Microcystin-LR triggers different endoplasmic reticulum stress pathways in the liver, ovary, and offspring of zebrafish (Danio rerio).

The existence of microcystins (MCs), the secondary metabolite of cyanobacteria, has become a growing public health concern. Previous researches have proved that MCs can trigger endoplasmic reticulum stress (ERS), but the underlying mechanisms remain unclear. In the present study, adult female zebrafish were exposed to MC-LR (0, 1, 5 and 20 μg/L) for 30 d, and the offspring derived from the treated females and healthy males were cultured in water without MC-LR until 96 h post fertilization (hpf). Our data suggested that MC-LR causes a significant increase in the eif2s1a, atf4, and eif2ak3 transcription levels in the liver and ovary. The mRNA levels of atf4, atf6, bcl-2, hspa5, eif2s1a and eif2ak3 upregulated notably in the offspring. JNK phosphorylation level and cleaved-caspase3 protein expression elevated obviously in the liver and ovary, but had no remarkable change in the offspring. Furthermore, TUNEL results showed that MC-LR significantly induced apoptosis in the liver and ovary, while acridine orange (AO) staining indicated that MC-LR did not cause abnormal apoptosis in offspring. Concisely, the present study indicated that MC-LR leads to apoptosis through different ERS pathways in the liver, ovary and offspring, and also provides a new perspective for understanding the apoptosis caused by MC-LR.

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