Ultrastructural alteration of lymphocytes in spleen and pronephros of grass carp (Ctenopharyngodon idella) experimentally exposed to microcystin-LR

Wei, Li Li; Sun, Bao Jian; Nie, Pin

doi:10.1016/j.aquaculture.2008.05.015

Cited by 17 publications

(10 citation statements)

References 21 publications

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“…Spleen-to-body weight ratios increased with 30 µg/kg MCLR exposure in the control and HFHC groups, primarily due to increased spleen weight. Published data for MCLR effects on spleen are limited, but our data are consistent with previous observations of spleen toxicity in fish and immunosuppression in isolated splenocytes [3,42,43]. This change in spleen weight may reflect increased portal hypertension and progression towards cirrhosis in these groups [44].…”

Section: Resultssupporting

confidence: 90%

Sub-Chronic Microcystin-LR Liver Toxicity in Preexisting Diet-Induced Nonalcoholic Steatohepatitis in Rats

Arman

Lynch

Montonye

et al. 2019

Toxins

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Microcystin-LR (MCLR) is a hepatotoxic cyanotoxin reported to cause a phenotype similar to nonalcoholic steatohepatitis (NASH). NASH is a common progressive liver disease that advances in severity due to exogenous stressors such as poor diet and toxicant exposure. Our objective was to determine how sub-chronic MCLR toxicity affects preexisting diet-induced NASH. Sprague-Dawley rats were fed one of three diets for 10 weeks: control, methionine and choline deficient (MCD), or high fat/high cholesterol (HFHC). After six weeks of diet, animals received vehicle, 10 µg/kg, or 30 µg/kg MCLR via intraperitoneal injection every other day for the final 4 weeks. Incidence and severity scoring of histopathology endpoints suggested that MCLR toxicity drove NASH to a less fatty and more fibrotic state. In general, expression of genes involved in de novo lipogenesis and fatty acid esterification were altered in favor of decreased steatosis. The higher MCLR dose increased expression of genes involved in fibrosis and inflammation in the control and HFHC groups. These data suggest MCLR toxicity in the context of preexisting NASH may drive the liver to a more severe phenotype that resembles burnt-out NASH.

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Section: Resultssupporting

confidence: 90%

Sub-Chronic Microcystin-LR Liver Toxicity in Preexisting Diet-Induced Nonalcoholic Steatohepatitis in Rats

Arman

Lynch

Montonye

et al. 2019

Toxins

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“…The toxic effects of MC-LR on fish have been reported in a large number of studies including behavioral, histological and biochemical investigations (Baganz et al, 2004;Fischer and Dietrich, 2000;Li et al, 2007;Malécot et al, 2009;Wang et al, 2010;Wei et al, 2008a), and various other effects on fish have also been reported, including genotoxicity, neurotoxicity and immunotoxicity (Gaudin et al, 2009;Wang et al, 2010;Wei et al, 2008bWei et al, , 2009. In chronic intoxication, it promotes liver tumor formation (Sekijima et al, 1999), but high doses of and the acute toxicity of MC-LR can lead to an excessive phosphorylation of proteins and to alterations in cytoskeleton, loss of cell shape with subsequent destruction of liver cells causing intrahepatic hemorrhage or hepatic insufficiency and necrosis/ apoptosis of hepatocytes (Hooser, 2000;van Apeldoorn et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Identification of apoptosis-related genes and transcription variations in response to microcystin-LR in zebrafish liver

2012

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There is growing evidence that the effects of microcystin-LR (MC-LR) are closely related to apoptosis. This study utilized microarray to identify the apoptosis-related genes induced by MC-LR in zebrafish liver. The messenger RNA abundance of some apoptosis-related genes was found to be increased, including five tumor necrosis factor (TNF)-related members (apoptosis regulatory protein siva, tumor necrosis factor-a (tnfa) TNF (ligand) superfamily member 10 (tnfsf10), TNF-inducible protein 6 (tnfaip6) and TNF receptor associated factor 2 binding protein (traf2bp)), three p53-related genes (tumor protein p53 inducible nuclear protein 1 (tp53inp1), p53-induced protein phosphatase 1 (ppm1d) and a novel apoptosis stimulating protein of p53 (aspp2)), bcl 2 family members (proapoptosis gene bax and antiapoptosis gene mcl 1), caspases (caspase y (caspy) and a PYD and CARD domain-containing protein (pycard)) and the transforming growth factor beta (TGF-b) induced apoptosis protein 2 (taip2). Real-time polymerase chain reaction was used to study the kinetic transcriptional changes in seven apoptosis-related genes. Elevated transcription of p53, tp53inp1, mcl 1 and taip2 could only be detected at 6 h, increased transcription of the antagonist molecules, bcl 2 and bax could be detected at most time points and the significant change of caspy could be found at 48 h and 72 h after stimulation. Taken together, the results obtained in the present study clearly demonstrate that large amount of apoptosis-related genes are involved in the regulation of MC-LR-induced apoptosis.

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“…The quail spleens were enlarged to double the size of the control spleens after administration of MCRR, whereas the livers did not change [15]. The ultrastructural alteration of lymphocytes was examined in the spleen of grass carp Ctenopharyngodon idella injected experimentally with MCLR [16]. The changes in the transcription levels of immunerelated genes induced by MCLR confirmed its effect on inhibiting immune function in grass carp C. idella [17].…”

Section: Introductionmentioning

confidence: 83%

“…Thus, the injury of spleen might lead to great damage to the immune function of the organism. It has been verified that MCs exert prominent immunotoxicity to animals, and result in pathological changes, inhibition of lymphocyte proliferation and transcriptional disruption [15][16][17][18]. In fact, the lysozyme activity is a useful tool in monitoring the immune system function [26].…”

Section: Discussionmentioning

confidence: 99%

Global effects of subchronic treatment of microcystin-LR on rat splenetic protein levels

Li¹,

Yan²,

Qiao³

et al. 2012

Journal of Proteomics

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Ultrastructural alteration of lymphocytes in spleen and pronephros of grass carp (Ctenopharyngodon idella) experimentally exposed to microcystin-LR

Cited by 17 publications

References 21 publications

Sub-Chronic Microcystin-LR Liver Toxicity in Preexisting Diet-Induced Nonalcoholic Steatohepatitis in Rats

Sub-Chronic Microcystin-LR Liver Toxicity in Preexisting Diet-Induced Nonalcoholic Steatohepatitis in Rats

Identification of apoptosis-related genes and transcription variations in response to microcystin-LR in zebrafish liver

Global effects of subchronic treatment of microcystin-LR on rat splenetic protein levels

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