest in patients receiving sodium phosphate (p < 0.02). Scores of left-colon cleansing for flexible sigmoidoscopy were equally high for the three methods. Scores for taste and symptom side effects were similar for each preparation. There were no recognized signs or symptoms of hypocalcemia in the sodium phosphate group. Because of the low cost of oral sodium phosphate combined with the lowest repeat endoscopy rate for inadequate cleansing, patient savings were projected to be $5000 per 100 patients at this center. Oral sodium phosphate is a cost-effective colonoscopy preparation that is better tolerated and more effective than the polyethylene glycol-electrolyte lavage solution or castor oil.

Administration, Oral↗
PubMed1989

Molecular and immunological characterization of plastid and cytosolic pyruvate kinase isozymes from castor-oil-plant endosperm and leaf.

1. Monospecific antiserum was raised in rabbits to homogeneous cytosolic pyruvate kinase isolated from 5-day-old germinating endosperm of the castor oil plant, Ricinus communis. An earlier study demonstrated that the purified enzyme is putatively heterotetrameric, composed of two subunits which migrate as 57-kDa and 56-kDa proteins upon sodium dodecyl sulfate/polyacrylamide gel electrophoresis [Plaxton, W. C. (1988) Plant Physiol. (Bethesda) 86, 1065-1069]. Both proteins were detected on Western blots of extracts prepared under denaturing conditions from 4-8-day-old, but not 0-3-day-old, germinating-endosperm tissue. This suggests that both subunits exist in vivo, and that the large increase in pyruvate kinase activity which occurs around the fourth day of germination is due to an increase in pyruvate kinase concentration. 2. The cytosolic and plastidic pyruvate kinase isozymes (termed PKc and PKp, respectively) from castor-oil-plant developing endosperm and expanding leaf tissue were separated by anion-exchange chromatography on Q-Sepharose. The antigenic reaction of the partially purified enzyme preparations to rabbit polyclonal antibodies raised against homogeneous germinating-castor-bean PKc was tested by immunoprecipitation and Western blotting. Although developing-endosperm and leaf PKc appeared to be antigenically very similar to germinating-endosperm PKc, they differed from the heterotetrameric germinating-endosperm enzyme by being composed of a single type of subunit with a molecular mass of about 56 kDa. No cross-reactivity of the PKc antibodies was observed with either developing-endosperm or leaf PKp, nor with rabbit muscle or Bacillus stearothermophilus pyruvate kinase. Conversely, none of the castor-oil-plant pyruvate kinase preparations showed significant cross-reactivity with antibodies raised against purified yeast or rabbit muscle pyruvate kinases. 3. To investigate the structural relationship between the two germinating-endosperm-PKc subunits, each polypeptide was characterized by amino acid composition analysis and peptide mapping by CNBr fragmentation. The amino acid compositions and CNBr cleavage patterns of the two subunits were similar, but not identical, suggesting that these polypeptides are related, but distinct, proteins. Mild tryptic attack of native enzyme led to an approximate 6-kDa reduction in the apparent molecular mass of both subunits, further indicating sequence similarity between the two polypeptides. 4. Native molecular masses of the various castor-oil-plant pyruvate kinases were estimated by Superose-6 gel-filtration chromatography.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acids↗
PubMed1978

[Pharmacological studies of loperamide, an anti-diarrheal agent. I. Effects on diarrhea induced by castor oil and prostaglandin E. (author's transl)].

Effects of loperamide on diarrhea induced by castor oil and prostaglandin E1 were investigated in rats and mice and compared with those of narcotic analgesics, atropine, mecamylamine and local anesthetics. The following results were obtained. Loperamide markedly suppressed the appearance of diarrhea induced by oral administration of castor oil in rats and the ED50 values for 1 and 2 hr protection was 0.082 and 0.42 mg/kg p.o., respectively. Loperamide markedly suppressed the appearance of diarrhea induced by i.v. administration of prostaglandin E1 and the ED50 value for 2 hr protection was 0.24 mg/kg p.o. in rats. The ID120 min value of loperamide which was calculated on the basis of the dose producing a 20% or more inhibition of the charcoal transport in the small intestine for 120 min was 0.8 mg/kg p.o. in mice and this activity was 9.2 times more potent than that of morphine. The analgesic ED50 value (Haffner's method) and LD50 value of loperamide was 149 and 249 mg/kg p.o., respectively. These results suggest that loperamide has a potent anti-diarrheal activity and specificity to the gastrointestinal tract and inhibits the effect of prostaglandin E1 and ricinoleic acid on the intestinal tract in rats.

Analgesics↗
PubMed1989

Castor oil increases intestinal formation of platelet-activating factor and acid phosphatase release in the rat.

1. When castor oil was administered by gavage to rats, the duodenum and jejunum but not ileum and colon produced large amounts (5-6 fold greater than control) of platelet activating factor (Paf). 2. Intraluminal release of acid phosphatase (AP) was also markedly increased (5-6 fold greater than control) in the duodenum and jejunum of castor oil-treated rats and there was a correlation between the elevated release of AP and intestinal hyperaemia. 3. These findings support a role for Paf as a mediator of intestinal damage induced by castor oil.

Acid Phosphatase↗
PubMed1994

Mutagenicity tests of polyoxyethylene hydrogenated castor oil 60 (HCO-60).

The genotoxicity of polyoxyethylene hydrogenated castor oil 60 (HCO-60) was examined in reverse mutation test in bacteria, chromosome aberration test in vitro and micronucleus test in mice. The in vitro tests were done with and without metabolic activation using rat liver microsomal fraction. HCO-60 did induce neither reverse mutation in Salmonella typhimurium TA100, TA98, TA1535, and TA1537 and in Escherichia coli WP2uvrA, nor chromosome aberrations in Chinese hamster V79 cells. In addition, no increase in micronucleated polychromatic erythrocytes was elicited in the bone marrow of BDF1 male and female mice. It is concluded that HCO-60 was not genotoxic in these in vitro and in vivo assays.

Animals↗
PubMed1976

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↗
PubMed1986

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↗
PubMed1993

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↗