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Protein oxidation and aggregation in UVA‐irradiated Escherichia coli cells as signs of accelerated cellular senescence
Author(s) -
Bosshard Franziska,
Riedel Kathrin,
Schneider Thomas,
Geiser Carina,
Bucheli Margarete,
Egli Thomas
Publication year - 2010
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/j.1462-2920.2010.02268.x
Subject(s) - biology , escherichia coli , senescence , protein aggregation , catalase , protein carbonylation , microbiology and biotechnology , protein biosynthesis , reactive oxygen species , chaperone (clinical) , photoprotection , biochemistry , cell , enzyme , biophysics , photosynthesis , glutathione , gene , medicine , pathology
Summary Solar disinfection (SODIS) is a simple drinking water treatment method that improves microbiological water quality where other means are unavailable. It makes use of the deleterious effect of solar irradiation on pathogenic microbes and viruses. A positive impact on health has been documented in several epidemiological studies. However, the molecular mechanisms damaging cells during this simple treatment are not yet fully understood. Here we show that protein damage is crucial in the process of inactivation by sunlight. Protein damages in UVA‐irradiated Escherichia coli cells have been evaluated by an immunoblot method for carbonylated proteins and an aggregation assay based on semi‐quantitative proteomics. A wide spectrum of structural and enzymatic proteins within the cell is affected by carbonylation and aggregation. Vital cellular functions like the transcription and translation apparatus, transport systems, amino acid synthesis and degradation, respiration, ATP synthesis, glycolysis, the TCA cycle, chaperone functions and catalase are targeted by UVA irradiation. The protein damage pattern caused by SODIS strongly resembles the pattern caused by reactive oxygen stress. Hence, sunlight probably accelerates cellular senescence and leads to the inactivation and finally death of UVA‐irradiated cells.

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