Association between children death and consumption of Cassia occidentalis seeds: Clinical and experimental investigations

[Display omitted] •Biochemical changes in liver are similar in experimental animals and HME patients.•Myopathy observed in CO treated rats is similar to HME patients muscle biopsy.•Modulation of GFAP and β-tubulin suggests neurodegeration in rats.•Overall, CO seed is the etiological factor for inducing HME in children. Recently, children with high mortality rate have been observed in northern parts of India, for which the etiology is still not established, although a case control study has been linked to the consumption of Cassia occidentalis (CO) seeds. In the present investigation toxicity of CO seeds (0.5, 1 and 2% w/w) in diet were carried out in wistar rats. After 28days it was observed that CO seeds caused significant increases in the serum markers viz transaminases, alkaline phosphatase and lactate dehydrogenase along with histopathological lesions in hepatic tissue. CO consumption also showed decrease in grip strength, vacuolization and myopathy of skeletal muscles along with increases in serum creatinine and creatinine phosphokinase suggesting muscular damage in animals. Neuronal damage in CO treated animals was evident by a marked increase in glial fibrilar acidic protein and decrease in β-tubulin III. The experimental findings of CO consumption showed liver, muscles and brain to be the target organs, which were similar to that of the clinical data of poisoning cases as observed in the present study. Overall, the study suggests that CO seed consumption is the main etiological factor in children population suffering from hepatomyoencephalopathy in India.