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Embryogenesis is one of the most important life stages because it determines an organism’s healthy growth. However, embryos of externally fertilizing species, such as most fish, are directly exposed to the environment during development and may be threatened by DNA damaging factors (pollutants, UV, reactive oxygen species). To counteract the negative effects of DNA fragmentation, fish embryos evolved complex damage response pathways. DNA repair pathways have been extensively studied in some fish species, such as zebrafish (Danio rerio). Our literature review, on the other hand, revealed a paucity of knowledge about DNA damage response and repair in non-model aquaculture fish species. Further, several pieces of evidence underlie the additional role of DNA repair genes and proteins in organogenesis, spatiotemporal localization in different tissue, and its indispensability for normal embryo development. In this review, we will summarize features of different DNA repair pathways in course of fish embryo development. We describe how the expression of DNA repair genes and proteins is regulated during development, their organogenetic roles, and how the expression of DNA repair genes changes in response to genotoxic stress. This will aid in addressing the link between genotoxic stress and embryo phenotype. Furthermore, available data indicate that embryos can repair damaged DNA, but the effects of early-life stress may manifest later in life as behavioral changes, neoplasia, or neurodegeneration. Overall, we conclude that more research on DNA repair in fish embryos is needed.

The present study aimed to evaluate cryo-injury during the cryopreservation process in sterlet (Acipenser ruthenus) sperm, focusing on ultrastructural characteristics. Post-thaw sperm quality parameters, including total motility rate, curvilinear velocity (VCL), linearity (LIN), plasma membrane integrity, antioxidant status, DNA damage, and fine ultrastructure were examined on fresh and cryopreserved sperm with/without addition of a single optimal dose of AFPI (10 μg/mL). A lower motility rate, VCL and plasma membrane integrity, and increased DNA damage (p < 0.05) were observed in frozen-thawed spermatozoa with/without AFPI compared to fresh spermatozoa. The morphology and ultrastructure of spermatozoa were affected during the cryopreservation process with/without supplementation of AFPI. Morphological abnormalities were observed in mitochondria (49–54%) and flagellum (55–57%) of cryopreserved spermatozoa with/without AFPI compared to fresh spermatozoa. In conclusion, the morphology and ultrastructure of spermatozoa were slightly changed after cryopreservation of sterlet spermatozoa with/without 10 μg/mL AFPI.

DNA damage during early life stages may have a negative effect on embryo development, inducing mortality and malformations that have long-lasting effects during adult life. Therefore, in the current study, we analyzed the effect of DNA damage induced by genotoxicants (camptothecin (CPT) and olaparib) at different stages of embryo development. The survival, DNA fragmentation, transcriptome, and proteome of the endangered sturgeon Acipenser ruthenus were analyzed. Sturgeons are non-model fish species that can provide new insights into the DNA damage response and embryo development. The transcriptomic and proteomic patterns changed significantly after exposure to genotoxicants in a stage-dependent manner. The results of this study indicate a correlation between phenotype formation and changes in transcriptomic and proteomic profiles. CPT and olaparib downregulated oxidative phosphorylation and metabolic pathways, and upregulated pathways involved in nucleotide excision repair, base excision repair, and homologous recombination. We observed the upregulated expression of zona pellucida sperm-binding proteins in all treatment groups, as well as the upregulation of several glycolytic enzymes. The analysis of gene expression revealed several markers of DNA damage response and adaptive stress response, which could be applied in toxicological studies on fish embryos. This study is the first complex analysis of the DNA damage response in endangered sturgeons.

DNA damage caused by exogenous or endogenous factors is a common challenge for developing fish embryos. DNA damage repair (DDR) pathways help organisms minimize adverse effects of DNA alterations. In terms of DNA repair mechanisms, sturgeons represent a particularly interesting model due to their exceptional genome plasticity. Sterlet (Acipenser ruthenus) is a relatively small species of sturgeon. The goal of this study was to assess the sensitivity of sterlet embryos to model genotoxicants (camptothecin, etoposide, and benzo[a]pyrene), and to assess DDR responses. We assessed the effects of genotoxicants on embryo survival, hatching rate, DNA fragmentation, gene expression, and phosphorylation of H2AX and ATM kinase. Exposure of sterlet embryos to 1 µM benzo[a]pyrene induced low levels of DNA damage accompanied by ATM phosphorylation and xpc gene expression. Conversely, 20 µM etoposide exposure induced DNA damage without activation of known DDR pathways. Effects of 10 nM camptothecin on embryo development were stage-specific, with early stages, before gastrulation, being most sensitive. Overall, this study provides foundational information for future investigation of sterlet DDR pathways.