Injury to hepatocytes induced by a peptide toxin from the cyanobacterium Microcystis aeruginosa

Toxicity and kinetics of [3H]microcystin-LR in isolated perfused rat livers

“…For example, serum glucose decreased in the whole animal model while in the perfused model, toxin stimulated the rate of glucose release. Stimulation of glucose release is consistent with the observation that MCYST activates phosphorylase a (Runnegar et al, 1987), the rate-limiting enzyme for glycogenolysis. MCYST stlmulation of glycoqenolysis probably occurs In vlvo uut was not reflected by a rise in serum glucose levels because of increased peripheral utilization of glucose.…”

Responses of antioxidant systems in the hepatocytes of common carp (Cyprinus carpio L.) to the toxicity of microcystin-LR

“…Degradation of MC in water is slow and the toxins often remain in the water supply used by people. There are many reports that Microcystis bloom leads to liver damage in human populations whose water supplies were contaminated by toxic Microcystis (Falconer et al, 1983;Carmichael et al, 1985;Carmichael, 1994;Bell and Codd, 1994 (Runnegar et al, 1987;Takenaka and Otsu, 1999). But little is known about the responses of antioxidant enzymes activities to microcystin-LR in freshwater fish hepatocytes and the relationship between ROS contents and MC shock.…”

Cytological alterations in isolated hepatocytes from common carp (Cyprinus carpio L.) exposed to microcystin-LR

“…The most conspicuous in vitro alterations were found within the nucleus, RER and cell membrane and these alterations were also observed in hepatocytes exposed to the toxin in vivo (Runnegar et al, 1987;Ito et al, 1997), as did ultrastructural change of RER and cell membrane including fragmentation, vesiculation, and transformation into concentric membrane whorls of RER (Dalholkar and Carmichael, 1987). Generally speaking, hepatocytes of animals died in two ways: either apoptosis or necrosis.…”