Deaths from
microcystin toxication have widely been attributed to
hypovolemic shock due to hepatic interstitial
hemorrhage, while some recent studies suggest that cardiogenic complication is also involved. So far, information on cardiotoxic effects of MC has been rare and the underlying mechanism is still puzzling. The present study examined toxic effects of
microcystins on heart muscle of rats intravenously injected with extracted MC at two doses, 0.16LD(50) (14 microg MC-LReq kg(-1)
body weight) and 1LD(50) (87 microg MC-LReq kg(-1)
body weight). In the dead rats, both TTC staining and maximum elevations of
troponin I levels confirmed
myocardial infarction after MC exposure, besides a serious interstitial
hemorrhage in liver. In the 1LD(50) dose group, the coincident falls in heart rate and blood pressure were related to
mitochondria dysfunction in heart, while increases in
creatine kinase and
troponin I levels indicated cardiac cell injury. The corresponding pathological alterations were mainly characterized as loss of adherence between cardiac myocytes and swollen or ruptured mitochondria at the ultrastructural level. MC administration at a dose of 1LD(50) not only enhanced activities and up-regulated
mRNA transcription levels of
antioxidant enzymes, but also increased GSH content. At both doses, level of
lipid peroxides increased obviously, suggesting serious oxidative stress in mitochondria. Simultaneously, complex I and III were significantly inhibited, indicating blocks in electron flow along the mitochondrial respiratory chain in heart. In conclusion, the findings of this study implicate a role for MC-induced
cardiotoxicity as a potential factor that should be considered when evaluating the mechanisms of death associated with
microcystin intoxication in Brazil.