Root crops, in common with most plants, contain small
amounts of potential toxins and antinutritional factors such as trypsin
inhibitors. Apart from cassava, which contains cyanogenic glucosides,
cultivated varieties of most edible tubers and roots do not contain any serious
toxins. Wild species may contain lethal levels of toxic principles and must be
correctly processed before consumption. These wild species are useful reserves
in times of famine or food scarcity. Local people are aware of the potential
risks in their use and have developed suilable techniques for detoxifying the
roots before consumption.
Cassava
toxicity
The main toxic principle which occurs in varying amounts in
all parts of the cassava plant is a chemical compound called linamarin (Nartey,
1981). It often coexists with its methyl homologue called methyl-linamarin or
lotaustralin. Linamarin is a cyanogenic glycoside which is converted to toxic
hydrocyanic acid or prussic acid when it comes into contact with linamarase, an
enzyme that is released when the cells of cassava roots are ruptured. Otherwise
linamarin is a rather stable compound which is not changed by boiling the
cassava. If it is absorbed from the gut to the blood as the intact glycoside it
is probably excreted unchanged in the urine without causing any harm to the
organism (Philbrick, 1977). However, ingested linamarin can liberate cyanide in
the gut during digestion.
Hydrocyanic acid or HCN is a volatile compound. It
evaporates rapidly in the air at temperatures over 28 C and dissolves readily
in water. It may easily be lost during transport, storage and analysis of
specimens. The normal range of cyanogen content of cassava tubers falls between
15 and 400 mg HCN/kg fresh weight (Coursey, 1973). The concentration varies
greatly between varieties (Fig. 7.1) and also with environmental and cultural
conditions. The concentration of the cyanogenic glycosides increases from the
centre of the tuber outwards (Bruijn, 1973). Generally the cyanide content is
substantially higher in the cassava peel. Bittemess is not necessarily a
reliable indicator of cyanide content.
Traditional processing and cooking methods for cassava can,
if efficiently carried out, reduce the cyanide content to non-toxic levels. An
efficient processing method will release the enzyme linamarase by
disintegrating the microstructure the cassava root. On bringing this enzyme
into contact with linamarin the glucoside is converted into hydrogen cyanide.
The liberated cyanide will dissolve in the water when fermentation is effected
by prolonged soaking, and will evaporate when the fermented cassava is dried.
Sun drying fresh cassava pieces for short periods is an inefficient detoxification
process. Cyanide will not be completely liberated and the enzyme will be
destroyed during drying. Sun drying processing techniques reduce only 60 to 70
percent of the total cyanide content in the first two months of preservation.
Cyanide residues can be quite high in the dry tubers, from 30 to 100 mg/kg
(Casadei, 1988). Simple boiling of fresh root pieces is not always reliable
since the cyanide may be only partially liberated, and only part of the
linamarin may be extracted in the cooking water. The reduction of cyanides
depends on whether the product is placed in cold water (27°C) or directly into
boiling water (100°C). After 30 minutes cooking, the remaining cyanides are, in
the first case, 8 percent of the initial value, and in the second case about 30
percent (Easers, 1986).
Figure 7-1 - Effect of traditional processing of
four varieties of cassava tuberous roots in the preparation of gari, on total
and free cyanide content at each respective stage of processing
Various authors have suggested different minimal levels for
toxicity. Rosling (1987) was of the opinion that an intake of over 20 mg per
100 g of cassava is toxic, while Bolhuis (1954) set the toxic level at an
intake of 50 to 60 mg daily for a European adult.
Table 7.1 shows the HCN content of various processed cassava
products. It indicates that a dramatic reduction in the hydrocyanic acid
content of the raw cassava has occurred during processing. Soaking in water
improves detoxification as cells are broken by osmosis and fermentation, which
facilitates hydrolysis of the glycosides. Short soaking (four hours) is
ineffective, but when longer periods are used (18 to 24 hours) cyanide levels
can be reduced by 50 percent (Table 7.2). Squeezing the product is a
fundamental step in the elimination of the soluble cyanides.
