Gastrointestinal toxicity induced by microcystins

Wu, Jinxia; Huang, Hui; Yang, Lijing; Zhang, Xiaofeng; Zhang, Shenshen; Liu, Hao-Hao; Wang, Yueqin; Yuan, Long; Cheng, Xuemin; Zhuang, Donggang; Zhang, Huizhen

doi:10.12998/wjcc.v6.i10.344

Cited by 32 publications

(18 citation statements)

References 56 publications

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“…Some previous studies have confirmed hepatotoxicity, neurotoxicity, gastrointestinal toxicity, and reproductive toxicity of MC-LR [29][30][31][32]. However, the study of nephrotoxicity induced by prolonged oral exposure to MC-LR is rare.…”

Section: Discussionmentioning

confidence: 99%

Effects of Chronic Exposure to Microcystin-LR on Kidney in Mice

Huang

et al. 2019

IJERPH

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Microcystin-LR (MC-LR) is a potent hepatotoxin, but a few studies suggested that it might also induce nephrotoxicity. However, nephrotoxicity induced by prolonged oral exposure to MC-LR is unknown. The aim of this study was to evaluate the potential influence of MC-LR on the kidney in mice following chronic exposure to MC-LR. In this study, we evaluated the nephrotoxicity of MC-LR in mice drinking water at different concentrations (1, 30, 60, 90, and 120 µg/L) for 6 months for the first time. The results showed that the kidney weights and the kidney indexes of mice were not altered in the MC-LR treated mice, compared with the control group. In addition, the renal function indicators revealed that the serum creatinine (SCr) levels were not significant changes after exposure to MC-LR. The blood urea nitrogen (BUN) levels were markedly decreased after exposure to 90 and 120 µg/L MC-LR for 3 months. The BUN levels were lower than that of the control group after exposure to 120 µg/L MC-LR for 6 months. The histopathological investigation revealed enlarged renal corpuscles, widened of kidney tubules, and lymphocyte infiltration in the interstitial tissue and the renal pelvis after exposure to 60, 90, and 120 µg/L MC-LR. Consequently, our results suggested that long-term exposure to MC-LR might be one important risk of kidney injury, which will provide important clues for the prevention of renal impairment.

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Section: Discussionmentioning

confidence: 99%

Effects of Chronic Exposure to Microcystin-LR on Kidney in Mice

Huang

et al. 2019

IJERPH

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“…Previous studies showed that animals and humans are mainly exposed to MC-LR through drinking polluted water, body contact, hemodialysis, consumption of contaminated food and algal dietary supplements [8,9,10]. When MC-LR is ingested, it first enters the intestine where most of these toxins are absorbed through the intestinal mucosal barrier (mucosal epithelial cells and mucosal lamina propria), and the absorbed MC-LR are transported through the bloodstream and distributed to the liver and other organs [11]. This may lead to the development of tumor and various acute liver diseases, nervous system damage, gastroenteritis problems and death [4,9,12,13,14,15].…”

Section: Introductionmentioning

confidence: 99%

Effects of Microcystin-LR on the Microstructure and Inflammation-Related Factors of Jejunum in Mice

Cao

Huang

Massey

et al. 2019

Toxins

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The increasing cyanobacterial blooms have recently been considered a severe environmental problem. Microcystin-leucine arginine (MC-LR) is one of the secondary products of cyanobacteria metabolism and most harmful cyanotoxins found in water bodies. Studies show MC-LR negatively affects various human organs when exposed to it. The phenotype of the jejunal chronic toxicity induced by MC-LR has not been well described. The aim of this paper was to investigate the effects of MC-LR on the jejunal microstructure and expression level of inflammatory-related factors in jejunum. Mice were treated with different doses (1, 30, 60, 90 and 120 μg/L) of MC-LR for six months. The microstructure and mRNA expression levels of inflammation-related factors in jejunum were analyzed. Results showed that the microstructure of the jejunum was destroyed and expression levels of inflammation-related factors interleukin (IL)-1β, interleukin (IL)-8, tumor necrosis factor alpha, transforming growth factor-β1 and interleukin (IL)-10 were altered at different MC-LR concentrations. To the best of our knowledge, this is the first study that mice were exposed to a high dose of MC-LR for six months. Our data demonstrated MC-LR had the potential to cause intestinal toxicity by destroying the microstructure of the jejunum and inducing an inflammatory response in mice, which provided new insight into understanding the prevention and diagnosis of the intestinal diseases caused by MC-LR.

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“…The mechanisms for microcystin-induced cell death involve protein phosphatase inhibition, ROS generation, and disruption of the cytoskeleton and calcium homeostasis [ 119 , 120 , 121 , 128 ]. For example, microcystin treatment activated Bid and induced apoptosis in hepatocytes through JNK activation [ 121 ].…”

Section: Microcystin Molecular Toxicologymentioning

confidence: 99%

Microcystin Toxicokinetics, Molecular Toxicology, and Pathophysiology in Preclinical Rodent Models and Humans

Arman

Clarke

2021

Toxins

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Microcystins are ubiquitous toxins produced by photoautotrophic cyanobacteria. Human exposures to microcystins occur through the consumption of contaminated drinking water, fish and shellfish, vegetables, and algal dietary supplements and through recreational activities. Microcystin-leucine-arginine (MCLR) is the prototypical microcystin because it is reported to be the most common and toxic variant and is the only microcystin with an established tolerable daily intake of 0.04 µg/kg. Microcystin toxicokinetics is characterized by low intestinal absorption, rapid and specific distribution to the liver, moderate metabolism to glutathione and cysteinyl conjugates, and low urinary and fecal excretion. Molecular toxicology involves covalent binding to and inhibition of protein phosphatases, oxidative stress, cell death (autophagy, apoptosis, necrosis), and cytoskeleton disruption. These molecular and cellular effects are interconnected and are commonly observed together. The main target organs for microcystin toxicity are the intestine, liver, and kidney. Preclinical data indicate microcystins may also have nervous, pulmonary, cardiac, and reproductive system toxicities. Recent evidence suggests that exposure to other hepatotoxic insults could potentiate microcystin toxicity and increase the risk for chronic diseases. This review summarizes the current knowledge for microcystin toxicokinetics, molecular toxicology, and pathophysiology in preclinical rodent models and humans. More research is needed to better understand human toxicokinetics and how multifactorial exposures contribute to disease pathogenesis and progression.

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Gastrointestinal toxicity induced by microcystins

Cited by 32 publications

References 56 publications

Effects of Chronic Exposure to Microcystin-LR on Kidney in Mice

Effects of Chronic Exposure to Microcystin-LR on Kidney in Mice

Effects of Microcystin-LR on the Microstructure and Inflammation-Related Factors of Jejunum in Mice

Microcystin Toxicokinetics, Molecular Toxicology, and Pathophysiology in Preclinical Rodent Models and Humans

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