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Content of the neurotoxins cycasin (methylazoxymethanol ß-D-glucoside) and BNLAA (ß-N-methylamino-L-alanine) in cycad flour prepared by Guam Chamorros

Center for Research on Occupational and Environmental Toxicology (Drs. Kisby and Spencer) and Department of Neurology (Dr. Spencer), School of Medicine, Oregon Health Sciences University, Portland, OR; and Evergreen High School (Mr. Ellison), Vancouver, WA.

Exposure to cycad seed kernel is an etiologic factor for the western Pacific amyotrophic lateral sclerosis (ALS) and parkinsonism-dementia complex (PDC). Traditionally processed cycad flours (n = 17) obtained from Chamorro residents of Guam and the adjacent island of Rota at risk for neurodegenerative disease were extracted and analyzed by high-performance liquid chromatography for content of ß-N-methylamino-L-alanine (BMAA) and methylazoxymethanol ß-D-glucoside (cycasin). Cycasin (detection limit: picomole) was present in concentrations of 0.004 to 75.93 µg/g (mean, 12.45 ± 5.0 µg/g), and levels of BMAA (detection limit: subpicomole) ranged from 0.00 to 18.39 µg/g (mean, 5.44 ± 1.56 µg/g). On average, cycasin content was approximately 10 times higher than that of BMAA. The largest concentrations of cycasin were found in samples from villages with a high reported prevalence of ALS/PDC. Ingestion of cycad-derived food would result in estimated human exposure to milligram amounts of cycasin per day. The cytotoxic properties of cycasin merit consideration in relation to the etiology of western Pacific ALS/PDC.

Address correspondence and reprint requests to Dr. Glen E. Kisby, Center for Research on Occupational and Environmental Toxicology, Oregon Health Sciences University, 3181 S.W. Sam Jackson Park Rd., L606, Portland, OR 97201.

Supported in part by the NIH grant NS 19611, and grants from the Alzheimer and Related Disorders Foundation and M.J. Murdoch Charitable Trust.

Received October 8, 1991. Accepted for publication in final form December 2, 1991.

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