Cyanobacteria are capable of producing metabolites that are in some cases toxic to humans and other animals. Of these metabolites, the toxin cylindrospermopsin (CYN) is produced by a number of species of cyanobacteria including Cylindrospermopsis raciborskii, and its toxicity has been documented. The CYN analog deoxycylindrospermopsin (deoxyCYN) is commonly produced in varying proportions by the cyanobacteria that produce CYN. The toxicological profile of CYN suggests that it is primarily a hepatotoxin, but with the capacity to damage other organs and tissues. Limited in vivo information is available on the toxicity of deoxyCYN and suggests it to be of low potency. The aim of this research was to determine the comparative toxicology of deoxyCYN using in vitro systems. Using cell viability assays, it was shown that deoxyCYN had inhibitory effects on cell viability and proliferation of a similar magnitude to that of CYN. Morphological changes in deoxyCYN-treated cells were similar to those of CYN. Investigation of protein synthesis inhibition demonstrated that deoxyCYN was of similar potency to CYN. Inhibition of protein synthesis is an acknowledged mechanism of toxicity for CYN, and the results produced here suggest that deoxyCYN operates by similar toxicological mechanisms to CYN and that in vivo animal testing should be undertaken to clarify the potential for risk to humans from this toxin.

TGF-beta2 induces expression of elastin and ColVI and thereby could contribute to the increase of type VI collagen fibers in the tissue septae and the elastotic changes typically observed in POAG. With the concurrent activation of TIMP-1 and -3 and PAI-1 and the repression of tPA, TGF-beta2 could negatively regulate the activity and activation of MMPs. This effect could further amplify ECM accumulation and elastosis.

OPN is an age-dependent increased AH factor associated with degeneration of the optic nerve in D2J mice. By modulating the metabolism of neuronal cells, deregulated levels of OPN could be involved in degenerative processes affecting RGCs or optic nerve axons in the D2J model.

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