Exposure to β-N-methylamino-l-alanine (BMAA) might be linked to the incidence of amyotrophic lateral sclerosis, Alzheimer’s disease and Parkinson’s disease. Analytical chemistry plays a crucial role in determining human BMAA exposure and the associated health risk, but the performance of various analytical methods currently employed is rarely compared. A CYANOCOST initiated workshop was organized aimed at training scientists in BMAA analysis, creating mutual understanding and paving the way towards interlaboratory comparison exercises. During this workshop, we tested different methods (extraction followed by derivatization and liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS) analysis, or directly followed by LC-MS/MS analysis) for trueness and intermediate precision. We adapted three workup methods for the underivatized analysis of animal, brain and cyanobacterial samples. Based on recovery of the internal standard D₃BMAA, the underivatized methods were accurate (mean recovery 80%) and precise (mean relative standard deviation 10%), except for the cyanobacterium Leptolyngbya. However, total BMAA concentrations in the positive controls (cycad seeds) showed higher variation (relative standard deviation 21%–32%), implying that D₃BMAA was not a good indicator for the release of BMAA from bound forms. Significant losses occurred during workup for the derivatized method, resulting in low recovery (<10%). Most BMAA was found in a trichloroacetic acid soluble, bound form and we recommend including this fraction during analysis.

In the present review we have discussed the occurrence of β-N-methylamino-L-alanine (BMAA) and its natural isomers, and the organisms and sample types in which the toxin(s) have been detected. Further, the review discusses general pathogenic mechanisms of neurodegenerative diseases, and how modes of action of BMAA fit in those mechanisms. The biogeography of BMAA occurrence presented here contributes to the planning of epidemiological research based on the geographical distribution of BMAA and human exposure. Analysis of BMAA mechanisms in relation to pathogenic processes of neurodegeneration is used to critically assess the potential significance of the amino acid as well as to identify gaps in our understanding. Taken together, these two approaches provide the basis for the discussion on the potential role of BMAA as a secondary factor in neurodegenerative diseases, the rationale for further research and possible directions the research can take, which are outlined in the conclusions.

The aim of our study was to investigate the effects of binge drinking on prooxidant/antioxidant system in rat liver in acute cadmium (Cd) intoxication. In experiment male Wistar rats were used and divided into following groups: 1. control, 2. ethanol-treated group, in five subsequent doses of 2 g/kg administered by orogastric tube, 3. Cd-treated group in a single dose of 2.5 mg/kg intraperitoneally, 4. group that received Cd 12 hours after the last dose of ethanol. Blood and liver samples were collected for determination of oxidative stress parameters, 24 hours after treatment. When administered in combination, ethanol and Cd induced a more pronounced increase in serum and liver malondialdehyde level than either of these substances alone (p<0.01). Liver manganese superoxide dismutase (MnSOD) activity was increased both in ethanol and Cd-treated group (p<0.01), while liver copper/zinc superoxide dismutase (Cu/ZnSOD) activity was elevated in Cd group only. However, when administered in combination, ethanol and Cd induced a more pronounced decrease in liver MnSOD and Cu/ZnSOD activity 24 hours after treatment (p<0.01). Based on our study, it can be concluded that ethanol may act sinergistically with Cd in inducing lipid peroxidation and reduction in liver SOD activity.