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Aims: Dysfunction of the Hippo-Yes-Associated Protein (YAP) signaling pathway is known to be associated with hepatocellular carcinoma (HCC). Evodiamine (Evo), a plant-derived bioactive alkaloid, exerts inhibitory effects on cancer. However, the precise influence of Evo on HCC and its potential effects on Hippo-YAP signaling have yet to be ascertained. Here, the effects of Evo on cell proliferation and apoptosis were evaluated using HCC cell lines (HepG2 and Bel-7402) and nude mice with xenograft tumors. We further investigated whether Evo exerts anti-HCC activity through effects on Hippo-YAP signaling in vitro with the aid of XMU-MP-1, an inhibitor of the key component of this pathway, mammalian sterile 20-like kinase 1/2., Main Methods: Cell proliferation and apoptosis were assessed using 5-ethynyl-2'-deoxyuridine staining, colony formation, flow cytometry, hematoxylin-eosin and dUTP nick-end labeling experiments. Bioinformatics and real-time quantitative polymerase chain reaction (RT-qPCR) arrays were performed to determine the associations among Evo, HCC progression and the Hippo-YAP pathway. The expression patterns of components of Hippo-YAP signaling and apoptotic genes were further examined via RT-qPCR and immunoblotting., Key Findings: Evo inhibited proliferation and promoted apoptosis of HCC cell lines in vitro, and attenuated xenograft tumor formation in nude mice in vivo. Mechanistically, Evo treatment stimulated the Hippo-YAP signaling pathway. In vitro, the effects of Evo on HCC cell proliferation and apoptosis were alleviated by XMU-MP-1., Significance: Our collective results revealed that the anti-HCC effects of Evo were correlated with the Hippo-YAP signaling pathway., Competing Interests: Declaration of competing interest All authors declare that there are no conflicts of interest., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Oxidative stress, as mediated by ROS (reactive oxygen species), is a significant factor in initiating the cells damaged by affecting cellular macromolecules and impairing their biological functions; SelX, a selenoprotein also known as MsrB1 belonging to the methionine sulfoxide reductase (Msr) family, is the redox repairing enzyme and involved in redox-related functions. In order to more precisely analyze the relationship between oxidative stress, cell oxidative damage, and SelX, we stably overexpressed porcine Selx full-length cDNA in human normal hepatocyte (LO2) cells. Cell viability, cell apoptosis rate, intracellular ROS, and the expression levels of mRNA or protein of apoptosis-related genes under H 2 O 2 -induced oxidative stress were detected. We found that overexpression of SelX can prevent the oxidative damage caused by H 2 O 2 and propose that the main mechanism underlying the protective effects of SelX is the inhibition of LO2 cell apoptosis. The results revealed that overexpressed SelX reduced the H 2 O 2 -induced intracellular ROS generation, inhibited the H 2 O 2 -induced upregulation of Bax and downregulation of Bcl-2, and increased the mRNA and protein ratio of Bcl-2/Bax. Furthermore, it inhibited H 2 O 2 -induced p38 MAPK phosphorylation. Taken together, our findings suggested that SelX played important roles in protecting LO2 cells against oxidative damage and that its protective effect is partly via the p38 pathway by acting as a ROS scavenger.

Naringenin, a flavanone mainly derived from grapes and citrus fruits, has been reported to exhibit cardioprotective effects. Accumulating evidence has confirmed that endoplasmic reticulum (ER) stress-mediated apoptosis participates in the process of myocardial ischemia/reperfusion injury and inhibiting ER stress is a potential therapeutic target/strategy in preventing cardiovascular diseases. Herein, the current study was designed to investigate whether naringenin protects H9c2 myocardial cells against hypoxia/reoxygenation (H/R) injury via attenuating ER stress or ER stress-mediated apoptosis. Our results showed that naringenin treatment resulted in obvious increases in the viability of H9c2 cells and the expression of Bcl-2 (anti-apoptotic protein), and decreases in the morphological changes of apoptotic cells, the activity of caspase-3 and the expression of Bax (pro-apoptotic protein) in H/R-treated H9c2 cells, implying the protective effects of naringenin against H/R-induced injury. In addition, naringenin also significantly reversed H/R-induced ER stress as evidenced by the up-regulation of Glucose-regulated protein 78, C/EBP homologous protein and Cleaved caspase-12 proteins. Meanwhile, naringenin remarkably reversed H/R-induced the increases in the expression of cleaved activating transcription factor 6 (ATF6) and phosphorylation levels of phospho-extracellular regulated protein kinases (PERK) and inositol-requiring enzyme-1α (IRE1α) in H9c2 cells. Finally, we found that ATF6 siRNA, PERK siRNA or IRE1α siRNA abolished H/R-induced cytotoxicity and apoptosis in H9c2 cells. In conclusion, these results confirmed that ER stress-mediated apoptosis contributes to the protection effects of naringenin against H/R injury, which is potentially involved in ATF6, IRE1α and PERK signaling activation.

