Background Okadaic acid is often a marine toxin produced by sev eral dinoflagellate species. It was firstly isolated from the black sponge Halichondria okadai and is regularly discovered in various varieties of molluscs usual within the human eating plan as those from Mytilus or Ostrea genus. The inges tion of OA contaminated shellfish leads to a syndrome called diarrhoeic shellfish poisoning which can be characterized by extreme gastrointestinal symptoms such as nauseas, vomit, diarrhoea and abdominal ache. Despite the fact that fatalities associated with DSP contami nated shellfish have not been reported, this intoxication has come to be a severe dilemma for public overall health and for the economy of aquaculture industries in a number of components from the globe. OA was identified to be a very potent tumour promoter in two stage carcinogenesis experiments in vivo invol ving mouse skin or mucosa with the rat glandular sto mach.
OA was also reported description to induce different genotoxic, cytotoxic, and embryotoxic effects like micronuclei, oxidative DNA damage, DNA strand breaks and alterations in DNA repair, mito tic spindle alterations, apoptosis, cell cycle disruptions, anomalies from the embryonic improvement and teratogenicity. Apart from, in spite of the truth that DSP toxins are not classified as neurotoxins, some earlier research have currently reported neurotoxic effects induced by OA such as neuronal apoptosis and cytoskeleton alterations, deficits in spatial memory as well as cognitive deficits in rodents. Around the basis on these and also other preceding studies, OA represents other prospective threats to human well being in addition to DSP, even at concentrations within the nanomo lar range.
It is actually well-known that OA can inhibit specifi cally mtorc2 inhibitor the serinethreonine protein phosphatases 1 and 2A. the number of physiological pro cesses in which these phosphatases are involved is immense, like regulation of glycogen metabolism and coordination from the cell cycle and gene expression. So this role of phosphatase inhibition by OA could clarify most of the cell effects induced by this toxin. Even so the amount of controversial data in the literature continues growing and further investigations on biochemical and molecular OA action mechanisms are needed because the reality that non phosphatase targets for OA are certainly not known will not mean that they usually do not exist. Actually, the existence of OA binding proteins besides phosphatases was demonstrated in numerous marine organisms.
In this study, a suppression subtractive hybridization approach was employed to identify genes differentially expressed in SHSY5Y cells in response to OA exposure at diverse instances. Sequences obtained by SSH were utilized to search for homologyidentity to nucleotide and protein databases. Moreover, differen tial expression patterns of five chosen genes had been also studied in OA treated SHSY5Y cells at 3, 24 and 48 h by real time PCR.