Microcystin-LR and okadaic acid-induced cellular effects: a dualistic response
This review summarises the existing data on the molecular e¡ects of microcystin-LR inhibition of PP1 and PP2A both in vivo and in vitro, and where possible, compares this to the action of okadaic acid. ß 2003 Federation of European Biochemical Societies
As lipid peroxidation is a good indicator of oxidative stress in cells, the authors concluded that chronic exposure to sublethal doses of MCLR resulted in oxidative stress and suggested that it may play an important role in the chronic liver damage induced by MCLR toxicosis at sublethal levels
Whether the hepatocyte undergoes apoptosis or increased cellular proliferation appears to be dependent on the e¡ective concentration of toxin to which it is exposed as demonstrated in vitro
Either or both of these mechanisms could induce hepatic damage leading to necrosis/apoptosis and/or increased cellular proliferation
The extent of injury in vivo is in turn dependent on the level of exposure to the toxin, e⁄ciency of uptake and the detoxi¢cation process within the liver to remove both MC and MCLR-induced reactive oxygen species
In vivo studies indicate a clear role for MCLR to act as a tumour promoter at dose levels in the range of 1^10 Wg/kg i.p. or 382^693 Wg/kg orally, being associated with the development of liver, skin and possibly colon cancer
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