There is mounting evidence indicating that microcystins (MCs) are heptapeptide toxins. Recent studies have also shown that MCLR can transfer from mother to offspring, but it is unclear whether maternal MCLR can influence the liver of offspring or not. In this study, pregnant SD rats were injected intraperitoneally with a saline solution (control) or 10 μg/kg MCLR per day from gestational day 8 (GD8) to postnatal day 15 (PD15) for a total of 4 weeks. 2-DE and MALDI-TOF-TOF mass spectrometry were used to screen for MCLR target proteins in the livers of rat pups. Our results demonstrated that MCLR could accumulate in the livers of neonatal rats. Proteomics studies also showed that MCLR significantly influenced many proteins, including those involved in the cytoskeleton, metabolism and particularly oxidative stress. In addition, MCLR induced cellular structural damage and resulted in the production of intracellular reactive oxygen species (ROS) and lipid peroxidation. Moreover, protein phosphatase (PP) activity was inhibited and some serum biochemistry parameters were altered. These results suggest an early molecular mechanism behind the hepatotoxicity induced by maternal MC exposure and highlight the importance of monitoring MC concentrations in new-born mammals.
Keywords: Liver; MCLR; Oxidative damage; Proteomics; Rat pups.
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