Consumption of oil extracted from accidental or deliberate contamination of argemone seed to mustard seed is known to pose a clinical condition popularly referred to as Epidemic
Dropsy. Several outbreaks of Epidemic
Dropsy have occurred in the past in India as well as in Mauritius, Fiji Island, and South Africa. Clinico-epidemiological manifestations of
argemone oil poisoning include
vomiting,
diarrhea,
nausea, swelling of limbs,
erythema, pitting
edema,
breathlessness, etc. In extreme cases,
glaucoma and even death due to
cardiac arrest have been encountered. The toxicity of
argemone oil has been attributed to two of its physiologically active benzophenanthridine
alkaloids,
sanguinarine and
dihydrosanguinarine. Histopathological studies suggest that liver, lungs, kidney, and heart are the target sites for
argemone oil intoxication. Studies have shown to elucidate the cocarcinogenic potential of
argemone oil that can be correlated with the binding of
sanguinarine with
a DNA template. Pharmacological response in intestine revealed immediate stimulation of tone and peristaltic movements of the gut in the
sanguinarine-treated animals.
Argemone oil/
Sanguinarine caused a decrease in
hepatic glycogen levels which may be due to the activation of glycogenolysis leading to an accumulation of
pyruvate in the blood of Epidemic
Dropsy cases. The increase in
pyruvate levels causes uncoupling of oxidative phosphorylation leading to
breathlessness, as observed in patients.
Sanguinarine has been shown to inhibit Na+, K(+)-
ATPase activity of different organs such as brain, heart, liver, intestine, and skeletal muscle, which may be due to the interaction with the
glycoside receptor site on
ATPase enzyme, thereby causing a decrease in the active transport of
glucose.
Argemone oil/
alkaloid showed a Type II binding spectra with hepatic
cytochrome P-450 (P-450)
protein, thereby causing loss of P-450 content and an impairment of phase I and phase II
enzymes. A green fluorescent metabolite of
sanguinarine, benzacridine was detected in the milk of grazing animals. The delayed appearance of this metabolite in urine and feces of experimental animals suggests the slow elimination of the
alkaloid.
Argemone oil enhances hepatic microsomal and mitochondrial lipid peroxidation, indicating that these two organelles are the sites of membrane damage. Furthermore, studies suggest that
singlet oxygen and
hydroxyl radical are involved in
argemone oil toxicity. Several bioantioxidants show protective effect in
argemone oil-induced toxicity in experimental animals. The line of treatment in argemone-intoxicated epidemics has so far been only symptomatic, and specific therapeutic measures are still lacking, although it has been suggested that
diuretics, bioantioxidants,
steroids,
vitamins,
calcium- and
protein-rich diet had some beneficial effects on Epidemic
Dropsy cases.