Biomagnification Of Cycad Neurotoxins In Flying Foxes

Biomagnification Of Cycad Neurotoxins Inflying Foxesimplications For

Analyze the biomagnification process of cycad neurotoxins, specifically BMAA, within Guam's ecosystem and its implications for neurodegenerative diseases such as ALS-PDC. Discuss the evidence supporting biomagnification in flying foxes and how traditional dietary practices may have contributed to disease prevalence, including analysis of neurotoxin levels in museum specimens and cycad seeds. Explore the potential health impacts, mechanisms of neurotoxicity, and broader environmental and cultural considerations.

Paper For Above instruction

The phenomenon of biomagnification plays a critical role in understanding how environmental neurotoxins, particularly those derived from plants, accumulate through various levels of a biological ecosystem. In Guam, the neurotoxin beta-methylamino-L-alanine (BMAA) has garnered attention because of its suspected link to neurodegenerative diseases such as amyotrophic lateral sclerosis-parkinsonism dementia complex (ALS-PDC). The evidence of biomagnification of BMAA involves its presence in cycad seeds—the primary plant source—and in higher concentrations within flying foxes (Pteropus mariannus mariannus), a traditional food source for the Chamorro people. Investigations have shown that BMAA levels in museum specimens of flying foxes, preserved over decades, are significantly higher than those in cycad seeds, indicating that the toxin is not only accumulated but possibly amplified through the food chain.

Historical epidemiological data from Guam reveal that the incidence of ALS-PDC was once 50–100 times higher than in other regions, coinciding with high consumption rates of flying foxes during traditional feasts. The fact that this pattern declined as the consumption decreased suggests a causative relationship between neurotoxin ingestion and disease prevalence. Furthermore, chemical analyses employing high-performance liquid chromatography (HPLC), thin-layer chromatography (TLC), and mass spectrometry (MS) provided concrete evidence of elevated BMAA levels in flying fox tissues. Some Museum of Vertebrate Zoology specimens contained BMAA concentrations up to 7,502 micrograms per gram of tissue, contrasted with only about 9 micrograms per gram in cycad seed sarcotesta, underscoring an extraordinary degree of biomagnification.

This process likely results from the predation of cycad seeds, which contain neurotoxins, by flying foxes that feed on the plant’s sarcotesta and outer integument. As the bats consume contaminated seeds, BMAA, which is water-soluble and stable over long periods, accumulates in their tissues. Predators, including humans, who consume flying foxes in traditional settings, are thereby exposed to these neurotoxins in doses that can cause or contribute to neurodegeneration. For example, a single flying fox weighing approximately 500 grams could harbor an internal BMAA load equivalent to ingesting over a kilogram of processed cycad flour, the traditional food source, known to contain neurotoxic levels of BMAA. Such significant doses are believed to have contributed to the high incidence of ALS-PDC during the peak consumption period in Guam.

The biochemical mechanisms by which BMAA causes neurotoxicity involve its incorporation into proteins in place of amino acids like serine, leading to protein misfolding and aggregation, which are hallmarks of neurodegenerative processes. BMAA also induces excitotoxicity via overstimulation of glutamate receptors, leading to neuronal damage and apoptosis. The stability of BMAA in tissues and its capacity to cross the blood-brain barrier mechanistically support its potential role in human neurodegeneration. The presence of BMAA in museum specimens after fifty years indicates that neurotoxins can persist in tissues without significant degradation, thus representing ongoing risks for past and present populations who have consumed traditional diets.

The implications of such biomagnification extend beyond Guam, highlighting the importance of understanding environmental sources of neurotoxins and their pathways in food webs. It underscores the significance of dietary and cultural practices in disease epidemiology, especially in indigenous communities that rely on traditional food sources rich in potentially neurotoxic compounds. Conservation efforts for endangered flying fox populations are also intertwined with public health concerns, as ecological change could influence toxin levels and exposure patterns. Additionally, recognition of BMAA’s role in neurodegeneration has led to broader investigations into other environmental, dietary, and industrial neurotoxins globally, emphasizing the need for vigilant monitoring and regulatory measures.

In conclusion, the biomagnification of cycad neurotoxins like BMAA within Guam’s ecosystem exemplifies how environmental contaminants can ascend food chains, ultimately impacting human health. The historic and biochemical evidence supports a model where traditional dietary practices contributed to high ALS-PDC prevalence via ingestion of biomagnified neurotoxins in flying foxes. Understanding these pathways underscores the critical need for integrating ecological, biochemical, and socio-cultural perspectives in addressing neurodegenerative disease risk factors and preserving ecological as well as human health.

References

• Banack, S. A., & Cox, P. A. (2005). Biomagnification of neurotoxins in flying foxes (Pteropus spp.) of Guam and implications for ALS-PDC. Journal of Environmental Neurology, 10(2), 83–98.
• Cox, P. A., & Sacks, O. W. (2002). Cycad neurotoxins, consumption of flying foxes, and ALS-PDC disease in Guam. Neurology, 58(6), 956–959.
• Kurland, L. T., & Mulder, D. W. (1954). Epidemiologic investigations of amyotrophic lateral sclerosis. Neurology, 4(4), 355–378.
• Reed, D., et al. (1987). A cohort study of ALS and parkinsonism-dementia in Guam. American Journal of Epidemiology, 125(1), 92–100.
• Spencer, P. S., et al. (1987). Guam ALS-parkinsonism–dementia linked to plant neurotoxins. Science, 237(4814), 517–522.
• Kisby, G. E., et al. (1992). Content of neurotoxins in cycad flour from Guam. Neurology, 42(7), 1336–1340.
• Duncan, M. W., et al. (1990). Analysis of BMAA in cycad flour: implications for ALS. Neurology, 40(5), 767–772.
• Cox, P. A., & Sacks, O. W. (2002). Cycad neurotoxins and ALS in Guam. Neurology, 58(6), 956–959.
• Khabazian, I., et al. (2002). Neurotoxicity of sterol β-D-glucosides from Cycas seeds. Journal of Neurochemistry, 82(2), 516–528.
• Banack, S. A., & Cox, P. A. (2004). Environmental neurotoxin biomagnification. Environmental Toxicology, 19(3), 328–337.