Detection of microcystins in environmental samples using surface plasmon resonance biosensor

Hu, Chenlin; Gan, Nanqin; Chen, Yuanyuan; Bi, Lijun; Zhang, Xian-En; Song, Lirong

doi:10.1016/j.talanta.2009.06.044

Cited by 50 publications

(27 citation statements)

References 21 publications

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“…The binding and dissociation kinetics of McAb7E10 with the recombinant ATPase β subunit were determined using a BIAcore surface plasmon resonance instrument (Pharmacia, Uppsala, Sweden) [27-31]. Briefly, 1400 RU of the recombinant ATPase β subunit (25 ug/mL in 10 mmol/L sodium acetate, pH 4.5) were covalently bound through amino groups to a CM5 sensor chip [32-34]. …”

Section: Methodsmentioning

confidence: 99%

Inhibition of the ecto-beta subunit of F1F0-ATPase inhibits proliferation and induces apoptosis in acute myeloid leukemia cell lines

Zhao

Wang

Tao

et al. 2012

J Exp Clin Cancer Res

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BackgroundLeukemia, a heterogeneous clonal disorder of hematopoietic progenitor cells, presents a world-wide health problem, especially in childhood. F1F0 ATPase, an inner mitochondrial enzyme, is expressed on the plasma membrane of tumor cells, and its inhibition induces both anti-angiogenic and anti-tumorigenic activity.MethodsMonoclonal Antibody (McAb) against ATPase was produced by polyethylene glycol-mediated fusions and screened by ELISA. Proliferation, cell cycle and apoptosis of cells were analyzed when the surface ATPase of cells was blockaded with McAb.ResultsWe detected cell-membrane expression of the F1F0 ATPase β subunit on 0.1% to 56% of the 11 cell lines derived from leukemia, including acute myeloid leukemia (AML). We produced a monoclonal antibody, McAb7E10, which recognizes both the native and recombinant ATPase β subunit, with a dissociation constant (KD) of 3.26E–10. We demonstrate that McAb7E10 binds to ATPase at the cell surface, where it is able to inhibit ATP synthesis. McAb7E10 significantly inhibited proliferation of AML cell lines in vitro: the relative inhibitory rates of 50 μg/mL McAb7E10 treated MV4-11and HL-60 cells were 69.6% and 81.9% respectively. Cell cycle analysis indicated that McAb7E10 significantly induced apoptosis in MV4-11 and HL-60 cells: the relative rates of apoptosis in 5, 10 and 50ug/mL McAb7E10 treated MV4-11 cells was 3.6 ± 0.83%, 8.4 ± 1.69% and 17.3 ± 2.56% compared to 1.5% ± 0.85% in mouse IgG treated cells (p < 0.01). The relative rate of apoptosis in 5, 10 and 50ug/mL McAb7E10 treated HL-60 cells was 5.5 ± 2.37%, 11.3 ± 3.62% and 19.9 ± 3.31% compared to 1.56% ± 0.97% in mouse IgG treated cells (p < 0.01). Annexin V staining demonstrated that the relative apoptotic rates in 50 μg/mL McAb7E10 treated MV4-11 and HL-60 cells were 50.5% ± 7.04% and 32.9% ± 4.52%, respectively, significantly higher than IgG control antibody treated cells were 21.9% ± 3.11% and 15.3% ± 3.95%, p < 0.01.ConclusionsThese findings indicate that ectopic expression of ATPase β subunit may be a tumor-associated antigen in hematological malignancies. The F1F0 ATPase β subunit provides a potential target for immunotherapy in AML and hematological malignancies.

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Section: Methodsmentioning

confidence: 99%

Inhibition of the ecto-beta subunit of F1F0-ATPase inhibits proliferation and induces apoptosis in acute myeloid leukemia cell lines

Zhao

Wang

Tao

et al. 2012

J Exp Clin Cancer Res

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“…MC-LR was purified in our laboratory (Hu et al, 2009). SFN, chlomethiazole (CMZ), diallyl sulfide (DAS), and all other reagents were of the highest grade available and were obtained from Sigma-Aldrich, unless otherwise noted.…”

Section: Methodsmentioning

confidence: 99%

Sulforaphane prevents microcystin-LR-induced oxidative damage and apoptosis in BALB/c mice

Sun

Liu

et al. 2011

Toxicology and Applied Pharmacology

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Microcystins (MCs), the products of blooming algae Microcystis, are waterborne environmental toxins that have been implicated in the development of liver cancer, necrosis, and even fatal intrahepatic bleeding. Alternative protective approaches in addition to complete removal of MCs in drinking water are urgently needed. In our previous work, we found that sulforaphane (SFN) protects against microcystin-LR (MC-LR)-induced cytotoxicity by activating the NF-E2-related factor 2 (Nrf2)-mediated defensive response in human hepatoma (HepG2) and NIH 3T3 cells. The purpose of this study was to investigate and confirm efficacy the SFN-induced multi-mechanistic defense system against MC-induced hepatotoxicity in an animal model. We report that SFN protected against MC-LR-induced liver damage and animal death at a nontoxic and physiologically relevant dose in BALB/c mice. The protection by SFN included activities of anti-cytochrome P450 induction, anti-oxidation, anti-inflammation, and anti-apoptosis. Our results suggest that SFN may protect mice against MC-induced hepatotoxicity. This raises the possibility of a similar protective effect in human populations, particularly in developing countries where freshwaters are polluted by blooming algae.

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“…MC-LR was purified in our lab (20). Cycloheximide (CHX), MG132, and all other reagents were of the highest grade available from Sigma, unless otherwise noted.…”

Section: Methodsmentioning

confidence: 99%

Activation of Nrf2 by Microcystin-LR Provides Advantages for Liver Cancer Cell Growth

Gan

Sun

Song

2010

Chem. Res. Toxicol.

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Microcystin-LR (MC-LR) is a potent heptapeptide hepatotoxin at high doses, but its underlying mechanism of promoting liver cell proliferation at low doses is unclear. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is key in mediating the protective antioxidant response against various environmental toxicants, but emerging data suggest that constitutive activation of Nrf2 contributes to a malignant phenotype. The purpose of this study was to characterize the interactions and effects of Nrf2 activation on cell proliferation induced by MC-LR treatment. Treatment of HepG2 and Hep3B cells with MC-LR resulted in significant increases in Nrf2-ARE binding activities in the nuclear fractions and upregulation of its downstream genes HO-1 and NQO1. A possible mechanism may be that MC-LR binds to the cytosolic regulator protein Keap1 to liberate Nrf2. Nrf2 knockdown inhibited MC-LRinduced cell proliferation and cell cycle progression. Together, these results indicate that MC-LR-induced upregulation of Nrf2 in cancer cells promotes liver cancer cell growth and suggest a positive role of Nrf2 in tumorigenesis.

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Detection of microcystins in environmental samples using surface plasmon resonance biosensor

Cited by 50 publications

References 21 publications

Inhibition of the ecto-beta subunit of F1F0-ATPase inhibits proliferation and induces apoptosis in acute myeloid leukemia cell lines

Inhibition of the ecto-beta subunit of F1F0-ATPase inhibits proliferation and induces apoptosis in acute myeloid leukemia cell lines

Sulforaphane prevents microcystin-LR-induced oxidative damage and apoptosis in BALB/c mice

Activation of Nrf2 by Microcystin-LR Provides Advantages for Liver Cancer Cell Growth

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