Pharmacologic application of Fourier transform IR spectroscopy:In vivo toxicity of carbon tetrachloride on rat liver

Melin, Anne-Marie; Perromat, Annie; Déléris, Gérard

doi:10.1002/(sici)1097-0282(2000)57:3<160::aid-bip4>3.0.co;2-1

Cited by 74 publications

(51 citation statements)

References 34 publications

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“…Amide A and amide B bands are found in this spectral region. They both have contributions from mainly the N-H stretching of proteins with a small contribution from the O-H stretching of polysaccharides and intermolecular H bonding and contributions from C-N and N-H stretching of proteins, respectively [21].…”

Section: Resultsmentioning

confidence: 99%

A molecular and biophysical comparison of macromolecular changes in imatinib-sensitive and imatinib-resistant K562 cells exposed to ponatinib

et al. 2015

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Chronic myeloid leukemia (CML) is a type of hematological malignancy that is characterized by the generation of Philadelphia chromosome encoding BCR/ABL oncoprotein. Tyrosine kinase inhibitors (TKIs), imatinib, nilotinib, and dasatinib, are used for the frontline therapy of CML. Development of resistance against these TKIs in the patients bearing T315I mutation is a major obstacle in CML therapy. Ponatinib, the third-generation TKI, is novel drug that is effective even in CML patients with T315I mutation. The exact mechanism of ponatinib in CML has been still unknown. In this study, we aimed to determine the potential mechanisms and structural metabolic changes activated by ponatinib treatment in imatinib-sensitive K562 human CML cell lines and 3 μM-imatinib-resistant K562/IMA3 CML cell lines generated at our lab. Apoptotic and antiproliferative effects of ponatinib on imatinib-sensitive and 3 μM-imatinibresistant K562/IMA3 CML cells were determined by proliferation and apoptosis assays. Additionally, the effects of ponatinib on macromolecules and lipid profiles were also analyzed using Fourier transform infrared spectroscopy (FTIR). Our results revealed that ponatinib inhibited cell proliferation and induced apoptosis as determined by loss of mitochondrial membrane potential, increased caspase-3 enzyme activity, and transfer of phosphatidylserine to the plasma membrane in both K562 and K562/IMA-3 cells. Furthermore, cell cycle analyses revealed that ponatinib arrested K562 and K562/IMA-3 cells at G1 phase. Moreover, ponatinib treatment created a more ordered nucleic acid structure in the resistant cells. Although the lipid to protein ratio increased in imatinib-sensitive K562 cells with a little decrease in the K562/IMA-3 cells, ponatinib treatment indicated significant changes in the lipid composition such as a significant increase in the cellular cholesterol amounts much more in the K562/IMA-3 cells than the sensitive counterparts. Unsaturation in lipids was higher in the resistant cells; however, increases in lipids without phosphate and the number of acyl chains were much higher in the K562 cells. Taken together, all these results showed powerful antiproliferative and apoptotic effects of ponatinib in both imatinib-sensitive and imatinib-resistant CML cells in a dose-dependent manner, and hence, the use of ponatinib for the treatment of TKI-resistant CML patients may be an effective treatment approach in the clinic. More importantly, these results showed that FTIR spectroscopy can detect druginduced physiological changes in cancer drug resistance.

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Section: Resultsmentioning

confidence: 99%

A molecular and biophysical comparison of macromolecular changes in imatinib-sensitive and imatinib-resistant K562 cells exposed to ponatinib

et al. 2015

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“…First, we tested the levels of serum aminotransferases on an automated analyzer in the Biochemistry Department of Pellegrin Hospital in Bordeaux. Second, we analyzed the extent of liver peroxidation induced by CCl 4 in microsomal fractions of mouse liver by Fourier-transformed infrared (FT-IR) spectroscopy as previously described (29). Ward's algorithm was used on OPUS 4.0 software (Bruker, Ettlingen, Germany) for spectra classification on the spectral intervals that are the most representative of the (C-O) sugar absorptions (1,130 -930 cm Ϫ1 ).…”