To study the effect of ginseng saponin Rh₂ in inducing apoptosis of human leukemia K562 cells, and explore its mechanism from the aspect of autophagy pathway. CCK-8 assay was used to examine the growth inhibition of human leukemia cell lines K562 treated with ginsenoside Rh₂; flow cytometry (FCM) was used to detect cell apoptosis; Hoechst staining was used to observe the changes of cell morphological apoptosis; Acridine and MDC staining were used to detect the effects of the Rh₂ on autophagy; Western blot and RT-PCR were used to detect the expression levels of the proteins closely associated with autophagy and apoptosis. In order to study the effect of autophagy in proliferation and apoptosis, we used the autophagy inhibitor (3-MA).CCK-8 indicated that Rh₂ at low concentration could effectively inhibit the proliferation of leukemia cellsin dose- and time-dependent manners in K562 cells; FCM indicated that Rh₂ induced apoptosis; Hoechest staining showed that K562 cells had typical apoptotic morphological changes by treated Rh₂; Acridine and MDC staining showed that Rh₂ enhanced the green fluorescence and a large number of acidic autophagy vesicles were present; Western blot and RT-PCR results showed that Rh₂ increased the expression levels of Beclin-1, LC3A, LC3B, activated Caspase-3 and p-p38 in K562 cells; application of autophagy inhibitors(3-MA) could weaken the inhibition effect of Rh₂ on proliferation and induction effect on apoptosis in K562 cells. Ginsenoside Rh₂ inhibited the proliferation and induced apoptosis probably through activating p-p38, and inducing cell autophagy signaling pathway in K562 cells., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Chinese Pharmaceutical Association.)

Aim: To investigate the in vitro and in vivo activities and related mechanism of apogossypolone (ApoG2) alone or in combination with adriamycin (ADM) against human hepatocellular carcinoma (HCC)., Methods: The IC50 of ApoG2 in vitro was tested by WST assay, and the synergistic effect was analyzed using the CalcuSyn method. Cell apoptosis was determined using 4',6-diamidino-2- phenylindole staining and flow cytometric analysis. Western blotting was used to determine the expression of apoptosis-related proteins. In vivo activity was evaluated in the xenograft model in nude mice, and apoptosis in tumor tissues was determined by terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP nick-end labeling (TUNEL) assay., Results: The IC50 of ApoG2 in HCC cells was 17.28-30.63 micromol/L. When ApoG2 was combined with ADM, increased cytotoxicity and apoptosis were observed in SMMC-7721 cells compared to treatment with ApoG2 alone. The Western blotting results indicated that the ApoG2 induced apoptosis in SMMC-7721 cells by downregulating anti-apoptotic proteins Bcl-2, Mcl-1, and Bcl-XL, up-regulating pro-apoptotic protein Noxa, and promoting the activities of caspases-9 and -3. The tumor growth of xenograft SMMC-7721 was inhibited in nude mice when ApoG2 was administered orally without causing damage to the normal tissues. The in vivo study also indicated an increasing anti-tumoral effect when ApoG2 at 100 or 200 mg/kg dosages were used together with ADM at 5.5 mg/kg, with relative tumor proliferation rate (T/C) values of 0.456 and 0.323, respectively. Apoptosis induced in vivo by ApoG2 alone or combined with ADM was confirmed by TUNEL assay in tumor tissues., Conclusion: ApoG2 is a potential non-toxic target agent that induces apoptosis by upregulating Noxa, while inhibiting anti-apoptotic proteins and promoting the effect of chemotherapy agent ADM in HCC.

