The presence of cyanotoxins, mainly microcystins (MCs), in surface freshwater represents a serious health risk to aquatic organisms living in the water body, as well as terrestrial animals and plants that are in contact with contaminated water. Consequently, the use of MCs contaminated water for irrigation represents a hazard for cultivated plants and could induce severe economical losses due to crops' yield reduction. The experimental approach undertaken in this work was exposing Vicia faba seedlings (inoculated with a Rhizobium strain resistant to MCs), to water supplemented with cyanobacterial crude extract containing total microcystins at a concentration of 50 and 100 μg/L (environmental relevant concentrations of MCs dissolved in the raw irrigation water from Lalla Takerkoust Lake-Marrakesh region). After chronic MCs exposure (2 months), biological and physiological parameters (plant growth, nitrogen uptake, mineral assimilation, and oxidative defense mechanisms) were evaluated. The results obtained showed evidence that chronic exposure to cyanobacterial bloom extract containing MCs strongly affected the physiological and biological plants activities; reduction of dry matter, photosynthetic activity, nodule number, and nitrogen assimilation. At the same time, an increase of oxidative stress was observed, as deduced from a significant increase of the activities of peroxidase, catalase, polyphenoloxidase, and phenylalanine ammonia lyase in leaves, roots, and nodules of faba bean plants exposed to cyanotoxins, especially at 100 μg/L of MCs. This experimentation constitutes a simulation of the situation related to cyanotoxins chronic exposure of seedlings-plants via the contaminated irrigation water. For this reason, once should take into consideration the possibility of contamination of agricultural crops and the quality of irrigation water should be by the way monitored for cyanotoxins biohazard.

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A previously undescribed mutation of hereditary γ γ-glutamylcysteine synthetase (GCS) deficiency was found in a 5 year old boy of Moroccan origin. He presented with chronic haemolytic anaemia, delayed psychomotor development and progressive motor sensitive neuropathy of lower extremities. The parents were third degree relatives. The activity of glycolytic enzymes were found to be normal in the propositus, his parents and a sister, but and a complete lack of GSH was found in the propositus. Accordingly, the measurement of de novo GSH synthetic enzymes was undertaken, and severe GCS deficiency was found in the propositus. Both parents and his sister presented GCS activity ranging from 69% to 90% of normal. GCS gene sequencing showed that the propositus was homozygous for a 1241C>T mutation in exon 11 and both parents and his sister were heterozygous. This mutation predicts a Pro414Leu amino acid substitution. Even though the homology between GCS and crystallographically solved, functionally related proteins is not very high, a three-dimensional model of GCS was derived using Modeller Software. GCS deficiency is a very rare autosomal recessive disorder reported so far in only 8 unrelated probands with severe haemolytic anaemia. In only 3 of these was the anaemia associated with severe neurological dysfunction. We report here the fourth case of GCS deficiency presenting neuropathy, giving further support to the eventual relationship between this enzymopathy and neurological damage Haematologica 2007; 92:e102-e105

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