Section: Measure Of CCL 4 Acute Liver Toxicitymentioning

confidence: 99%

Protease-activated receptor 1 knockout reduces experimentally induced liver fibrosis

Rullier

Gillibert-Duplantier²,

Costet³

et al. 2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Thrombin inhibition protects against liver fibrosis. However, it is not known whether the thrombin profibrogenic effect is due to effects on blood coagulation or to signaling via protease-activated receptors (PARs). We took advantage of the lack of blood coagulation defects in PAR-1-knockout mice. Acute carbon tetrachloride (CCl4) toxicity was similar in wild-type (WT), PAR-1−/−, and PAR-1+/−mice as judged by aminotransferase levels, area of liver necrosis, and liver peroxidation measured by Fourier-transformed infrared spectroscopy. Fifteen mice/group received CCl4or its solvent for 6 wk (300 μl/kg, 3 times a week). Fibrosis area was increased 10-fold by CCl4treatment in WT mice. PAR-1 deficiency protected against fibrosis, with 36% and 56% decrease in PAR-1+/−and PAR-1−/−mice, respectively ( P < 0.001). Similar results were obtained for area of activated fibrogenic cells (64% and 79% decrease in PAR-1+/−and PAR-1−/−mice, respectively, P < 0.001). These findings were corroborated by measurements of type I collagen, matrix metalloproteinase-2, and PDGF-β receptor mRNA levels. There was also a significant decrease in T lymphocyte infiltration in PAR-1-deficient mice. Altogether, these results suggest that thrombin profibrogenic effects are independent of effects on blood coagulation and are instead due to direct effects on fibrogenic cells and possibly on T lymphocytes.

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“…3a shows the average FTIR spectra of control and HHP-treated blood cells in the 3100-3680 cm À1 spectral region. The FTIR spectrum in this region consists of amide A band which has contributions from mainly the N-H stretching of proteins with the little contribution from the O-H stretching of polysaccharides and intermolecular H bonding (Melin et al, 2000;Cakmak et al, 2011). All the control and treated spectra have almost the same overlapping absorption bands.…”

Section: Effects Of Hhp On Serum Studied By Ftirmentioning

confidence: 99%

Biophysical and microbiological study of high hydrostatic pressure inactivation of Bovine Viral Diarrheavirus type 1 on serum

Ceylan

Severcan

Özkul

et al. 2012

Veterinary Microbiology

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The effect of high hydrostatic pressure application on fetal bovine serum components and the model microorganism (Bovine Viral Diarrheavirus type 1 NADL strain) was studied at 132 and 220MPa pressure for 5min at 25°C. Protein secondary structures were found to be unaffected by an artificial neural network application on the amide I region for both untreated and HHP treated samples. FTIR spectroscopy study of both the HHP-treated and control samples revealed changes in the intensity of some bands in the finger-print region (1500-900cm -1) originating mainly from lipids which are thought to result from changes in the lipoprotein structure. The virus strain lost its infectivity completely after 220MPa HHP treatments. These results indicate that HHP can be successfully used for inactivation of pestiviruses while leaving structural and functional properties of serum and serum products unaffected. © 2011 Elsevier B.V

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Pharmacologic application of Fourier transform IR spectroscopy:In vivo toxicity of carbon tetrachloride on rat liver

Cited by 74 publications

References 34 publications

A molecular and biophysical comparison of macromolecular changes in imatinib-sensitive and imatinib-resistant K562 cells exposed to ponatinib

A molecular and biophysical comparison of macromolecular changes in imatinib-sensitive and imatinib-resistant K562 cells exposed to ponatinib

Protease-activated receptor 1 knockout reduces experimentally induced liver fibrosis

Biophysical and microbiological study of high hydrostatic pressure inactivation of Bovine Viral Diarrheavirus type 1 on serum

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