Fish embryo toxicity of cyanobacteria via mitochondria-mediated oxidative damage

In previous studies, cyanobacteria have been associated with embryonic toxicity, including teratogenic effects, though the underlying mechanism remains unclear. Here, we explored differential responses to Microcystis aeruginosa by endangered Sinocyclocheilus grahami and introduced Pseudorasbora parva from Lake Dianchi, China. We conducted fish embryo test under Microcystis aeruginosa exudates (MaE) exposure, and developmental responses, cell structure and metabolism were measured. We observed increased malformation, mortality rate and decreased fertilization, hatching rate and heartbeats in both fish species when exposed to MaE. Transmission electron microscopy revealed damage to brain cells of both species. Transcriptomics revealed that mitochondria were a MaE target in both species, with impairment occurring to respiratory enzyme complexes and oxidative stress enzymes. Oxidative stress induced by MaE was mainly associated with hydrogen peroxide, though the underlying mechanism differed: In Sinocyclocheilus grahami, hydrogen peroxide increased owing to its decreased degradation, whereas in Pseudorasbora parva, it increased owing to increased synthesis. All results were consistent in that the Sinocyclocheilus grahami was more vulnerable than Pseudorasbora parva to MaE exposure. Our work highlights that MaE may harm fish in species-specific ways and contribute to replacement of native by invasive species in Lake Dianchi.