Microcystin-leucine-arginine affects brain gene expression programs and behaviors of offspring through paternal epigenetic information.

Microcystin-leucine-arginine (MC-LR) adversely affects male reproduction and interferes with the development of the offspring. Here, we establish a zebrafish (Danio rerio) model to understand the cross-generational effects of MC-LR in a male-lineage transmission pattern. F0 embryos were reared in water containing MC-LR (0, 5, and 25 μg/L) for 90 days and the developmental indices of F1 and F2 embryos were then measured with no MC-LR treatment.

Microcystin-LR induced oxidative stress, inflammation, and apoptosis in alveolar type II epithelial cells of ICR mice in vitro.

Previous studies have shown that microcystin-LR (MC-LR) produced by toxic cyanobacterial blooms could inflict damage to the lung. However, the mechanisms underlying MC-induced pulmonary toxicity are not fully described. In this study, the primary' fetal alveolar type II epithelial cells (AEC II) from ICR mice, which are involved in formation of bioactive component of pulmonary epithelium and secretion of pulmonary surfactants, were exposed to MC-LR at different concentrations (0, 0.

Microcystin-LR exposure decreased the fetal weight of mice by disturbance of placental development and ROS-mediated endoplasmic reticulum stress in the placenta.

The placenta is essential for sustaining the growth of the fetus. The aim of this study was to investigate the role of the placenta in MCLR-induced significant reduction in fetal weight, especially the changes in placental structure and function. Pregnant mice were intraperitoneally injected with MCLR (5 or 20 μg/kg) from gestational day (GD) 13 to GD17.