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Abstract
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.