Abstract β-N-Methylamino-l-alanine (BMAA) is a neurotoxin that is suspected to play a role in the neurological diseases amyotrophic lateral sclerosis, Alzheimer's disease and Parkinson’s disease. BMAA has been detected in phytoplankton and globally, the main exposure routes for humans to BMAA are through direct contact with phytoplankton-infested waters and consumption of BMAA-contaminated fish and invertebrates. As BMAA can be transferred from mothers to offspring in mammals, BMAA exposure is expected to have transgenerational effects. The aim of our study was to determine whether maternal exposure to BMAA affects offspring fitness in zooplankton. We performed a multigenerational life history experiment and a multigenerational uptake experiment with the water flea Daphnia magna as a model species. In both experiments, offspring from nonexposed and exposed mothers were raised in clean and BMAA-containing medium. Direct exposure to 110 μg/l BMAA reduced survival, somatic growth, reproduction and population growth. Maternal exposure did not affect D. magna fitness: animals from exposed mothers that were raised in clean medium had a higher mortality and produced lighter neonates than the controls, but this did not result in lower population growth rates. No evidence of adaptation was found. Instead, multigeneration exposure to BMAA had a negative effect: animals that were exposed during two generations had a lower brood viability and neonate weight than animals born from unexposed mothers, but raised in BMAA-containing medium. Maternal transfer of BMAA was observed, but BMAA concentrations in neonates raised in BMAA containing medium were similar for animals born from exposed and unexposed mothers. Our results indicate that zooplankton might be an important vector for the transfer of BMAA along the pelagic food chain, but whether BMAA plays a role in preventing zooplankton from controlling cyanobacterial blooms needs further investigation.
|Status||Gepubliceerd - nov. 2015|