RESUMO
The peptic-tryptic-cotazym (PTC) digest, obtained from bread wheat gliadin by simulating in vivo protein digestion, was more active than the PTC-digest of durum wheat gliadin in reversibly inhibiting HEp-2 cell proliferation and in increasing cellular acid phosphatase. Colony-forming ability of the cells was not affected by treatment with both bread or durum wheat gliadin peptides. The peptic-tryptic (PT) digest of bread wheat gliadin also showed agglutinating activity of HEp-2 cells.
Assuntos
Gliadina/toxicidade , Proteínas de Plantas/toxicidade , Fosfatase Ácida/metabolismo , Aglutinação/efeitos dos fármacos , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Ensaio de Unidades Formadoras de Colônias , Humanos , Técnicas In Vitro , Peptídeos/toxicidade , TriticumRESUMO
A peptic-tryptic-cotazym digest, obtained from bread (hexaploid) wheat gliadins under experimental conditions mimicking in vivo protein digestion, was found to reduce in vitro viability of human embryo (MRC-5) and tumor cell (Hep-2) lines. Time of onset and extent of cytotoxic effects were largely dependent on initial peptide concentrations in the culture medium. The presence of 2% fetal calf serum was capable of delaying, but not of preventing, the onset of cytotoxic effects only in MRC-5 cultures. A peptic-tryptic-cotazim digest obtained from durum (tetraploid) wheat gliadins and tested under identical conditions did not show any cytotoxic activity on MRC-5 and Hep-2 cell lines. These results indicate that cell systems are useful to investigate pathogenetic mechanisms of coeliac disease (gluten-dependent enteropathy).
Assuntos
Doença Celíaca/etiologia , Gliadina/toxicidade , Proteínas de Plantas/toxicidade , Triticum/toxicidade , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Embrião de Mamíferos , Epitélio , Fibroblastos , Humanos , Neoplasias Laríngeas , Fragmentos de Peptídeos/toxicidadeRESUMO
Nitrofuran drugs have been studied on cellular systems in order to develop in vitro tests for safety assessment of food contaminants. In the present study we have tested furaltadone on three cell lines (HEp-2, Caco-2 and V79), using the same toxicity endpoints as in a previous study with furazolidone, namely cell viability and growth, colony-forming ability, LDH release, and O2 consumption. One of the aims of this investigation was to compare the two compounds in order to determine whether our models are able to discriminate among structurally related molecules. The other aim was to study the influence of the solvent used on the observed toxicity, because furaltadone is soluble both in water and in DMSO. The results show that the three cell lines used as differently affected by the two compounds, and that, at least in the case of furaltadone, the solvent is not relevant for the observed toxicity.
Assuntos
Dimetil Sulfóxido/farmacologia , Furazolidona/toxicidade , Inibidores do Crescimento/toxicidade , Nitrofuranos/toxicidade , Oxazolidinonas , Animais , Células CACO-2 , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Cricetinae , Humanos , L-Lactato Desidrogenase/análise , Estrutura Molecular , Consumo de Oxigênio/efeitos dos fármacos , Solventes , Células Tumorais CultivadasRESUMO
Two human cell lines have been used, HEp-2 and (de)differentiated Caco-2, derived from a larynx and a colon carcinoma, respectively, with the aim of evaluating and characterizing the cytotoxicity of okadaic acid (OA) and related toxins. Effects of OA and dinophysistoxin-1 (DTX-1) on cell viability (neutral red uptake) and on cell morphology/cytoskeleton structure have been observed in both cell lines, though at different time exposures and with different concentrations. The morphological alteration was detected earlier than the viability inhibition in HEp-2 cells with both toxins and in Caco-2 cells with DTX-1. HEp-2 cells have shown to be more sensitive than the intestinal cell line and thus possibly suitable for screening of contaminated samples, while Caco-2 cells could be used for further investigating the possible mechanisms involved in diarrhoeic shellfish poisoning (DSP) toxins.