BEET RED AND BETANINE
Beet red is the colour obtained from the red beetroot, the
principal component of which is betanine. This food colour was last
reviewed at the twenty-sixth meeting of the Committee (Annex 1,
reference 59), when the previously allocated temporary ADI "not
specified" was withdrawn because the additional information required
by the Committee at its eighteenth and twenty-second meetings was not
available, that is, data on metabolism and long-term toxicity (Annex
1, references 35 and 47).
Since the previous evaluation, additional data have become
available and are summarized and discussed in the following monograph.
Absorption, distribution, metabolism, and excretion
When betanine (4.5 µmole) was injected i.v. to rats, urinary
excretion was rapid, 88% of the dose appearing in urine within 4
hours, and the plasma half-life was 32 minutes. Orally-administered
betanine was poorly absorbed in rats and most of the dose was
metabolized in the gastrointestinal tract; approximately 3% of the
oral dose appeared in urine and a similar amount in faeces
(Krantz et al., 1980).
Special studies on carcinogenicity
In a two-generation study, rats were given 50-78 mg betanine/kg
b.w./day in drinking water throughout their lives. No evidence of
carcinogenicity was reported (Druckrey, 1959).
No increase in tumours was observed in rats given repeated doses
of betanine by subcutaneous injection (Druckrey, 1959).
A short-term study was performed to assess the ability of beet
red to initiate or promote hepatocarcinogenesis in rats. Groups of
female Sprague-Dawley rats (6-11 animals/group) were partially
hepatectomized and treated with four different beet pigment
preparations to assess their ability to initiate carcinogenesis;
fermented betacyanin solution (50 mg/kg), pure betanine (50 mg/kg),
degraded betanine (50 mg/kg), or a diet containing 2000 mg
betacyanin/kg. N-Nitrosodiethylamine (10 mg/kg) was used in a positive
control group. Another group previously initiated with
N-nitrosodiethylamine was given a betacyanin solution (100 ppm,
equivalent to 3.5 mg/rat/day) to determine the ability of betacyanin
to promote carcinogenesis after initiation relative to control and
phenobarbitone-pretreated rats. After 6 months (promotion studies) or
8 months (initiation studies) the livers were examined histologically
and histochemically for gamma-glutamyl peptidase foci. There was no
evidence that betalain preparations initiated or promoted
hepatocarcinogenesis (Schwartz et al., 1983).
Special studies on mutagenicity
Beet red was found to be non-mutagenic against 5 strains of
Salmonella typhimurium in the Ames test, with or without metabolic
activation by S-9 preparations, at concentrations of 500-2500 µg/plate
(von Elbe & Schwartz, 1981). At higher concentrations (50 mg/plate),
beet red was reported to be weakly mutagenic against S. typhimurium,
with or without metabolic activation (Ishidate et al., 1984).
No mutagenic activity was detected in studies using
Escherichia coli or S. typhimurium assays, with or without
metabolic activation by rat S-9 preparations, or intestinal microbial
preparations. No DNA damage was detected in the E. coli rec assay
Beet red did not induce chromosomal aberrations in Chinese
hamster fibroblast cells in culture (Ishidate et al., 1984).
No deaths were reported in rats given high oral doses of beetroot
red (Druckrey, 1959).
Single doses of betanine injected i.v. into anaesthetised rats
caused a transient increase in blood pressure and heart rate, the
effect of 0.9 µmole betanine being about equivalent to that of 2 µmole
adrenalin (Kranz et al., 1980).
Groups of six rats were fed beet red preparations containing
2000 ppm betalains in the diet for 7 days. No significant differences
were noted in body-weight gain, food intake, or gross pathological
features relative to controls (von Elbe & Schwartz, 1981).
(see "Special studies on carcinogenicity").
Observations in man
No information available.
COMMENTS AND EVALUATION
Previous Committees had considered beet red together with its
major colour component, betanine. This Committee decided that it would
be appropriate to evaluate these food colours separately and pointed
out that, for the compound betanine, insufficient data were available
to establish an ADI, since the information available to the Committee
did not meet currently accepted standards.
In evaluating beet red, the Committee took into account the
principles laid down by the Committee at its twenty-first meeting
(Annex I, reference 44) and endorsed in Annex III of "Principles for
the Safety Assessment of Food Additives and Contaminants in Food"
(Annex 1, reference 76). Thus, when the concentrate is used to enhance
the colour of beet products, it could be considered as food. If, on
the other hand, the concentrate is used more generally as a colourant,
careful specifications need to be established. Because nitrate is a
component of beet red, it is necessary to ensure that levels of
nitrate do not exceed the specifications. Under these conditions beet
red could be used according to good manufacturing practice with an ADI
"not specified", keeping in mind the need to limit the nitrate content
of foods produced for infants and young children.
Druckrey (1959). Unpublished data submitted to WHO.
von Elbe, J.H. & Schwartz, S.J. (1981). Absence of mutagenic activity
and a short-term toxicity study of beet pigments as food colourants.
Arch. Toxicol., 49, 93-98.
Haveland-Smith, R.B. (1981). Evaluation of the genotoxicity of some
natural food colours using bacterial assays. Mutation Res., 91, 285.
Ishidate, M., Sofuni, T., Yoshikawa, K., Hayashi, M., Nohmi, T.,
Sawada, M., & Matsuoka (1984). Primary mutagenicity screening of food
additives currently used in Japan. Fd. Chem. Toxicol., 22, 623.
Krantz, C., Monier, M., & Wahlstrom, B. (1980). Absorption, excretion,
metabolism and cardiovascular effects of beetroot extract in the rat.
Fd. Cosmet. Toxicol., 18, 363-366.
Schwartz, S.J., von Elbe, J.H., Pariza, M.W., Goldsworthy, T., &
Pitot, H.C. (1983). Inability of red beet betalain pigments to
initiate or promote hepatocarcinogenesis. Fd. Chem. Toxicol.,