Pathophysiology of cyanide intoxication
Cyanide is detoxicated in the body by conversion to
thiocyanate, a sulphurcontaining compound with goitrogenic properties. The
conversion is catalysed by an enzyme thiosulphate cyanide sulphur transferase
(rhodanase) present in most tissues in humans, and to a lesser extent by
mercaptopyruvate cyanide sulphur transferase which is present in red blood
cells (Fielder and Wood, 1956). The essential substrates for conversion of
cyanide to thiocyanate are thiosulphate and 3-mercaptopyruvate, derived mainly
from cysteine, cystine and methionine, the sulphur-containing aminoacids. Vitamin
B12 in the form of hydroxycobalamin probably influences the conversion of
cyanide to thiocyanate. Hydroxycobalamin has been reported to increase the
urinary excretion of thiocyanate in experimental animals given small doses of
cyanide (Wokes and Picard, 1955; Smith and Duckett, 1965). About 60 to 100
percent of the injected cyanide in toxic concentration is converted to
thiocyanate within 20 hours and enzymatic conversion accounts for more than 80
percent of cyanide detoxification (Wood and Cooley, 1956). Thiocyanate is
widely distributed throughout body fluids including saliva, in which it can
readily be detected. In normal health, a dynamic equilibrium between cyanide
and thiocyanate is maintained. A low protein diet, particularly one which is
deficient in sulphurcontaining amino-acids may decrease the detoxification
capacity and thus make a person more vulnerable to the toxic effect of cyanide
(Oke 1969, 1973). Excessive consumption of cassava, as the sole source of
dietary energy and main source of protein, could thus increase vulnerability to
cyanide toxicity.
TABLE 7.1 - HCN content of various cassava products during
processing Remaining HCN
Food
item
|
Detoxification stage
|
Remaining HCN
|
|
Mean (mg/kg)
|
(percentage)
|
||
Mpondu
|
Fresh leaves
|
68.6
|
100.0
|
Washed leaves (cold waler)
|
63.9
|
93.1
|
|
Dried leaves
|
66.1
|
96.3
|
|
Boiled leaves (15 min in water)
|
3.7
|
5.4
|
|
Boiled leaves (30 min in water)
|
1.2
|
1.7
|
|
Boiled cassava
|
|||
Fresh roots (sweet)
|
10.7
|
100.0
|
|
Boiled roots (20 min In water)
|
1.3
|
12.1
|
|
Fufu
|
Fresh roots (sweet and bitter)
|
111.5
|
100.0
|
Soaked roots (3 days)
|
19.4
|
17.4
|
|
Dried roots (3 days)
|
15.7
|
14.1
|
|
Uncooked fufu (flour and water)
|
2.5
|
2.2
|
|
Cooked fufu
|
1.5
|
1.3
|
|
Fuku
|
Fresh roots (sweet)
|
25.5
|
100.0
|
Uncooked fuku (heated)
|
4.2
|
16.4
|
|
Cooked fuku
|
1.2
|
4.7
|
|
Gari
|
Mash
|
90.1
|
100.0
|
24 h fermentation
|
73.2
|
81.2
|
|
48 h fermentation
|
55.3
|
61.3
|
|
48 h pressing
|
36.0
|
40.0
|
|
Roasting
|
25.8
|
28.6
|
|
Lafun
|
Mash
|
16.5
|
100.0
|
5 day soaking
|
35.9
|
21.8
|
|
5-day soaking + 48 h drying
|
25.5
|
15.5
|
|
5-day soaking + 96 h drying
|
19.6
|
11.9
|
|
Source: Bourdoux et al. 1982; Oke, 1984.
Diseases related to cassava toxicity
Several diseases have been associated with the toxic effects
of cassava. Its causative role has been confirmed in the pathological condition
of acute cyanide intoxication and in goitre. There is also some evidence
linking two types of paralysis to the combined effects of a high cyanide and
low sulphur intake, such as could result from a diet dominated by inefficiently
processed cassava. In these two diseases, tropical atoxic neuropathy and
epidemic spastic paraparesis, paralysis follows damage to the spinal cord. The
role of cyanide toxicity in the causation of tropical diabetes, and in
congenital malformation has not been established. Similarly its supposed
beneficial effects on sickle cell anaemia, shistosomiasis and malignancies are
still hypothetical.
Acute cyanide intoxication. Symptoms appear four to hours
after after of raw or insufficiently processed cassava and consist of vertigo,
vomiting, collapse and in some cases death within one or two hours. Treatment
is quite effective and cheap. The principle is to increase the detoxicating
capacity of the patient by giving an intravenous injection of thiosulphate and
thereby making more sulphur available for conversion of cyanide to thiocyanate.
