Microcystin-LR exposure to adult zebrafish (Danio rerio) leads to growth inhibition and immune dysfunction in F1 offspring, a parental transmission effect of toxicity.

Microcystins (MCs) are algal toxins produced intracellularly within the cyanobacteria cells. MCs exposure exerts great harm to the reproductive system of fish and deteriorates the quality of eggs and sperms, and has further adverse effects on early developmental stages of fish. Whether the MC toxicity can be parentally transmitted to offspring, even though the embryos and larvae are free of MC exposure? In the present study, adult zebrafish were continuously exposed to MC-LR (with dose of 1, 5 and 20 μg/L) for 30 days. After MC-LR exposure, fertilized eggs were collected and the following F1 generation was reared in water containing no MC-LR until 60 days post fertilization (dpf). In F1 offspring, both body weight and body length were evidently dropped. Some growth and immune related genes were detected using the real-time PCR. The transcriptional levels of these genes significantly decreased in F1 offspring of zebrafish whose parents were treated with 5 and 20 μg/L MC-LR. The activities of some antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) significantly dropped in 5 and 20 μg/L MC-LR groups, and the malondialdehyde (MDA) levels markedly increased in all the three treatment groups. Furthermore, distinct pathological changes in liver were observed in F1 zebrafish. Our findings show that the MC-LR exposure to parental zebrafish results in liver damage and evidently influences the growth and immune function in F1 offspring. We consider this damage as a parental transmission effect of microcystin toxicity. Further mechanism studies are necessary to elucidate this transmission effect.