CASTOR OIL
Explanation
Castor oil is obtained from the seeds of the castor bean plant
(Ricinus communis L., Euphorbiaceae). The oil consists of a
triglyceride of fatty acids. The fatty acid content of castor oil
consists of about 88-90% ricinoleic acid, 4-5% linoleic acid, 2-3%
oleic acid, 1% palmitic acid, 1% stearic acid, about 1%
dihydroxystearic acid, and trace amounts of other fatty acids (Binder
et al. 1962).
BIOLOGICAL DATA
BIOCHEMICAL ASPECTS
About 7% of the ricinoleic acid present in a 1 ml oral dose of
castor oil given by stomach tube to fasted Sprague-Dawley rats was
absorbed into the chyle within a 24-hour period. About 24% of the
ricinoleic acid was absorbed if the substance was given to fed rats.
Seven weanling rats were given a diet containing 20% castor oil, the
animals gained weight on the diet, although at a lower rate than
animals fed an olive oil supplemented diet. After eight weeks on the
castor oil diet, the amount of ricinoleic acid in the animals' fat
pads was about 9.7%. When animals were fed the castor oil diet for
four weeks then switched to an olive oil diet for 14 days, the amount
of ricinoleic acid in the fat pads decreased to about 2% (Watson &
Gordon, 1962).
Studies in humans indicated that the percentage absorption of
castor oil is inversely proportional to the dose given. A dose of 4 g
of castor oil was almost completely absorbed; whereas, 64% of a dose
of 50 g appeared in the faeces within 24 hours, and almost 90% of 60 g
dose was excreted in the faeces. Doses of 10 g or more of castor oil
produced either mild laxation of purgation (Watson et al., 1963).
TOXICOLOGICAL STUDIES
Special studies on cytotoxicity
Ricinoleic acid was cytotoxic in vitro to isolated intestinal
epithelial cells from hamsters as based on release of radiolabelled
chromium, inhibition of 3-O-methylglucose transport and failure to
exclude trypan blue. The cytotoxicity began to occur at ricinoleic
acid concentrations greater than about 0.1 mM (Caginella et al.,
1977).
Special studies on intestinal histology
No microscopic changes were noted in the villus architecture of
the small intestine of random bred white mice following daily oral
dosing with 0.3 ml per day of castor oil for 12 weeks (Gibbins & John,
1970).
Substantial architectural changes were seen upon light or
electron microscopic examination of the mucosal cells of hamster small
intestine perfused in vivo in the presence of 8 mM sodium
ricinoleate. After treatment, the villus tips were capped with
vaccuolated epithelial cells with disintegrating brush borders; the
tight junctions were, however, not altered. Ricinoleate treatment was
accompanied by increased mucosal cell exfoliation as evidenced by
appearance of DNA in the perfusate. Membrane damage was accompanied by
increased sucrase activity and appearance of phospholipid in cell-free
aliquots of luminal fluid. There was also an increased clearance of
inulin and a 16 000 molecular weight dextran (Cline et al., 1976).
Dose-related epithelial damage and increased mucosal permeability
was seen upon perfusion of rabbit colon in vivo with 0, 2.5, 5.0,
7.5 and 10.0 mM concentrations of ricinoleate. Only occasional focal
epithelial damage was seen with 2.5 mM ricinoleate. Severe damage
was seen at 7.5 and 10.0 mM ricinoleate. There were also large dose-
related increases in the plasma to lumen clearances of urea and
creatinine (Gaginella et al., 1976).
Special studies on the incorporation of ricinoleic acid into phospholipids
Adult rats were fed for 25-40 days on a diet containing 48%
castor oil. Judging from the absence of hydroxy fatty acids, none of
the ricinoleic acid from the castor oil was incorporated into the
phospholipids of the liver, skeletal muscle, and small intestine. The
animals did not eat during the first few days of the experiment and
weight loss occurred. Aversion to the diet was soon overcome and in
most cases the initial body weight was restored. At no time during the
experiment was there any evidence of cartharsis (Steward & Sinclair,
1945).
Special studies on gastrointestinal motility and water absorption
Sodium ricinoleate at 2 mM concentration caused a 48% reduction
in net water absorption in vitro by isolated segments of hamster
jejunum. The substance also caused a significant decrease in sodium
and chloride absorption, but not potassium absorption (Stewart et al.,
1975a).
In vivo studies carried out with dogs indicated that 45 ml of
castor oil given by stomach tube decreased the activity of circular
smooth muscle in the intestine (Stewart et al., 1975a).
Ricinoleic acid depressed the spontaneous or induced contractile
activity of smooth muscle preparations from rat colon, rabbit jejunum
and guinea-pig taenia coli and ileum (Stewart et al. 1975b).
Studies with perfused human subjects showed that ricinoleic acid
caused a decrease in water absorption by the ileum at intraluminal
concentrations of 0.5 mM or higher. Concentrations of about 2 mM
or higher caused net secretion of water in the jejunum. Ricinoleic
acid was absorbed at about half the rate of oleic acid by the perfused
subjects (Ammon et al. 1974).
Acute toxicity
No data available.
Short-term studies
No data available.
Long-term studies
No data available.
Comments
At low doses castor oil is readily absorbed by man. As the oral
dose increases, per cent. absorption decreases and laxation occurs.
Castor oil has a long history of use as a laxative and aside from
these effects it has been used apparently without harm. At laxation
levels castor oil might be expected to inhibit the absorption of fat
soluble nutrients, notably vitamins A and D. Therefore, food additive
use of castor oil should be kept well below levels where absorption
would be inhibited. At doses of 4 g in adults absorption appears to be
complete and may be considered as a no-effect level.
However in light of the lack of adequate long-term studies of
immediate relevance the Committee applied a more conservative margin
of safety.
EVALUATION
Level causing no toxicological effect
Man: 70 mg/kg bw.
Estimate of acceptable daily intake for man
0-0.7 mg/kg bw.
REFERENCES
Ammon, H. V., Thomas, P. J. & Phillips, S. F. (1974) J. Clin.
Invest., 53, 374
Binder, R. G. et al. (1962) J. Amer. Oil Chem. Soc., 39, 513
Cline, W. S. et al. (1976) J. Clin. Invest., 58, 380
Gaginella, T. S. et al. (1976) Clin. Res., 24, 534A
Gaginella, T. S. et al. (1977) J. Pharmacol. exp. Ther., 201, 259
Gibbins, R. L. & John, T. J. (1971) J. Path., 103, 57
Stewart, J. J. et al. (1975a) J. Pharmacol. exp. Ther., 192, 458
Stewart, J. J., Gaginella, T. S. & Bass, P. (1975b) J. Pharmacol. exp.
Ther., 195, 347
Stewart, W. C. & Sinclair, R. G. (1945) Arch. Biochem., 8, 7
Watson, W. C. & Gordon, R. S. (1962) Biochem. Pharmacol., 11, 229
Watson, W. C. et al. (1963) J. Pharm. Pharmacol., 15, 183