Endemic goitre. Cyanide taken in the diet is detoxified in the body,
resulting in the production of thiocyanate. Thiocyanate has the same molecular
size as iodine and interferes with iodine uptake by the thyroid gland (Bourdoux
et al., 1978). Under conditions of high ingestion of inefficiently processed
cassava, there may be a chronic cyanide overload leading to a high level of
serum thiocyanate of 1 to 3 mg/100 ml, compared to a normal level of about 0.2
mg/100 ml. Under such conditions there is an increased excretion of iodine and
a reduced iodine uptake by the thyroid gland, resulting in a low
thiocyanate/iodine (SCN/I) excretion ratio. The value of the threshold level
for this ratio seems to be three (Derange et al., 1983) after which endemic
goitre appears. This phenomenon can occur only when the iodine intake is below
about 100 mg per day. At SCN/I ratios of lower than two there is a risk of
endemic cretinism, a condition characterized by severe mental retardation and
severe neurologic abnormalities (Ermans et al., 1983).
Studies in Zaire have shown that the population of Ubangi,
who consume a high amount of sun dried but unfermented cassava products, have a
low SCN/I ratio of 2 to 4 and suffer from endemic goitre and cretinism. Whereas
in Kim, where fermented and dried cassava paste is eaten, the SCN/I ratio goes
up to three to five and there is a low incidence of goitre. In Bas Zaire, where
properly processed cassava products are eaten, the SCN/I ratio is higher than
seven and there is no goitre. A low ratio leads to abnormal levels of the
thyroid stimulating hormone (TSH) and low thyroxine (T4). Ayangade et al.,
(1982) found that in pregnant women the thiocyanate level of the cord blood was
proportional to the maternal serum thiocyanate level, indicating that
thiocyanate can cross the placental barrier and affect the foetus. However,
there is very little thiocyanate in breast milk indicating that the mammary
gland does not concentrate thiocyanate and so breast-fed infants are not
affected.
When iodine supplements are given, for example, by adding
potassium iodide to local supplies of salt, goitre is reduced in spite of a
continued high intake of cassava products. Where salt intake is small or
variable, iodized oil, given by mouth, provides protection for one to two
years. In the Amazon jungle some tribal people eat as much as one kg of cooked
fresh cassava per person per day and consume up to three litres of fermented
cassava beer, but there have been no reported eases of either goitre or ataxic
neuropathy. These tribes also consume a considerable amount of animal and fish
protein and thus have high levels of sulphur-amino acids and iodine in their
diet.
Neurological disorders
Cyanide intake from a cassava-dominated diet has been
proposed as a contributing factor in two forms of nutritional neuropathies,
tropical ataxic neuropathy in Nigeria (Osuntokun, 1981) and epidemic spastic
paraparesis (Cliff et al., 1984). These disorders are also found in some
cassava growingareas of Tanzania and Zaire.
Tropical ataxic neuropathy. This disease is common in a
particular area in Nigeria where a lot of cassava is consumed without the
addition of sufficient protein-rich supplementary foods to provide an adequate
supply of sulphur amino-acids for the detoxification of ingested cyanide. The
consumed cassava product, called purupuru, is processed by an insufficient
fermentation of the cassava, which leaves a residual cyanide content of up to
0.10 M mole/g. As much as two kg of this foodstuff is consumed daily, leading
to the ingestion of about 50 mg of cyanide. The toxic level for an adult is
about 60 ma. The clinical picture is dominated by damage to one of the sensory
tracts in the spinal cord resulting in an uncoordinated gait called ataxia.
When patients are brought to the hospital they have a high
plasma thiocyanate level. On admission they are put on a hospital diet which is
highly nutritious and includes cassava only twice a week. Within a short period
the plasma thiocyanate level returns to normal, and the patients recover.
However, on discharge, they go back to their original diet of cassava and so
the condition reappears (Osuntokun, 1968).
All the cases reported came from the area where cassava is
cultivated and eaten in large quantities, with no cases in the nearby areas
where yam predominates. A change in the diet of the population at risk in
Nigeria has reduced the incidence of this disease.
