BMAA and ALS: A Close Look at Eutrophication

The overall equation representing one of life’s ultimate achievements, photosynthesis, is the biggest oversimplification you will find in any basic science book on the planet. It shows water, carbon dioxide and sunlight as reactants and glucose and oxygen as products. It does not hint at the intricate cascade of events that have to transfer electrons from water to carriers to chlorophyll; on to more carriers and other chlorophyll molecules and still more shuttle bus-like molecules and eventually to carbon dioxide and other reactants of the Calvin cycle.


It overlooks the accessory pigments that help chlorophyll capture more energy from the sun. It ignores the components of the membranes that separate hydrogen ion concentrations supplying the voltage needed to make the reaction facilitator, ATP, and all the enzymes that accelerate the entire food-making process of plants.

Reaction rates in chemistry are controlled by their slow intermediary steps. Photosynthesis and subsequent plant growth rates are controlled by the amount of light, which initiates the process; by temperature, which controls the carbon-dioxide fixing rate; by water-availability and by certain limiting ions. In other words, there is usually ample carbon dioxide available, but other minor, yet crucial substances are often scarce and control the growth of both land and aquatic plants. For algae, such limiting ions, mainly phosphate(PO43- and nitrate(NO3) are needed to make those behind the scene-molecules just mentioned: nitrogen-containing enzymes and ATP, which have N-compounds and phosphate, and they are also needed to synthesize genetic material.

But what happens when limiting ions suddenly become available in greater quantities to bodies of water? They cause eutrophication, which is a state of excess plant and algal growth. Although the process can occur naturally, humans are masters at accentuating it. Runoff fertilizer from nearby agricultural activities, sewage and industrial effluents all contain nitrates and phosphates, which directly lead to population explosions of algae, so called algal blooms.


As algal growth goes out of control, light has a harder time penetrating the water and its pH rises, both of which impact certain predators and shore plants. When excess algae die as part of their life cycles, their decomposition consumes dissolved oxygen, killing fish. Such hypoxic events are affecting over 245 000 square kilometers worldwide.

The foul smell of algal blooms is also a sign of more chemistry gone awry. Depending on the algal species that proliferate, eutrophication at times produces toxins that threaten drinking water supplies, recreational swimming and consumption of seafood. More specifically species of a group of photosynthetic bacteria, cyanobacteria,  produce compounds such as an enzyme-binding microcystin and the neurotoxin anatoxin-a, which mimics the neurotransmitter acetylcholine.

One of several microcytins, the LR refers to variant amino acids
One of several microcytins, microcystin-LR— the LR refers to the variant amino acids leucine and arginine.

In Canada, the Federal-Provincial-Territorial Subcommittee on Drinking Water recommends a maximum acceptable concentration of 0.0015 mg/L for total microcystins in drinking water, based on the toxicity of microcystin-LR. That is equivalent to 1.5 parts per billion, attesting to their high toxicity and to the fact that these compounds resist boiling.

Another cyanobacterial neurotoxin , β-methylamino-ʟ-alanine (BMAA), found in contaminated seafood and shellfish, drinking water supplies, and recreational waters—may be a factor in Lou Gehrig’s disease (amyotrophic lateral sclerosis, or ALS) and possibly other neurodegenerative conditions.


The toxin is produced by 95% of the cyanobacteria genera tested, and although it is not one of the 20 amino acids building blocks used by organisms, it does get mistakenly incorporated into proteins.

Accumulation of BMAA in the proteins of nerve cells, which need to last a lifetime, would provide a mechanism for how the toxin might biomagnify. “The problem with neurons is they do not divide, as a general rule, so over time they accumulate damaged proteins, and once they reach a critical level, it causes the cell to undergo apoptosis [cell death],” explains Rachael Dunlop, a researcher with the Heart Research Institute in Sydney, Australia.

Dunlop and others also found that at least in test tubes, a transfer RNA enzyme mistakenly picks up BMAA and incorporates it into proteins. More recently Dunlop and another researcher have mentioned that genes in certain individuals make them more sensitive to BMAA, which unfortunately is not presently screened for in municipal water analyses.


One thought on “BMAA and ALS: A Close Look at Eutrophication

  1. Apparently, excess phosphates and nitrates in streams causes algae to “hog” carbon compounds to the detriment of forest ecosystems.
    The abstract: Nutrient pollution of freshwater ecosystems results in predictable increases in carbon (C) sequestration by algae. Tests of nutrient enrichment on the fates of terrestrial organic C, which supports riverine food webs and is a source of CO2, are lacking. Using whole-stream nitrogen (N) and phosphorus (P) additions spanning the equivalent of 27 years, we found that average terrestrial organic C residence time was reduced by ~50% as compared to reference conditions as a result of nutrient pollution. Annual inputs of terrestrial organic C were rapidly depleted via release of detrital food webs from N and P co-limitation. This magnitude of terrestrial C loss can potentially exceed predicted algal C gains with nutrient enrichment across large parts of river networks, diminishing associated ecosystem services.


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