Oxidative damage and apoptosis induced by microcystin-LR in the liver of Rana nigromaculata in vivo

Zhang, Hangjun; Cai, Chenchen; Fang, Wendi; Wang, Jia; Zhang, Yue; Liu, Jiayu; Jia, Xiao‐Bin

doi:10.1016/j.aquatox.2013.05.009

Cited by 49 publications

(27 citation statements)

References 46 publications

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“…16,61,62 in vivo studies have shown that MC-LR could induce severe oxidative damage and increase the protein expression of bax, Cyt-c, caspase-3, and caspase-9 to induce the apoptosis of frog liver. 63 In the present study, MC-LR was also found to induce a decrease in MMP, the release of Cyt-c from the mitochondria into the cytoplasm, and promote the activation of caspase-3 in co-cultured Sertoli-germ cells. However, the MMP was recovered to a large extent, and the release of Cyt-c was strongly inhibited after pretreatment with PFT-α, indicating that MC-LR can impair mitochondrial function, and p53-dependent pathways are also involved in this process.…”

Section: Effect Of Pft-α On the Expression Of Apoptosisrelated Protsupporting

confidence: 64%

“…Studies have found that MC‐LR could increase the content of Cyt‐c, ROS, and Bax in co‐cultured Sertoli‐germ cells and human bronchial epithelial cells and could also decrease the content of MMP in A549 cells (human lung cancer cells), SK‐Hep‐1 cells (human hepatic adenocarcinoma cells), and FL cells (human amniotic normal cells) . in vivo studies have shown that MC‐LR could induce severe oxidative damage and increase the protein expression of bax, Cyt‐c, caspase‐3, and caspase‐9 to induce the apoptosis of frog liver . In the present study, MC‐LR was also found to induce a decrease in MMP, the release of Cyt‐c from the mitochondria into the cytoplasm, and promote the activation of caspase‐3 in co‐cultured Sertoli‐germ cells.…”

Section: Discussionmentioning

confidence: 99%

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p53‐Dependent pathway and the opening of mPTP mediate the apoptosis of co‐cultured Sertoli‐germ cells induced by microcystin‐LR

Liu

Huang

et al. 2019

Environmental Toxicology

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Microcystin‐LR (MC‐LR), a potent endotoxin, can induce reproductive toxicity. In order to investigate the role and mechanisms of apoptosis (p53‐dependent and mitochondrial pathways) of germ cells induced by MC‐LR, the co‐cultured primary Sertoli‐germ cells from Sprague‐Dawley rats were used for the experiments. Expression levels of proteins, genes, and mitochondrial membrane potential (MMP) were obtained after exposing co‐cultured Sertoli‐germ cells to MC‐LR with or without the addition of the p53 inhibitor, pifithrin‐α (PFT‐α), and MMP inhibitor, cyclosporin A (CsA). Results indicated that MC‐LR could activate p53‐dependent pathway‐associated proteins in Sertoli‐germ cells, leading to a decrease in MMP (indicating the opening of mitochondrial permeability transition pore [mPTP] and the release of Cytochrome‐c [Cyt‐c]) from the mitochondria into the cytoplasm and eventually the induction of apoptosis. PFT‐α inhibited the expression ofp53, ameliorated the MMP of the co‐cultured Sertoli‐germ cells, and prevented the release of Cyt‐c from the mitochondria into the cytoplasm, which reduces the occurrence of apoptosis. Similarly, the decreased release of Cyt‐c from the mitochondria into the cytoplasm and the declined level of apoptosis in Sertoli‐germ cells induced by MC‐LR were observed after the addition of CsA. These results indicated that the apoptosis of the co‐cultured Sertoli‐germ cells induced by MC‐LR was mediated by the p53‐dependent pathway, with the involvement of the opening of mPTP.

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Section: Effect Of Pft-α On the Expression Of Apoptosisrelated Protsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 99%

p53‐Dependent pathway and the opening of mPTP mediate the apoptosis of co‐cultured Sertoli‐germ cells induced by microcystin‐LR

Liu

Huang

et al. 2019

Environmental Toxicology

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“…Western blot was done as described by [51]. Briefly, approximately 20 lg (20 lL) protein per gel well was loaded and resolved by 10% sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE).…”

Section: Western Blot Assay For Tight Junction Injurymentioning

confidence: 99%

Blueberry anthocyanins-enriched extracts attenuate the cyclophosphamide-induced lung toxicity

Liu

Shi

et al. 2014

Chemico-Biological Interactions

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“…Liver is the organ that presents the highest tropism for MCs (so-called “target”), since it is rich in a few liver-specific OATP members possessing high affinities and capacities to MCs. Several studies have reported the acute hepatotoxicity of MCs characterized by hepatocellular apoptosis (Zhang et al, 2013), necrosis (Mattos et al, 2014), intrahepatic hemorrhaging (Hou et al, 2015), and cytoskeleton disruption (Zhou et al, 2015). Additionally, the distribution of MCs in the liver has been detected using immunohistochemical methods in mice (Guzman and Solter, 2002; Yoshida et al, 1998) and fish (Djediat et al, 2011; Fischer and Dietrich, 2000; Marie et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Subcellular localization of microcystin in the liver and the gonad of medaka fish acutely exposed to microcystin-LR

Qiao

Djédiat

Huet

et al. 2018

Preprint

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Among the diverse toxic components produced by cyanobacteria, microcystins (MCs) are one of the most toxic and notorious cyanotoxin groups. Besides their potent hepatotoxicity, MCs have been revealed to induce potential reproductive toxicity in various animal studies. However, little is still known regarding the distribution of MCs in the reproductive organ, which could directly affect reproductive cells. In order to respond to this question, an acute study was conducted in adult medaka fish (model animal) gavaged with 10 µg.g-1 body weight of pure MC-LR. The histological and immunohistochemical examinations reveal an intense distribution of MC-LR within hepatocytes along with a severe liver lesion in the toxin-treated female and male fish. Besides being accumulated in the hepatocytes, MC-LR was also found in the connective tissue of the ovary and the testis, as well as in oocytes and degenerative spermatocyte-like structures. Both liver and gonad play important roles in the reproductive process of oviparous vertebrates. This observation constitutes the first observation of the presence of MC-LR in the reproductive cell of a vertebrate model with in vivo study. Our results, which provide intracellular localization of MC-LR in the gonad, advance our understanding of the potential reproductive toxicity of MC-LR in fish.

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Oxidative damage and apoptosis induced by microcystin-LR in the liver of Rana nigromaculata in vivo

Cited by 49 publications

References 46 publications

p53‐Dependent pathway and the opening of mPTP mediate the apoptosis of co‐cultured Sertoli‐germ cells induced by microcystin‐LR

p53‐Dependent pathway and the opening of mPTP mediate the apoptosis of co‐cultured Sertoli‐germ cells induced by microcystin‐LR

Blueberry anthocyanins-enriched extracts attenuate the cyclophosphamide-induced lung toxicity

Subcellular localization of microcystin in the liver and the gonad of medaka fish acutely exposed to microcystin-LR

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