Epidemic spastic paraparesis. This is a situation of depending
on very toxic varieties of cassava as a food security crop (Cliff et al.,
1984). In parts of Mozambique a bitter toxic type of cassava is often planted
as a food reserve because of its high yield. As cassava constitutes about 80
percent of the basic diet, there is nominally a standard method of preparation
which makes the cassava safe for consumption. Cassava, containing about 327 mg
HCN/ kg, is peeled, sliced and sun dried for about three weeks after which the
cyanide level is reduced to about 95 mg/kg. It is then pounded to a flour which
is mixed with hot water to make a paste called chima. This paste is normally
eaten with a relish of beans, fish or vegetables, to provide a well balanced meal.
During a prolonged period of drought all the food crops in
this area were lost except the toxic variety of cassava. The foodstores were
depleted and many families had no alternative, but to resort to the toxic
cassava. Normal processing time was reduced because of the emergency and so
there was no proper detoxification. The people knew this but they had no other
choice of action except to die of starvation. On eating the underprocessed
chima without their usual protein-rich supplement they complained that it was
more bitter than normal. After about four to six hours they suffered from
nausea, vertigo and confusion. Sufferers showed a high serum thiocyanate level
and a urinary thiocyanate excretion of about ten times that of
non-cassava-eating groups in Mozambique. There followed a sudden appearance of
many cases of spastic paraparesis, indicating an extensive epidemic. This
disease affects mainly women and children. It damages the nerve tract in the
spinal cord that transmits signals for movement, thus causing a spastic
paralysis of both legs (Rolling, 1983). Outbreaks have been reported during the
dry season from two areas in Zaire (Nkamany and Kayinge, 1982) and during
droughts in one area in Mozambique (Cliff et al., 1984) and one area in
Tanzania (Howlett, 1985).
During these drought periods about 500 g of dried cassava,
or 1.5 kg on a fresh weight basis, is consumed daily, representing an intake of
1 500 kcal and 50 mg cyanide per day. This level approaches the toxic level of
60 ma. The body can safely detoxify about 20 mg cyanide per day but when this
level increases to 30 mg symptoms of acute intoxication develop in many
consumers and hence the epidemics. If there is a period during which a high
cassava intake and a low protein-rich food intake, to supply sulphur
amino-acids for detoxification, coincide, this combination precipitates the
outbreak of this disease. The situation may be compared to the epidemics of
lathyrism that occured in drought-affected areas of India owing to the
high-level intake of the drought-resistant pea, Lathyrus saliva.
Production of low-cyanide foods
The development of a more sensitive method for cyanide
determination in foods by Cooke (1978a) and an in-depth study of some
traditional cassava foods have led to a better understanding of the
detoxification mechanism of cyanide in foods and to improved recommendations
for processing cassava.
Cyanide occurs in cassava and cassava products in two forms,
the glucosidic form, which is the linamarin itself, and the non-glucosidic or bound
form which is cyanohydrin. Under normal conditions of hydrolysis, when the
enzyme linamarase reacts with linamarin, it is hydrolysed to cyanohydrin which,
on decomposition, gives acetone and hydrocyanic acid. However, under acid
conditions, of pH4 or less, which tend to occur in some lactic acid
fermentations of cassava, the cyanohydrin decomposition is hindered and it
becomes stable. It is relatively easy to get rid of free cyanide, which is
present at about 10 percent in both peeled and fresh cassava, especially in
solution, but the non-glucosidic cyanide may hydrolyse very slowly and result
in a lot of residual cyanide in cassava products. Thus drying cassava chips in
an air oven at 47° and 60°C causes a decrease in the bound cyanide content of
25 to 30 percent, whereas faster drying at 80°C or 100°C gave only a 10 to 15
percent decrease of the bound cyanide. However, losses of free cyanide were 80
to 85 percent and 95 percent respectively (Cooke and Maduagwu, 1978b). Drying
results in an apparent increase in cyanide concentration because of loss of
water (Bourdoux et al., 1982). The longer the drying the higher the amount of
water removed. About 14 percent of the water can be removed during the first
day, reaching a level of up to 70 percent after eight days. This leads to an
increase in cyanide concentration from 70 mg/kg on the first day to 91 mg/kg
after eight days.
Soaking in water at 30°C, boiling or cooking removes free
cyanide but only about 55 percent of the bound cyanide is released after 25 minutes.