Objective: To investigate the effects of telmisartan on endoplasm reticulum (ER) stress signal pathways and cardiomyocyte apoptosis in abdominal aortic banded rats., Methods: Male SD rats were randomly divided into sham-operated group, abdominal aortic banding group (AAB) and AAB + telmisartan (5 mgxkg(-1)xd(-1) per gavage, beginning at 1 week before AAB for 8 weeks, n = 10 each). Ten weeks post AAB, hemodynamic measurements were performed, whole heart and left ventricular weights were obtained, cardiomyocyte apoptosis was measured by TUNEL method. Myocardial GRP78 and CHOP protein expressions were detected by Western blot and immunohistochemistry., Results: The ratio of left ventricular weight to body weight, the ratio of heart weight to body weight, left ventricular end diastolic pressure and the apoptosis index were significantly increased while left ventricular end systolic pressure and +/- dp/dt(max) were significantly decreased in AAB group than those in sham-operated group (all P < 0.01), these changes could be significantly attenuated by telmisartan (all P < 0.01). Moreover, myocardial GRP78 and CHOP expressions were significantly upregulated in AAB group than those in sham-operated group and telmisartan could significantly downregulate the increased GRP78, CHOP expressions (all P < 0.01)., Conclusions: Increased ER stress might be responsible for enhanced cardiomyocyte apoptosis in AAB rats. Telmisartan effectively attenuated the cardiomyocyte apoptosis and cardiac hypertrophy in AAB rats possibly through reducing ER stress.

The physiological response of symbiotic Symbiodiniaceae to high temperature is believed to result in coral bleaching. However, the potential effect of nitrogen availability on heat acclimatization of symbiotic Symbiodiniaceae is still unclear. In this study, physiological responses of Symbiodiniaceae Cladocopium goreaui to temperature and nitrogen nutrient stress conditions were investigated. Nitrogen deficiency caused significant declines in cell concentration and chlorophyll content per cell, but significant increases in nitric oxide synthase activity, caspase3 activation level, and cellular carbon content of C. goreaui at normal temperature. Algal cells under high temperature and nitrogen deficiency showed significant rises in Fv/Fm, catalase activity, and caspase3 activation level, but no significant changes in cell yield, cell size, chlorophyll content, superoxide dismutase, nitric oxide synthase activity, and cellular contents of nitrogen and carbon, in comparison with those under normal temperature and nitrogen deficiency. Growth, chlorophyll, and nitrogen contents of algal cells under the high temperature and nitrogen‐replete conditions were significantly higher than those under high temperature or nitrogen deficiency alone, whereas nitric oxide synthase activity, superoxide dismutase activity, catalase activity, carbon content, and caspase3 activation level exhibited opposite trends of variation. Transcriptomic and network analyses revealed ion transport and metabolic processes mainly involved in regulating these physiological activities under different temperature and nitrogen nutrient. The totality of results shows that high temperature activates stress responses, induces antioxidant capacity of apoptosis, and limits the growth rate of C. goreaui. Adequate nitrogen nutrient can improve the resilience of this Symbiodiniaceae against heat stress through repressed apoptosis, promoted ion transport, and optimized metabolism. [ABSTRACT FROM AUTHOR]

Background/Aims: Cerebral ischemia-reperfusion (I/R) injury involves multiple independently fatal terminal pathways. CK2α/NADPH oxidase is an important signaling pathway associated with ischemia-reperfusion injury, and miR-125b can regulate oxidative stress-related injury. In this study, we investigated whether the effect of miR-125b in rat brain I/R injury occurs through its modulation of the CK2α/NADPH oxidase pathway. Methods: Rats were subjected to 2 h of cerebral ischemia followed by 24 h of reperfusion to establish an I/R injury model. Neurological deficit was evaluated using a five-point score. Infarct volume was evaluated with 2, 3, 5-triphenyltetrazolium chloride (TTC) staining, and RT-PCR was used to detect expressions of miR125b and CK2α. We then examined the association between miR-125b expression and the CK2α/NADPH oxidative signaling pathway in a PC-12 cell oxygen-glucose deprivation and reoxygenation (OGD/R) injury model. Transfection with miR-125b mimics, an miR-125b inhibitor, and luciferase reporter gene plasmid was accomplished using commercial kits. In these cells, Western blots were used to detect the levels of expression of CK2α, cleaved caspase-3, NOX2, and NOX4. RT-PCR was used to detect the expressions of CK2α, miR125b, NOX2, and NOX4. We evaluated Lactate Dehydrogenase (LDH) level, NADPH oxidase activity, and caspase-3 activity using commercial kits. Mitochondrial reactive oxygen species (ROS) were measured by fluorescence microscopy. For both PC-12 cells and rat brains, histological analyses were conducted to observe morphological changes, and apoptosis was measured using a commercial kit. Results: I/R rats exhibited an increase in neurological deficit score, infarct volume, and cellular apoptosis, along with miR-125b elevation and CK2α downregulation. OGD/R treatment increased PC-12 cells’ injuries, cellular apoptosis, and ROS levels. These changes were associated with miR-125b elevation, CK2α downregulation and activations of NOX2 and NOX4, mimicking our in vivo findings. All of these effects were reversed by the inhibition of miR-125b, confirming a strong correlation between miR-125b activity and the CK2α/NADPH oxidase signaling pathway. Conclusions: Based on these observations, we conclude that inhibition of miR-125b protects the rat brain from I/R injury by regulating the CK2α/NADPH oxidative signaling pathway. [ABSTRACT FROM AUTHOR]

