composed of insoluble Ca2+ salts of
sapogenin glucuronides derived from the
saponins in the respective plants. These
saponins are thought to be the hepatotoxin,
and characteristic lesions include varying
degrees of necrosis of hepatocytes, concen-
tric lamellar periductal fibrosis and
proliferation of the bile duct epithelium.
Occlusion or obstruction of the biliary
system causes the accumulation of the
photosensitizing agent, phylloerythrin
derived by the action of rumen micro-
organisms on chlorophyll. Retention of
phylloerythrin may also arise from the
inability of damaged hepatocytes to
dispose of this compound into the biliary
system. Any phylloerythrin reaching the
skin, through inefficient hepatic and biliary
elimination, is able to react with sunlight
to cause photosensitization.
Lantana camara intoxication is another
example of hepatogenous photosensitiza-
tion disorders, in this instance caused by
pentacyclic triterpene acids, primarily lan-
tadene A and B. Incidence of L. camara
intoxication has been reported almost
exclusively in cattle in Australia, India,
South Africa and the USA. Liver lesions
include swelling and hydropic degenera-
tion of hepatocytes, single cell necrosis of
hepatocytes and bile duct damage leading
to impaired disposal of phylloerythrin.
Abnormal liver function with photo-
sensitization may also occur after con-
sumption of certain mycotoxins. Thus,
phomopsin A causes lupinosis which is
essentially a hepatic disorder of sheep
grazing lupin stubble. Manifestations
include ill-thrift, jaundice, photosensitiza-
tion and death. The mycotoxin interferes
with microtubule-dependent intracellular
transport mechanisms and acts as an anti-
mitotic agent in the liver. Sporidesmin A is
another mycotoxin with the capacity to
induce liver lesions with photosensitiza-
tion in ruminants. Effects include inflam-
mation of the bile ducts, progressive
obliterative cholangitis, obstructive jaundice
and phylloerythrin accumulation.
The aflatoxins are well recognized for
their potential to cause liver damage.
Indeed, the high mortality of turkey poults
in the ‘turkey X disease’ incident of 1960,
referred to above, arose from acute necrosis
of the liver and hyperplasia of the bile
duct. Current disquiet about the aflatoxins
centres on their capacity to induce liver
cancer in humans.Nephrotoxicity
In addition to photosensitization, certain
plants will induce renal damage. Thus,
Narthecium ossifragum may cause nephro-
toxicity in cattle, sheep and goats, although
current indications are that the agent is
distinct from that involved in hepato-
genous photosensitization (Flaoyen and
Froslie, 1997). Lantana poisoning may be
accompanied by kidney failure due to
tubular degeneration and necrosis.
Oxalates present in certain tropical grasses
such as those in the genera Cenchrus,
Setaria, Pennisetum, Digitaria and
Brachiaria may cause chronic renal failure
in grazing ruminants due to formation of
oxalate crystals and urinary calculi
(Marais, 1997).
Ochratoxin A frequently is implicated
in porcine nephropathy (Abramson, 1997).
Its action in the kidney may be exacerbated
by the co-occurring mycotoxin, citrinin.
Field cases of porcine nephropathy,
associated with the consumption of moist
cereal grains, have been reported in
Denmark, where the condition is endemic.
Affected kidneys are enlarged and pale
while, internally, sections of the renal
cortex show interstitial, peritubular and
periglomerular fibrosis. Tubular function
and efficiency may be impaired, consistent
with tubular degeneration and atrophy.
Balkan endemic nephropathy is a disorder
of humans which has also been linked with
OA and, in addition, there is evidence that
an OA-related nephropathy may be wide-
spread among Tunisians.Neurotoxicity
Of the secondary compounds occurring in
plants, the lathyrogenic non-protein amino
acids, -cyanoalanine, -(N-oxalylamino)
alanine and , -diaminobutyric acid are
notable for their neurotoxic properties.
Whether this neurotoxicity accounts for theAnti-nutritional Factors and Mycotoxins 395