PubMed:17035713 JSONTXT 24 Projects

Annnotations TAB TSV DIC JSON TextAE

Id Subject Object Predicate Lexical cue
T1 0-104 Sentence denotes Chloroacetaldehyde as a sulfhydryl reagent: the role of critical thiol groups in ifosfamide nephropathy.
T2 105-269 Sentence denotes Chloroacetaldehyde (CAA) is a metabolite of the alkylating agent ifosfamide (IFO) and putatively responsible for renal damage following anti-tumor therapy with IFO.
T3 270-371 Sentence denotes Depletion of sulfhydryl (SH) groups has been reported from cell culture, animal and clinical studies.
T4 372-479 Sentence denotes In this work the effect of CAA on human proximal tubule cells in primary culture (hRPTEC) was investigated.
T5 480-608 Sentence denotes Toxicity of CAA was determined by protein content, cell number, LDH release, trypan blue exclusion assay and caspase-3 activity.
T6 609-659 Sentence denotes Free thiols were measured by the method of Ellman.
T7 660-784 Sentence denotes CAA reduced hRPTEC cell number and protein, induced a loss in free intracellular thiols and an increase in necrosis markers.
T8 785-876 Sentence denotes CAA but not acrolein inhibited the cysteine proteases caspase-3, caspase-8 and cathepsin B.
T9 877-930 Sentence denotes Caspase activation by cisplatin was inhibited by CAA.
T10 931-1055 Sentence denotes In cells stained with fluorescent dyes targeting lysosomes, CAA induced an increase in lysosomal size and lysosomal leakage.
T11 1056-1153 Sentence denotes The effects of CAA on cysteine protease activities and thiols could be reproduced in cell lysate.
T12 1154-1343 Sentence denotes Acidification, which slowed the reaction of CAA with thiol donors, could also attenuate effects of CAA on necrosis markers, thiol depletion and cysteine protease inhibition in living cells.
T13 1344-1449 Sentence denotes Thus, CAA directly reacts with cellular protein and non-protein thiols, mediating its toxicity on hRPTEC.
T14 1450-1494 Sentence denotes This effect can be reduced by acidification.
T15 1495-1586 Sentence denotes Therefore, urinary acidification could be an option to prevent IFO nephropathy in patients.