The survival of corals worldwide has been seriously threatened by eutrophication events concomitant with the increase in ocean pollution. In the present study, whole transcriptomes of the stony coral Pocillopora damicornis exposed to elevated ammonium were sequenced. A total of 121,366,983 pair-end reads were obtained, and 209,337 genes were assembled, including 42,399 coral-derived and 54,874 zooxanthella-derived genes. Further, a comparison of the control versus stress group revealed 6572 differentially expressed genes. For 1015 significantly upregulated genes, 24 GO terms were overrepresented, among which 3 terms related to apoptosis and cell death induction included one caspase, five bcl-2-like proteins, and two tumor necrosis factor receptor superfamily member genes. For 5557 significantly downregulated genes, the top 10 overrepresented terms were related to metabolism and signal transduction. These results indicate that apoptosis and cell death could be induced under elevated ammonium, suggesting that metabolic regulation and signal transduction might be involved in the reconstruction of the coral–zooxanthellae symbiotic balance in the stony coral P. damicornis . [ABSTRACT FROM AUTHOR]

Polycyclic aromatic hydrocarbons (PAHs) are highly toxic environmental pollutants and are threatening scleractinian corals. In this study, PAHs treatment did not induce significant physiological responses of the coral Pocillopora damicornis and its algal symbionts, but biological processes including response to toxin, drug metabolic, and oxidation reduction were triggered at the mRNA level. These results implied that PAHs could be a group of slow-acting environmental toxicants, whose effects were moderate but persistent. Besides, it was interesting to find that PAHs activated the neuroendocrine system in the coral by triggering the expression of monoaminergic and acetylcholinergic system related genes, indicating that PAHs might function as environmental hormones. Moreover, the combined treatments of PAHs and heat caused a much obvious effect on the coral and its algal symbionts by elevating antioxidant activity and suppressing photosynthesis in the symbionts. Results from the transcriptome data further indicated that corals might perform stress responses upon PAHs and heat challenges through the TNF and apoptosis pathways, which perhaps was modulated by the neuroendocrine system of corals. Collectively, our survey demonstrates that the PAHs can function as environmental hormones and activate the neuroendocrine regulation in scleractinian corals, which may contribute to the stress responses of symbiotic association by modulating photosynthesis, antioxidation, and apoptosis. [Display omitted] • PAHs imposed a long-term impact on the scleractinian coral and its symbionts. • PAHs activated the neuroendocrine regulation of the coral. • PAHs + heat treatment elevated symbiont antioxidation and suppressed photosynthesis. • PAHs + heat treatment inhibited meiotic process in the coral. • The coral responded to PAHs and heat challenges under neuroendocrine modulation. [ABSTRACT FROM AUTHOR]

Oxidative stress plays a critical role in normal functioning of cardiac and vascular cells as well as in the pathogenesis of cardiovascular disease. Growth arrest and DNA damage-inducible gene 153 (GADD153), which is upregulated by oxidative stress, regulates the cell cycle and apoptosis. Previously an AP-1 was reported to contribute significantly to GADD153 gene transcriptional activation by oxidative stress. Recently, we have reported that GADD153 gene promoter activity is negatively regulated by nuclear factor 1 (NF1), in vascular smooth muscle cells (VSMCs). The aim of this study was to elucidate the roles of AP-1 and NF1 in GADD153 gene induction by oxidative stress in VSMCs. H2O2 induced GADD153 mRNA and reduced NF1 mRNA expression. In the electromobility shift assay, H2O2 induced AP-1-binding activity and reduced NF1-binding activity. Overexpression of NF1 significantly suppressed the induction of the GADD153 gene after treatment with H2O2. These results revealed that induction of the GADD153 gene by oxidative stress is regulated mainly by two nuclear factors, NF1 and AP-1. [Copyright &y& Elsevier]

