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Microcystin-LR (MCLR) produced by cyanobacterial blooms have received global attention. MCLR has been recognized as a reproductive toxin to fish and poses a threat to ecosystem stability. It has been proven that probiotic dietary management can improve reproductive performance of fish. It is worth paying attention to exploring whether probiotic management can alleviate the reproductive toxicity caused by MCLR. In this investigation, adult zebrafish were exposed to different doses of MCLR solution (0, 2.2, and 22 μg/L) with or without the Lactobacillus rhamnosus GG supplementation for a duration of 28 days. The results showed that female zebrafish spawning was reduced after exposure to MCLR, but this reduction was reversed when L. rhamnosus GG was added. To elucidate how L. rhamnosus GG mitigates reproductive toxicity caused by MCLR, we examined a series of indicators of MCLR accumulation, ovarian histology, hormones, and transcriptome levels. Our study showed that L. rhamnosus GG could alleviate oogenesis disorders and ultimately attenuate MCLR-induced reproductive toxicity by reducing MCLR accumulation in the gonads, modulating the expression of endocrine system and auto/paracrine factors. The transcriptome results revealed that single or combined exposure of MCLR and L. rhamnosus GG mainly affected the endocrine system, energy metabolism, and RNA degradation and translation. Overall, our results provide new insights for alleviating MCLR-induced reproductive toxicity and help promote healthy aquaculture., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Cyanobacteria (blue-green algae) have been present on Earth for over 2 billion years, and can produce a variety of bioactive molecules, such as cyanotoxins. Microcystins (MCs), the most frequently detected cyanotoxins, pose a threat to the aquatic environment and to human health. The classic toxic mechanism of MCs is the inhibition of the protein phosphatases 1 and 2A (PP1 and PP2A). Immunity is known as one of the most important physiological functions in the neuroendocrine-immune network to prevent infections and maintain internal homoeostasis in fish. The present review aimed to summarize existing papers, elaborate on the MC-induced immunotoxicity in fish, and put forward some suggestions for future research. The immunomodulatory effects of MCs in fish depend on the exposure concentrations, doses, time, and routes of exposure. Previous field and laboratory studies provided strong evidence of the associations between MC-induced immunotoxicity and fish death. In our review, we summarized that the immunotoxicity of MCs is primarily characterized by the inhibition of PP1 and PP2A, oxidative stress, immune cell damage, and inflammation, as well as apoptosis. The advances in fish immunoreaction upon encountering MCs will benefit the monitoring and prediction of fish health, helping to achieve an ecotoxicological goal and to ensure the sustainability of species. Future studies concerning MC-induced immunotoxicity should focus on adaptive immunity, the hormesis phenomenon and the synergistic effects of aquatic microbial pathogens.

The combined toxicity effects of microcystins-LR (MCLR) and polystyrene nanoplastics (PSNPs) on the hatching of F1 zebrafish (Danio rerio) embryos were investigated in this study due to the increasing concerns of both plastic pollution and eutrophication in aquatic environments. Three-month-old zebrafish were used to explore the molecular mechanisms underlying the combined effect of MCLR (0, 0.9, 4.5, and 22.5 μg/L) on egg hatching in the existence of PSNPs (100 μg/L). The results demonstrated the existence of PSNPs further increased the accumulation of MCLR in F1 embryos. The hatching rates of F1 embryos were inhibited after exposure to 22.5 μg/L MCLR, and the presence of PSNPs aggravated the hatching inhibition induced by MCLR. The decrease of hatching enzyme activity and the abnormality of spontaneous movement were observed. We examined the altered expression levels of the genes associated with the hatching enzyme (tox16, foxp1, ctslb, xpb1, klf4, cap1, bmp4, cd63, He1.2, zhe1, and prl), cholinergic system (ache and chrnα7), and muscle development (Wnt, MyoD, Myf5, Myogenin, and MRF4). The results suggested the existence of PSNPs exacerbated the hatching inhibition of F1 embryos through decreasing the activity of enzyme, interfering with the cholinergic system, and affecting the muscle development., Competing Interests: Declaration of competing interest The authors do not have conflict of interest to declare., (Copyright © 2021. Published by Elsevier B.V.)

