The suppression of hematopoiesis function in Balb/c mice induced by prolonged exposure of microcystin-LR

Zhou, Wenshan; Zhang, Xuezhen; Xie, Ping; Liang, Haihua; Zhang, Xin

doi:10.1016/j.toxlet.2013.02.011

Cited by 11 publications

(9 citation statements)

References 39 publications

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“…Moreover, the fluorescence in situ hybridization (FISH) analysis of the MN content (HepG2 cells) suggested that MC-LR induces both chromosome breaks and loss [84]. Significantly elevated MN frequency was also observed in bone marrow cells of MC-LR-treated mice [85]. In contrast, Zhan et al [86] demonstrated that oral exposure to MC-LR (1 mg/kg b.w., 0.1 LD 50 , once every week for 4 weeks) did not increase either MN frequency in the peripheral blood cells or mutant frequencies of the lacZ and cII genes in liver and lungs of the λ/lacZ transgenic mouse.…”

Section: Genotoxicitymentioning

confidence: 99%

Mechanisms of Microcystin-induced Cytotoxicity and Apoptosis

Chen¹,

Xie

2016

MRMC

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Abstract:In recent years, cyanobacterial blooms have dramatically increased and become an ecological disaster worldwide. Cyanobacteria are also known to produce a wide variety of toxic secondary metabolites, i.e. cyanotoxins. Microcystins (MCs), a group of cyclic heptapeptides, are considered to be one of the most common and dangerous cyanobacterial toxins. MCs can be incorporated into the cells via organic anion transporting polypeptides (Oatps). It's widely accepted that inhibition of protein phosphatases (PPs) and induction of oxidative stress are the main toxic mechanisms of MCs. MCs are able to induce a variety of toxic cellular effects, including DNA damage, cytoskeleton disruption, mitochondria dysfunction, endoplasmic reticulum (ER) disturbance and cell cycle deregulation, all of which can contribute to apoptosis/programmed cell death. This review aimed to summarize the increasing data regarding the intracellular biochemical and molecular mechanisms of MC-induced toxicity and cell death.

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Section: Genotoxicitymentioning

confidence: 99%

Mechanisms of Microcystin-induced Cytotoxicity and Apoptosis

Chen¹,

Xie

2016

MRMC

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“…Recent studies suggest that MC-LR may promote the migration and invasion of colorectal cancer and it has been implicated in renal-function impairment 25 , 26 . MC-LR has also been shown to cause apoptosis and changes to the permeability of the mitochondrial membrane in mice 27 and can cause suppression of haematopoiesis function in mice leading to normocytic anaemia through prolonged exposure 28 . To date, the only human study looking at daily exposure and subsequent health effects of chronic exposure to MCs was conducted by Chen et al .…”

Section: Introductionmentioning

confidence: 99%

Uptake and accumulation of Microcystin-LR based on exposure through drinking water: An animal model assessing the human health risk

Greer

Meneely

Elliott

2018

Sci Rep

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Harmful Algal Blooms (HABs) in freshwater systems and intensified aquaculture have increased the risk to human health through exposure to cyanotoxins such as microcystin-LR (MC-LR). To understand the uptake and processing of MC-LR in humans, the pig was chosen as an animal model. This was assessed by repeated exposure for 13 weeks of eight animals dosed daily with MC-LR at 0.04 µg/kg bw, repeated with six animals over five weeks at a dose 50 times higher at 2 µg/kg bw. An analytical method was developed for MC-LR in porcine serum and also to analyse levels of free MC-LR in harvested porcine tissues, with Lemieux Oxidation employed to determine bound MC-LR in these tissues. MC-LR was not detected in the serum of treated animals from either experiment but free MC-LR was observed in the large intestine and kidney from two animals from the higher dosed group at levels of 1.4 and 1.9 µg/kg dry weight (dw) respectively. The results indicated 50% of higher dosed animals accumulated bound MC-LR in liver tissue, averaging 26.4 µg, approximately 1.1% of the dose administered. These results point to the potential uptake and accumulation of MC-LR in human liver tissue exposed chronically to sub-acute doses.

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“…19 Spontaneous frequency average of bone marrow micronucleus was 0.8% to 2.3% in ICR mouse species with the weighted average of 1.5%. In our micronucleus test, the ratio of PCE-RBC of mice in each dose group was basically consistent with the reported results of normal range which was from 0.6 to 1.2, 20 indicating no suppression of PCE formation.…”

Section: Feed Safety Of the Acidolysis Productsmentioning

confidence: 94%

Valuable ingredients and feed toxicity evaluation of Microcystis aeruginosa acidolysis product in mice

Han

Zhou

Yudi

et al. 2015

Exp Biol Med (Maywood)

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This research studied the extraction from Microcystis aeruginosa using hydrochloric acid method as a potentially valuable protein resource from eutrophic lakes. Amino acid composition, residual algal toxins, and heavy metals of the acidolysis product were studied. After 18 h of hydrochloric acid treatment, the product of M. aeruginosa contained 17 amino acids, 51.34% of total amino acid requirements, and 30.25% of the livestock and poultry essential amino acid (Eaa). The residual microcystin-LR (MC-LR) was 0.94 mg kg À1 , which was less than WHO drinking water limit of microcystins. The removal ratio of microcystins was higher than 99.99% during the process of hydrolysis. The concentration of heavy metals of the product was in compliance with feed standards. Furthermore, using Horn's method, Mouse Micronucleus Test and Sperm Shape Abnormality Test were conducted to study the forage safety of the product. Half lethal dose (LD 50 ) of acidolysis product in mice was >9.09 g kg À1 body weight, actually belonging to non-toxic grade. Every dose treatment did not significantly increase activities of alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and g-glutamyltransferase (g-GT). The results of both micronucleus test and sperm shape abnormality test were negative, which suggested the product with no mutagenicity and sperm malformation effects. This study indicated that the acidolysis product of M. aeruginosa was safe to be used as a feed ingredient.

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The suppression of hematopoiesis function in Balb/c mice induced by prolonged exposure of microcystin-LR

Cited by 11 publications

References 39 publications

Mechanisms of Microcystin-induced Cytotoxicity and Apoptosis

Mechanisms of Microcystin-induced Cytotoxicity and Apoptosis

Uptake and accumulation of Microcystin-LR based on exposure through drinking water: An animal model assessing the human health risk

Valuable ingredients and feed toxicity evaluation of Microcystis aeruginosa acidolysis product in mice

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