Homoharringtonine (HHT), an approved anti-leukemic alkaloid, has been reported effectively in many types of tumor cells. However, its effect on melanoma cells has not been investigated. And the anti-melanoma mechanism of HHT is still unknown. In this study, we detected the effects of HHT on two melanoma cell lines (A375 and B16F10) and on the A375 xenograft mouse model. HHT significantly inhibited the proliferation of melanoma cells as investigated by the CCK8 method, cell cloning assay, and EdU experiment. HHT induced A375 and B16F10 cells DNA damage, apoptosis, and G2/M cell cycle arrest as proved by TdT-mediated dUTP Nick-End Labeling (TUNEL) and flow cytometry assay. Additionally, the loss of mitochondrial membrane potential in HHT-treated cells were visualized by JC-1 fluorescent staining. For the molecule mechanism study, western blotting results indicated the protein expression levels of ATM, P53, p-P53, p -CHK2, γ-H2AX, PARP, cleaved-PARP, cleaved caspase-3, cleaved caspase-9, Bcl-2, Bax, Aurka, p -Aurka, Plk1, p -Plk1, Cdc25c, CDK1, cyclin B1, and Myt1 were regulated by HHT. And the relative mRNA expression level of Aurka, Plk1, Cdc25c, CDK1, cyclin B1, and Myt1 were ascertained by q-PCR assay. The results in vivo experiment showed that HHT can slow down the growth rate of tumors. At the same time, the protein expression levels in vivo were consistent with that in vitro. Collectively, our study provided evidence that HHT could be considered an effective anti-melanoma agent by inducing DNA damage, apoptosis, and cell cycle arrest. [ABSTRACT FROM AUTHOR]

Microplastics are emerging contaminants and widespread in the ocean, but their impacts on coral reef ecosystems are poorly understood, and in situ study is still lacking. In the present study, the distribution patterns of microplastics in the environment and inhabiting organisms were investigated along the east coast of Hainan Island, South China Sea, and the physiological impacts of the microplastics on scleractinian corals were analyzed. We documented average microplastic concentrations of 14.90 particles L−1 in seawater, 343.04 particles kg−1 in sediment, 4.97 particles cm−2 in corals, and 0.67–3.12 particles cm−1 in Tridacnidae, Trochidae and fish intestines. Further analysis revealed that the characteristics of microplastics in the organisms were different from those in the environment, indicating preferential enrichment in the organisms. Furthermore, there was an obvious correlation between microplastic concentration and symbiotic density in corals. Furthermore, caspase3 activity was significantly positively correlated with the microplastic content in the small-polyp coral Pocillopora damicornis , but the large-polyp coral Galaxea fascicularis showed higher tolerance to microplastics. Taken together, our results suggest that microplastics are selectively enriched in corals and other reef-dwellers, in which they exact differential stress (apoptotic) effects, with the potential to impact the coral-Symbiodiniaceae symbiosis and alter the coral community structure. ga1 • Microplastics distributed in the environment in the coral reefs around Hainan Island. • Scleractinian corals and other reef-dwellers ingested preferential microplastics. • Caspase3 activity of small-polyp coral was positively affected by microplastic content. • Large-polyp coral showed higher tolerance to microplastics. [ABSTRACT FROM AUTHOR]