However, the bound cyanide is removed by prolonged soaking as fermentation
begins (Table 7.2) through the action of the enzyme linamarase which is
released by disruption of the tuberous tissues. If water is added at this stage
most of the cyanide is removed. Meuser and Smolnik (1980) were able to improve
the production of gari by washing the mash after fermentation to remove the
residual bound cyanide which was still present as cyanohydrin because of its
higher stability at the lower pH.
The result of different drying techniques is shown in Table
7.3. Freeze drying or rash-drying eliminated only the free cyanide, which
accounted for about 50 percent of the total cyanide present. Roller-drying of
the fresh pulp at a pH of 5.5 to 5.7 removed virtually all the cyanide, whereas
if the fermented pulp was dried on rollers or on drums high amounts of cyanide
were retained in the dried product because of the acid condition (pH 3.8) of
the fermented pulp. In the detoxification of cassava products fermentation is
most effective when accompanied by squeezing and washing of the acidic pulp.
Residual cyanide can be reduced further by sun drying or frying. This had been
confirmed by Hahn (1983) as shown in Fig. 7.1. In traditional preparations of
various food products from cassava, there may be some residual cyanide because
of insufficient tissue disintegration during processing and insufficient
washing. It is the residual cyanide that is responsible for toxicity. Some of
these preparations have been simulated in the laboratory and modified to give
much lower cyanide levels (Bourdoux et al., 1983).
TABLE 7.2 - Effects of soaking on the HCN content of six
bitter cassava roots
Soaking period (days)
|
Remaining HCN (percentage)
|
0
|
100.0
|
1
|
55.0
|
2
|
42.3
|
3
|
19.0
|
4
|
10.9
|
5
|
2.7
|
Source: Bourdoux et al., 1983
Sweet
potato
Sweet potato contains raffinose, one of the sugars
responsible for flatulence. Three of the sugars which occur in plant tissues,
raffinose, stachyose and verbascose are not digested in the upper digestive tract,
and so are fermented by colon bacteria to yield the flatus gases, hydrogen and
carbon dioxide. The level of raffinose present depends on the cultivar. In some
parts of Africa the cultivars used are considered too sweet and cause
flatulence (Palmer, 1982), Lin et al. (1985) have established that sweet potato
shows trypsin inhibitor activity (TIA) ranging from 90 percent inhibition in
some varieties to 20 percent in others. There is a significant correlation
between the trypsin inhibitor content and the protein content of the sweet
potato variety. Heating to 90°C for several minutes inactivates trypsin
inhibitors. Lawrence and Walker (1976) have implicated TIA in sweet potato as a
contributory factor in the disease enteritis necroticans. This seems doubtful
since sweet potato is not usually eaten raw and the activity of the trypsin
inhibitor present is destroyed by heat.
In response to injury, or exposure to infectious agents, in
reaction to physiological stimulation or on exposure of wounded tissue to fungal
contamination, sweet potato will produce certain metabolites. Some of these
compounds, especially the furano-terpenoids are known to be toxic (Uritani,
1967). Fungal contamination of sweet potato tubers by Ceratocystis fimbriata
and several Fusarium species leads to the production of ipomeamarone, a
hepatoxin, while other metabolites like 4-ipomeanol are pulmonary toxins.
Baking destroys only 40 percent of these toxins. Catalano et al. (1977)
reported that peeling blemished or diseased sweet potatoes from 3 to 10 mm
beyond the infested area is sufficient to remove most of the toxin.
TABLE 7.3 - Effect of drying on HCN consent of cassava
Drying
process
|
HCN (ppm)
|
|
Freeze
drying
|
Pulp
|
439
|
Flash
drying
|
Slices
|
432
|
Air
drying 40°C
|
Chips. pulp
|
13
|
Heated
air drying 180°C
|
Chips
|
14
|
Fermented pulp
|
77
|
|
Drum
drying
|
Pulp
|
8
|
Fermented pulp
|
121
|
|
HCN
of pulp
|
free and bound
|
900
|
Source: Meuser & Smolnik, 1980.
Potato
Potato contains the glycoalkaloids alpha-solanine and
alpha-chaconine (Maya, 1980), concentrated mainly in the flowers and sprouts
(200 to 500 mg/100 g). In healthy potato tubers the concentration of the
glycoalkaloids is usually less than 10 mg/100 g and this can normally be
reduced by peeling (Wood and Young, 1974; Bushway et al., 1983). In bitter
varieties the alkaloid concentration can go up to 80 mg/100 g in the tuber as a
whole and up to 150220 mg/100 g in the peel. The presence of these
glycoalkaloids is not perceptible to the taste buds until they reach a
concentration of 20 ma/100 g when they taste bitter. At higher concentrations
they cause a burning and persistent irritation similar to hot pepper. At these
concentrations solanine and other potato glycoalkaloids are toxic. They are not
destroyed during normal cooking because the decomposition temperature of
solanine is about 243 C.
