Microcystin Contamination in Sea Mussel Farms from the Italian Southern Adriatic Coast following Cyanobacterial Blooms in an Artificial Reservoir

An experimental study was performed in 2009-2010 to investigate the polluting effect of eutrophic inland waters communicating with the sea coast. The study was planned after a heavy and long-lasting Planktothrix rubescens bloom occurred in the Lake Occhito, an artificial reservoir. The waters of the reservoir flow into the southern Adriatic Sea, near several marine breeding of Mytilus galloprovincialis mussels, a typical seafood from the Apulia region (Southern Italy). A monitoring study of water and mussels from the sea coast of northern Apulia region and on the Occhito reservoir was carried out over twelve months, to get more information regarding the contamination by cyanobacteria and related cyanotoxins. Elisa immunoassay analyses estimated total microcystin amounts from 1.73 to 256？ng/g in mussels, up to 0.61？μg/L in sea water and up to 298.7？μg/L in lake water. Analyses of some samples of free-living marine clams as well as of marine and freshwater fish proved microcystin contamination. Selective confirmatory analyses by LC/ESI-Q-ToF-MS/MS on some mussel samples identified the microcystin desMe-MC-RR as the major toxin; this compound has been reported in the literature as a specific marker toxin of Planktothrix rubescens blooms. Our study describes for the first time the direct relationship between environmental pollution and food safety, caused by seafood contamination from freshwater toxic blooms. 1. Introduction Most poisoning risks from cyanobacteria blooms are due to microcystins (MC), a group of cyclic heptapeptides causing acute and chronic effects derived from their endocellular activity and protein phosphatase inhibition. Microcystins are hepatotoxins [1–6] acting as specific inhibitors of protein phosphatases 1, 2A [4], 3 (MC-LA) [7], 4 and 5 [8], and to a minor extent PP 2B [9]. They dephosphorylate serine and threonine residues in animals and plants. The inhibition of PP1 and PP2A increases the phosphorylation of proteins in liver cells, affecting several processes like metabolism, cell contractility, membrane transport, secretion, cell division, and gene transcription and translation. MCs are responsible for liver failure and death in humans [3, 10], wild animals, livestock, and aquatic life [11, 12]. Hepatotoxic [3, 4] endocrine disrupting [13–17] and oncogene activating [18] effects have been described for these toxins, classified as 2B compounds in the IARC oncogenic scale [19]. Indirect evidence supporting tumour promotion of human cancer from exposure to MCs is derived from the studies of Yu [20], Ueno et al. [21], and Zhou et