Heavy metals have become one of the main pollutants in the marine environment and a major threat to the growth and reproduction of stony corals. In the present study, the density of symbiotic zooxanthellae, levels of crucial physiological activities and the transcriptome were investigated in the stony coral Pocillopora damicornis after the acute exposure to elevated cadmium concentration. The density of symbiotic zooxanthellae decreased significantly during 12–24 h period, and reached lowest at 24 h after acute cadmium stress. No significant changes were observed in the activity of glutathione S-transferase during the entire stress exposure. The activities of superoxide dismutase and catalase, and the concentration of glutathione decreased significantly, but the activation level of caspase3 increased significantly after cadmium exposure. Furthermore, transcriptome sequencing and bioinformatics analysis revealed 3538 significantly upregulated genes and 8048 significantly downregulated genes at 12 h after the treatment. There were 12 overrepresented GO terms for significantly upregulated genes, mostly related to unfolded protein response, endoplasmic reticulum stress and apoptosis. In addition, a total of 32 GO terms were overrepresented for significantly downregulated genes, and mainly correlated with macromolecular metabolic processes. These results collectively suggest that acute cadmium stress could induce apoptosis by repressing the production of the antioxidants, elevating oxidative stress and activating the unfolded protein response. This cascade of reactions would result to the collapse of the coral-zooxanthella symbiosis and the expulsion of symbiotic zooxanthellae in the stony coral P. damicornis , ultimately leading to coral bleaching. [ABSTRACT FROM AUTHOR]

Apoptosis is orchestrated by a family of cysteine proteases known as the caspases, and caspase3 is the primary executioner caspase in the apoptosis. In the present study, the potential role of caspase3 was investigated under the exposure to high temperature and elevated ammonium in stony coral Pocillopora damicornis . The cDNA of a caspase3 (PdCaspase3) was identified to encode a polypeptide of 344 amino acids, and the encoded protein contained one CASc domain (Caspase, interleukin-1 beta converting enzyme homologues, from Val76 to Asn333). The recombinant protein of the mature PdCaspase3 was expressed in Escherichia coli BL21 (DE3)-Transetta, and it displayed caspase3-like activity which catalyzed the reaction of DEVD-p-nitroanilide cleavage. The expression level of PdCaspase3 mRNA increased significantly at 24 h after acute heat stress and 12 h after acute ammonium stress, reached 2.28-fold ( P < 0.05) and 1.76-fold ( P < 0.05) of that in the blank group, respectively. The activation level of caspase3 began to increase at 12 h (1.41-fold, P < 0.05), and reached the peak at 24 h (1.54-fold, P < 0.05) after acute heat stress. Furthermore, the activation level of caspase3 increased significantly during 6–24 h, with the highest level at 24 h (1.44-fold, P < 0.05) after acute ammonium stress. These results collectively suggested that PdCaspase3, as a homologue of caspase3, was involved in the response to high temperature and elevated ammonium, which might further regulate the symbiosis between the host and zooxanthellae in the stony coral P. damicornis . [ABSTRACT FROM AUTHOR]

Microplastics are widespread emerging marine pollutants that have been found in the coral reef ecosystem. In the present study, using Cladocopium goreaui as a symbiont representative, we investigated cytological, physiological, and molecular responses of a Symbiodiniaceae species to weeklong microplastic exposure (Polystyrene, diameter 1.0 μm, 9.0 × 109 particles L−1). The density and size of algal cells decreased significantly at 7 d and 6–7 d of microplastic exposure, respectively. Chlorophyll a content increased significantly at 7 d of exposure, whereas Fv/Fm did not change significantly during the entire exposure period. We observed significant increases in superoxide dismutase activity and caspase3 activation level, significant decrease in glutathione S-transferase activity, but no change in catalase activity during the whole exposure period. Transcriptomic analysis revealed 191 significantly upregulated and 71 significantly downregulated genes at 7 d after microplastic exposure. Fifteen GO terms were overrepresented for these significantly upregulated genes, which were grouped into four categories including transmembrane ion transport, substrate-specific transmembrane transporter activity, calcium ion binding, and calcium-dependent cysteine-type endopeptidase activity. Thirteen of the significantly upregulated genes encode metal ion transporter and ammonium transporter, and five light-harvesting protein genes were among the significantly downregulated genes. These results demonstrate that microplastics can act as an exogenous stressor, suppress detoxification activity, nutrient uptake, and photosynthesis, elevate oxidative stress, and raise the apoptosis level through upregulating ion transport and apoptotic enzymes to repress the growth of C. goreaui. These effects have implications in negative impacts of microplastics on coral-Symbiodiniaceae symbiosis that involves C. goreaui. Image 1 • The growth and density of algal cells were repressed by microplastic exposure. • Microplastics declined detoxification activity, nutrient uptake, and photosynthesis. • Microplastics raised oxidative stress, apoptosis level and ion transport. [ABSTRACT FROM AUTHOR]