Levels of glycoalkaloids may build up in potatoes which are
exposed to bright light for long periods. They may also result from wounding
during harvest or during post-harvest handling and storage, especially at
temperatures below 10°C (Jadhav and Salunkhe, 1975). Glycoalkaloids are
inhibitors of choline esterase and cause haemorrhagic damage to the
gastrointestinal tract as well as to the retina (Ahmed, 1982). Solanine
poisoning has been known to cause severe illness but it is rarely fatal (Jadhav
and Salunkhe, 1975).
Potato also contains proteinase inhibitors which act as an
effective defense against insects and micro-organisms but are no problem to
humans because they are destroyed by heat. Lectins or haemogglutenins are also
present in potato. These toxins are capable of agglutinating the erythocytes of
several mammalian species including humans (Goldstein and Hayes, 1978), but
this is of minimal nutritional significance as haemogglutenins are also
destroyed by heat, and potatoes are normally cooked before they are eaten.
Cocoyam
The high content of calcium oxalate crystals, about 780 mg
per 100 g in some species of cocoyam, Colocasia and Xanthosoma, has been
implicated in the acridity or irritation caused by cocoyam. Oxalate also tends
to precipitate calcium and makes it unavailable for use by the body. Oke (1967)
has given an extensive review of the role of oxalate in nutrition including the
possibility of oxalaurea and kidney stones. The acridity of high oxalate
cultivars of cocoyam can be reduced by peeling, grating, soaking and fermenting
during processing.
Acridity can also be caused by proteolytic enzymes as in
snake venoms. Attempts have been made to isolate such enzymes from taro, Colocasia
esculenta, and the principal component has been called "taroin" by
Pena et al. (1984).
Banana
and plantain
Banana and plantain do not contain significant levels of any
toxic principles. They do contain high levels of serotonin, dopamine and other
biogenic amines. Dopamine is responsible for the enzymic browning of sliced
banana. Serotonin intake at high levels from plantain has been implicated in
the aetiology of endomyocardial fibrosis (EMF) (Foy and Parratt, 1960).
However, Ojo (1969) has shown that serotonine is rapidly removed from the
circulating plasma and so does not contribute to elevated levels of biogenic
amines in healthy Nigerians. It has been confirmed by Shaper (1967) that there
is insufficient evidence for regarding its level in plantain as a factor in the
aetiology of EMF.
Yam
The edible, mature, cultivated yam does not contain any
toxic principles. However, bitter principles tend to accumulate in immature
tuber tissues of Dioscorea rotundata and D. cayenensis. They may be polyphenols
or tanninlike compounds (Coursey, 1983). Wild forms of D. dumetorum do contain
bitter principles, and hence are referred to as bitter yam. Bitter yams are not
normally eaten except at times of food scarcity. They are usually detoxified by
soaking in a vessel of salt water, in cold or hot fresh water or in a stream.
The bitter principle has been identified as the alkaloid dihydrodioscorine,
while that of the Malayan species, D. hispida, is dioscorine (Bevan and Hirst,
1958). These are water soluble alkaloids which, on ingestion, produce severe
and distressing symptoms (Coursey, 1967). Severe cases of alkaloid intoxication
may prove fatal. There is no report of alkaloids in cultivated varieties of D.
dumetorum.
Dioscorea bulbifera is called the aerial or potato yam and
is believed to have originated in an Indo-Malayan centre. In Asia
detoxification methods, involving water extraction, fermentation and roasting
of the grated tuber are used for bitter cultivars of this yam. The bitter
principles of D. bulbifera include a 3furanoside norditerpene called
diosbulbin. These substances are toxic, causing paralysis. Extracts are
sometimes used in fishing to immobolize the fish and thus facilitate capture.
Toxicity may also be due to saponins in the extract. Zulus use this yam as bait
for monkeys and hunters in Malaysia use it to poison tigers. In Indonesia an
extract of D. bulbifera is used in the preparation of arrow poison (Coursey,
1967).