The Kidney Vero-E6 Cell Line: A Suitable Model to Study the Toxicity of Microcystins

Menezes, Carina; Valério, Elisabete; Dias, Elsa

doi:10.5772/54463

Cited by 28 publications

(30 citation statements)

References 85 publications

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“…At lower MC-LR concentrations, autophagy is triggered as a survival mechanism of Vero-E6 cells, in an attempt to eliminate the toxin and/or the MC-LR-induced cellular damages [31][32][33]. However, the presence of a significant increase in apoptosis/ necrosis at sub-cytotoxic MC-LR concentrations, suggests that in this case, autophagy was ineffective in attenuating the MC-LR-induced cellular damages, triggering a drastic cell death pathway.…”

Section: Mc-induced Toxicity and Cell Deathmentioning

confidence: 87%

“…MC-LR also has a binary effect in Vero-E6 cells (African green monkey-Cercopithecus aethiops kidney epithelial cells): the stimulation of cell proliferation at low MC-LR concentrations and the induction of autophagy/ apoptosis at (sub)cytotoxic concentrations of MC-LR [30]. Alverca et al [31] and Menezes et al [32,33] indicated that Vero-E6 cells respond to MC-LR-induced stress through autophagy, apoptosis or ultimately through necrosis, and the type of response seems to be highly dependent on the strength of the stimulus, i.e. the dose and/or the exposure time.…”

Section: Mc-induced Toxicity and Cell Deathmentioning

confidence: 99%

“…Apoptosis and proliferation are intimately coupled and are linked by cell cycle regulators and apoptotic stimuli that affect both processes [156]. MCs promoted cell survival and growth at lower doses, while induced apoptosis/cell death at higher doses in liver cells [29,157], lymphocytes [158], kidney cells [30][31][32][33]56], HeLa cells [139]. It is accepted that both survival and death signals could be activated by MCs, and the cell responded to the stronger signals, so the outcome of the MCs on the cells depends on concentration of the toxin as well as duration of exposure [139,142,159,160].…”

Section: Cell Cycle Regulationmentioning

confidence: 99%

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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: Mc-induced Toxicity and Cell Deathmentioning

confidence: 87%

Section: Mc-induced Toxicity and Cell Deathmentioning

confidence: 99%

Section: Cell Cycle Regulationmentioning

confidence: 99%

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Mechanisms of Microcystin-induced Cytotoxicity and Apoptosis

Chen¹,

Xie

2016

MRMC

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“…Oatp-mediated and MC-congener-dependent transport is responsible for MC-induced neuronal toxicity (Feurstein et al, 2009b). MCs are mainly excreted by the hepatocytes, but up to 9 % can be eliminated by urine (Bischoff, 2001) which makes the kidneys a potential target for MC-LR toxicity (Menezes et al, 2013). Furthermore, OATP-A, one of the known MC active transporters, has been identified recently at mRNA level in the human kidney (Hagenbuch & Meier, 2003).…”

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confidence: 99%

Microcystin-LR-induced cytotoxicity and apoptosis in human embryonic kidney and human kidney adenocarcinoma cell lines

et al. 2015

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Microcystin-LR (MC-LR) is a potent hepatotoxin, and increasing evidence suggests that it might also induce kidney injury. The aim of the present work was to evaluate the cytotoxicity and possible apoptotic effects of MC-LR on a human embryonic kidney cell line (HEK-293) and human kidney adenocarcinoma cell line (ACHN). Cells were exposed for 24 h to pure MC-LR (1.0-200 mM) and the cytotoxic effects were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and sulphorhodamine B (SRB) cell viability assays. Cell viability in both cell lines was significantly decreased after treatment with MC-LR at 50 mM for 24 h (P,0.001). Moreover, MC-LR-treated ACHN and HEK-293 cells exhibited a marked dosedependent loss of confluence as judged by phase-contrast microscopy. Similarly, fluorescence microscopic observations following acridine orange-ethidium bromide (AO/EB) staining confirmed that both cell types were undergoing apoptosis after treatment with MC-LR for 24 h. Expression of three apoptosis-related genes, Bax, Survivin and p53, was analysed by quantitative reverse transcriptase PCR analysis. Both Bax and p53 functioned as promoters of MC-LRmediated apoptosis in ACHN and HEK-293 cells. The Survivin gene acted as a suppressor of apoptosis at lower MC-LR concentration (1 mM) and the gene was upregulated at higher MC-LR concentration (10 mM) (P,0.001). Significant increases of caspase 3 (P,0.0001) and caspase 9 (P,0.0001) activity were detected in both cell lines after exposure to MC-LR for 24 h, indicating the MC-LR induces cytotoxicity and a marked apoptosis in both ACHN and HEK-293 kidney cell lines.

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“…Sugar-sweetened beverages, food additives, sodium, drugs, toxins, and smoking cause renal failure. (3)(4)(5)(6)(7) In this modern age (computer age), computers are essential to our routine life. On the other hand, the waste products of computers will accumulate in our environment.…”

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confidence: 99%

Personal Computers : Risk Factors for Renal Failure

Gowder¹

2015

IJHS

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Kidneys perform various biological functions in the human body, and hence, they are called multitalented powerhouses in our physiological system. Increased blood flow, occurrence of metabolizing enzymes, and transport proteins are important factors enhancing the sensitivity of the kidney. In this context, the kidney is an important candidate organ for the evaluation of the adverse effects of environmental chemicals. Although kidneys reside in the abdominal cavity and are protected by other tissues, they still behave like security forces working at the border of a country facing the onslaughts of external agents.With reference to its structure, the kidney is a complicated organ, comprising various cell types and having a neatly designed three-dimensional organization. Due to this complexity, the intact kidney is difficult to use for an adequate study of many biochemical, pharmacological and physiological processes. Renal proximal tubule cells derived from primary cultures have been considered an appropriate model for the study of either proximal tubule cell function or renal intact function. Culturing of renal proximal tubule cells derived from primary culture is a critical issue in renal research. The newly designed protocol of Gowder and McMartin will provide an appropriate method to grow good quality renal proximal tubule cells to evaluate toxicity and transport properties of drugs/chemicals.( 1) Since reductionism (Einsteinian theory) dominates over the holism (Newtonian theory) in personal medicine, investigation of cells will provide more compromising results than that of whole individuals.(2) Kidney damage has been considered to be a major public health hazard in recent years. Common lifestyle diseases, such as diabetes, hypertension, and infectious diseases, are significant causes of renal failure. Sugar-sweetened beverages, food additives, sodium, drugs, toxins, and smoking cause renal failure.(3-7)

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The Kidney Vero-E6 Cell Line: A Suitable Model to Study the Toxicity of Microcystins

Cited by 28 publications

References 85 publications

Mechanisms of Microcystin-induced Cytotoxicity and Apoptosis

Mechanisms of Microcystin-induced Cytotoxicity and Apoptosis

Microcystin-LR-induced cytotoxicity and apoptosis in human embryonic kidney and human kidney adenocarcinoma cell lines

Personal Computers : Risk Factors for Renal Failure

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