The coexistence of nanoplastics (NPs) and various pollutants in the environment has become a problem that cannot be ignored. In order to identify the microcystin-LR (MCLR) bioaccumulation and the potential impacts on the early growth of F1 zebrafish (Danio rerio) offspring in the presence of polystyrene nanoplastics (PSNPs), PSNPs and MCLR were used to expose adult zebrafish for 21days. The exposure groups divided into MCLR (0, 0.9, 4.5 and 22.5μgL -1 ) alone groups and PSNP (100μgL -1 ) and MCLR co-exposure groups. F1 embryos were collected and developed to 120 h post-fertilization (hpf) in clear water. Compared with the exposure to MCLR only, the combined exposure increased the parental transfer of MCLR to the offspring and subsequently exacerbated the growth inhibition of F1 larvae. Further research clarified that combined exposure of PSNPs and MCLR could reduce the levels of thyroxine (T4) and 3, 5, 3'-triiodothyronine (T3) by altering the expression of hypothalamus-pituitary-thyroid (HPT) axis-related genes, eventually leading to growth inhibition of F1 larvae. Our results also exhibited combined exposure of PSNPs and MCLR could change the transcription of key genes of the GH/IGF axis compared with MCLR single exposure, suggesting the GH/IGF axis was a potential target for the growth inhibition of F1 larvae in PSNPs and MCLR co-exposure groups. The present study highlights the potential risks of coexistence of MCLR and PSNPs on development of fish offspring, and the environmental risks to aquatic ecosystems., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Owing to the eutrophication in freshwater and industrial emissions, the detected concentrations of MCLR and nano-TiO 2 in nature water increase year by year. The purpose of this study was to evaluate the joint effect of microcystin-LR (MCLR) and titanium dioxide nanoparticles (nano-TiO 2 ) on the zebrafish brain and to investigate the underlying mechanisms. In this study, four-month old zebrafish were exposed to 0, 0.5, 4, and 32 μg/L MCLR and MCLR-co-nano-TiO 2 (100 μg/L) for 45 days. Obvious brain injury characterized by formation of glial scars and ventriculomegaly was observed in both MCLR groups and MCLR-co-nano-TiO 2 groups. In addition, our results showed the existence of nano-TiO 2 aggravated MCLR-induced abnormity of swimming behavior and social behavior of zebrafish. To clarify the mechanisms of nano-TiO 2 aggravated MCLR-induced brain injury, we firstly examined the reactive oxygen species (ROS) generation in the zebrafish brain. The results showed that co-exposure with nano-TiO 2 could further increase ROS content compared with MCLR only groups. We also detected a significant change of lipid peroxidation products (MDA, malondialdehyde) content, antioxidant enzyme (SOD, superoxide dismutase) activity, and non-enzymatic antioxidant (GSH, glutathione) content in MCLR-co-nano-TiO 2 groups. Transcriptional analysis indicated the expression of genes related to the antioxidant system was significantly altered in the zebrafish brain. Collectively, the observations in this study showed that the existence of nano-TiO 2 could exacerbate the damage of the zebrafish brain through the aggravation of MCLR-induced oxidative stress, ultimately leading to the abnormity of swimming behavior and social behavior., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Microcystin-LR (MCLR) has been reported to cause developmental neurotoxicity in zebrafish, but there are few studies on the mechanisms of MCLR-induced transgenerational effects of developmental neurotoxicity. In this study, zebrafish were exposed to 0, 1, 5, and 25 μg/L MCLR for 60 days. The F1 zebrafish embryos from the above-mentioned parents were collected and incubated in clean water for 120 h for hatching. After examining the parental zebrafish and F1 embryos, MCLR was detected in the gonad of adults and F1 embryos, indicating MCLR could potentially be transferred from parents to offspring. The larvae also showed a serious hypoactivity. The contents of dopamine, dihydroxyphenylacetic acid (DOPAC), serotonin, gamma-aminobutyric acid (GABA) and acetylcholine (ACh) were further detected, but only the first three neurotransmitters showed significant reduction in the 5 and 25 μg/L MCLR parental exposure groups. In addition, the acetylcholinesterase (AChE) activity was remarkably decreased in MCLR parental exposure groups, while the expression levels of manf, bdnf, ache, htr1ab, htr1b, htr2a, htr1aa, htr5a, DAT, TH1 and TH2 genes coincided with the decreased content of neurotransmitters (dopamine, DOPAC and serotonin) and the activity of AChE. Neuronal development related genes, α1-tubulin, syn2a, mbp, gfap, elavl3, shha and gap43 were also measured, but gap43 was the gene only up-regulated. Our results demonstrated MCLR could be transferred to offspring, and subsequently induce developmental neurotoxicity in F1 zebrafish larvae by disturbing the neurotransmitter systems and neuronal development., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Microcystin-LR is the most poisonous and commonly encountered hepatotoxin produced by cyanobacteria in an aquatic ecosystem, and it may cause thyroid dysfunction in fish. The present study aimed to reveal the effects of transgenerational toxicity of MCLR on the thyroid endocrine system under sub-chronic exposure conditions. Adult zebrafish (F0) were exposed to environmentally relevant concentrations (1, 5 and 25 μg/L) of MCLR for 45 days. The produced F1 embryos were then tested without further MCLR treatment. In the F0 generation, exposure to 25 μg/L MCLR reduced thyroxine (T4) but not 3, 5, 3'-triiodothyronine (T3) levels in females, while the T4 and T3 levels were unchanged in males. After parental exposure to MCLR, we observed a decreased hatching and growth retardation correlated with reduced thyroid hormone levels in the F1 offspring. The gene transcription and protein expression along the hypothalamic-pituitary-thyroid axis were detected to further investigate the possible mechanisms of MCLR-induced thyroid disruption. Our results indicated MCLR could disturb the thyroid endocrine system under environmentally relevant concentrations and the disrupting effects could be remarkably transmitted to its F1 offspring. We regard these adverse effects as a parental transgenerational toxicity of MCLR., (Copyright © 2017 Elsevier Ltd. All rights reserved.)