Antioxidant responses of triangle sail mussel Hyriopsis cumingii exposed to toxic Microcystis aeruginosa and thermal stress

Liu, Yimeng; Yang, Min; Zheng, Liang; Nguyen, Huong Minh; Ni, Liangping; Song, Shanshan; Sui, Yanming

doi:10.1016/j.scitotenv.2020.140754

Cited by 25 publications

(15 citation statements)

References 72 publications

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“…Crustacea, for instance, have survival rates of 100%, even for exposures to concentrations of cyanotoxins like those in bloom episodes [ 30 , 128 ]. Long-term macroinvertebrates exposure to cyanotoxins via feeding may involve bioaccumulation levels higher than cell-free or dissolved exposures, which suggests that different absorption and metabolization pathways likely exist [ 30 , 122 , 129 ]. However, another fact is that the macroinvertebrates that cohabit with cyanobacteria or are long-term/chronically exposed to cyanotoxins show more tolerance to toxicity than those that have not been exposed [ 47 , 130 ].…”

Section: Resultsmentioning

confidence: 99%

Cyanobacteria and Macroinvertebrate Relationships in Freshwater Benthic Communities beyond Cytotoxicity

Ubero-Pascal,

Aboal

2024

Toxins

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Cyanobacteria are harmful algae that are monitored worldwide to prevent the effects of the toxins that they can produce. Most research efforts have focused on direct or indirect effects on human populations, with a view to gain easy accurate detection and quantification methods, mainly in planktic communities, but with increasing interest shown in benthos. However, cyanobacteria have played a fundamental role from the very beginning in both the development of our planet’s biodiversity and the construction of new habitats. These organisms have colonized almost every possible planktic or benthic environment on earth, including the most extreme ones, and display a vast number of adaptations. All this explains why they are the most important or the only phototrophs in some habitats. The negative effects of cyanotoxins on macroinvertebrates have been demonstrated, but usually under conditions that are far from natural, and on forms of exposure, toxin concentration, or composition. The cohabitation of cyanobacteria with most invertebrate groups is long-standing and has probably contributed to the development of detoxification means, which would explain the survival of some species inside cyanobacteria colonies. This review focuses on benthic cyanobacteria, their capacity to produce several types of toxins, and their relationships with benthic macroinvertebrates beyond toxicity.

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Section: Resultsmentioning

confidence: 99%

Cyanobacteria and Macroinvertebrate Relationships in Freshwater Benthic Communities beyond Cytotoxicity

Ubero-Pascal,

Aboal

2024

Toxins

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“…Therefore, we investigated the effect of acacetin on protein levels of reactive antioxidant enzymes in cardiomyocytes. Protein levels of SOD, an important antioxidant enzyme [ 26 ], were significantly decreased by H/R but increased with acacetin pretreatment ( Figure 2(a) ). In addition, the activities of MDA and LDH were reduced in acacetin pretreatment groups, indicating that cell injury was inhibited by acacetin pretreatment (Figures 2(b) and 2(c) ).…”

Section: Resultsmentioning

confidence: 99%

Acacetin Protects Myocardial Cells against Hypoxia-Reoxygenation Injury through Activation of Autophagy

Liu

Hong

et al. 2021

Journal of Immunology Research

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Ischemic heart disease is a leading cause of mortality and morbidity worldwide. We previously demonstrated that acacetin protects against myocardial ischemia reperfusion injury in rats, although the underlying mechanism remains to be elucidated. In the present study, we investigated the effects of acacetin on autophagy during hypoxia/reoxygenation (H/R) injury by exposing H9c2 myocardial cells to H/R with or without acacetin pretreatment during hypoxia. Our results show that acacetin significantly increased cell viability in a dose-dependent manner, enhanced antioxidant capacity, and suppressed protein apoptosis of rat cardiomyocytes H9c2 cells following H/R injury. In addition, lentiviral infection of H9c2 cardiomyocytes revealed that acacetin pretreatment significantly enhanced the fluorescence intensity of autophagy proteins Beclin 1, LC3-II, and p62. These results indicate that acacetin protected H9c2 cardiomyocytes from H/R damage by enhancing autophagy. Moreover, we found that application of acacetin increased activation of the PI3K/Akt signaling pathway, whereas cotreatment with the PI3K inhibitor LY294002 reversed the inhibition of apoptosis and autophagy induced by acacetin. In conclusion, acacetin mitigated H/R injury by promoting autophagy through activating the PI3K/Akt/mTOR signaling pathway.

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“…As noted above, oxidative stress exerts a significant effect on hepatocyte injury induced by D-GalN, the progression of liver injury was associated with the level of oxidative stress. As a result, MDA, the lipid peroxidation toxic product, is also an important biomarker of oxidative injury [ 24 , 25 ]. Hepatotoxic drugs or harmful substances usually increase the concentration of MDA in liver tissue, thereby influencing the activities of antioxidant enzymes [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

Protective effects of Schisandrin B against D-GalN-induced cell apoptosis in human hepatocyte (L02) cells via modulating Bcl-2 and Bax

et al. 2021

Bioengineered

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Schisandrin B is a dibenzocyclooctadiene derivative extracted fromSchisandra chinensis (Turcz.) Baill., that exhibits anti-oxidation, anti-inflammation, anti-tumor and hepatoprotective activities. To understand the hepatoprotective mechanism of schisandrin B, this study investigated the efficacy of schisandrin B on L02 cells after treatment with D-GalN. Following pretreatment with 40 μM schisandrin B, L02 cells were stimulated with 40 mM D-GalN. Cell viability, apoptosis, the expression levels of genes associated with apoptosis, and the intracellular oxidative stress indexes were measured. The viability of L02 cells was determined using MTT assay, and the Annexin V-FITC/PI assay kit was utilized for the assessment of apoptosis. The activities of GSH-Px and SOD, the level of MDA were assessed, separately, using relative detection kits. Moreover, RT-PCR as well as Western blot was applied to measure the mRNA and protein expression of Bax and Bcl-2. The results indicated that schisandrin B significantly prevented D-GalN-induced oxidative damage in L02 cells (P<0.05), decreased GSH-Px and SOD activities (P<0.05), increased MDA content (P<0.05). Furthermore, schisandrin B inhibited D-GalN-induced apoptosis in L02 cells (P<0.05), regulated the expression of Bax and Bcl-2 (P<0.05). The results indicated that schisandrin B decreased the D-GalN-induced intracellular oxidative stress indexes generation, and inhibited the down-regulation of Bcl-2 and up-regulation of Bax induced by D-GalN. In conclusion, schisandrin B was shown to exert protective effect against oxidative damage of L02 cells, which, in part, was achieved by regulating the mRNA and protein levels of Bax and Bcl-2.

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Antioxidant responses of triangle sail mussel Hyriopsis cumingii exposed to toxic Microcystis aeruginosa and thermal stress

Cited by 25 publications

References 72 publications

Cyanobacteria and Macroinvertebrate Relationships in Freshwater Benthic Communities beyond Cytotoxicity

Cyanobacteria and Macroinvertebrate Relationships in Freshwater Benthic Communities beyond Cytotoxicity

Acacetin Protects Myocardial Cells against Hypoxia-Reoxygenation Injury through Activation of Autophagy

Protective effects of Schisandrin B against D-GalN-induced cell apoptosis in human hepatocyte (L02) cells via modulating Bcl-2 and Bax

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