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• W2059646751 endingPage "1850" @default.
• W2059646751 startingPage "1841" @default.
• W2059646751 abstract "Aminoacetone (AA), triose phosphates, and acetone are putative endogenous sources of potentially cytotoxic and genotoxic methylglyoxal (MG), which has been reported to be augmented in the plasma of diabetic patients. In these patients, accumulation of MG derived from aminoacetone, a threonine and glycine catabolite, is inferred from the observed concomitant endothelial overexpression of circulating semicarbazide-sensitive amine oxidases. These copper-dependent enzymes catalyze the oxidation of primary amines, such as AA and methylamine, by molecular oxygen, to the corresponding aldehydes, NH4+ ion and H2O2. We recently reported that AA aerobic oxidation to MG also takes place immediately upon addition of catalytic amounts of copper and iron ions. Taking into account that (i) MG and H2O2 are reportedly cytotoxic to insulin-producing cell lineages such as RINm5f and that (ii) the metal-catalyzed oxidation of AA is propagated by O2•- radical anion, we decided to investigate the possible pro-oxidant action of AA on these cells taken here as a reliable model system for pancreatic β-cells. Indeed, we show that AA (0.10−5.0 mM) administration to RINm5f cultures induces cell death. Ferrous (50−300 μM) and Fe3+ ion (100 μM) addition to the cell cultures had no effect, whereas Cu2+ (5.0−100 μM) significantly increased cell death. Supplementation of the AA- and Cu2+-containing culture medium with antioxidants, such as catalase (5.0 μM), superoxide dismutase (SOD, 50 U/mL), and N-acetylcysteine (NAC, 5.0 mM) led to partial protection. mRNA expression of MnSOD, CuZnSOD, glutathione peroxidase, and glutathione reductase, but not of catalase, is higher in cells treated with AA (0.50−1.0 mM) plus Cu2+ ions (10−50 μM) relative to control cultures. This may imply higher activity of antioxidant enzymes in RINm5f AA-treated cells. In addition, we have found that AA (0.50−1.0 mM) plus Cu2+ (100 μM) (i) increase RINm5f cytosolic calcium; (ii) promote DNA fragmentation; and (iii) increase the pro-apoptotic (Bax)/antiapoptotic (Bcl-2) ratio at the level of mRNA expression. In conclusion, although both normal and pathological concentrations of AA are probably much lower than those used here, it is tempting to propose that excess AA in diabetic patients may drive oxidative damage and eventually the death of pancreatic β-cells." @default.
• W2059646751 created "2016-06-24" @default.
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• W2059646751 date "2008-08-26" @default.
• W2059646751 modified "2023-10-16" @default.
• W2059646751 title "Aminoacetone, a Putative Endogenous Source of Methylglyoxal, Causes Oxidative Stress and Death to Insulin-Producing RINm5f Cells" @default.
• W2059646751 cites W120247693 @default.
• W2059646751 cites W1490906767 @default.
• W2059646751 cites W1583699416 @default.
• W2059646751 cites W1605991890 @default.
• W2059646751 cites W1768247331 @default.
• W2059646751 cites W1943794713 @default.
• W2059646751 cites W1966621383 @default.
• W2059646751 cites W1968130661 @default.
• W2059646751 cites W1969445527 @default.
• W2059646751 cites W1970451002 @default.
• W2059646751 cites W1974985242 @default.
• W2059646751 cites W1986846402 @default.
• W2059646751 cites W1990630457 @default.
• W2059646751 cites W1996428972 @default.
• W2059646751 cites W1998015077 @default.
• W2059646751 cites W1998228104 @default.
• W2059646751 cites W1999527102 @default.
• W2059646751 cites W2008596858 @default.
• W2059646751 cites W2010290591 @default.
• W2059646751 cites W2012297152 @default.
• W2059646751 cites W2015930146 @default.
• W2059646751 cites W2019407191 @default.
• W2059646751 cites W2020816386 @default.
• W2059646751 cites W2023189641 @default.
• W2059646751 cites W2027203159 @default.
• W2059646751 cites W2030463887 @default.
• W2059646751 cites W2035396795 @default.
• W2059646751 cites W2039400792 @default.
• W2059646751 cites W2046686737 @default.
• W2059646751 cites W2049492732 @default.
• W2059646751 cites W2050415187 @default.
• W2059646751 cites W2054308266 @default.
• W2059646751 cites W2054621083 @default.
• W2059646751 cites W2055589739 @default.
• W2059646751 cites W2056007774 @default.
• W2059646751 cites W2056964101 @default.
• W2059646751 cites W2060526888 @default.
• W2059646751 cites W2061953105 @default.
• W2059646751 cites W2062622163 @default.
• W2059646751 cites W2067138582 @default.
• W2059646751 cites W2077260619 @default.
• W2059646751 cites W2077293904 @default.
• W2059646751 cites W2078116198 @default.
• W2059646751 cites W2078892596 @default.
• W2059646751 cites W2079952067 @default.
• W2059646751 cites W2080294402 @default.
• W2059646751 cites W2081583688 @default.
• W2059646751 cites W2086365629 @default.
• W2059646751 cites W2088385191 @default.
• W2059646751 cites W2089816337 @default.
• W2059646751 cites W2092055474 @default.
• W2059646751 cites W2104595034 @default.
• W2059646751 cites W2105361286 @default.
• W2059646751 cites W2111675700 @default.
• W2059646751 cites W2116587224 @default.
• W2059646751 cites W2128085053 @default.
• W2059646751 cites W2131798140 @default.
• W2059646751 cites W2132411546 @default.
• W2059646751 cites W2138774341 @default.
• W2059646751 cites W2146169493 @default.
• W2059646751 cites W2149081316 @default.
• W2059646751 cites W2154362965 @default.
• W2059646751 cites W2156044622 @default.
• W2059646751 cites W2157198098 @default.
• W2059646751 cites W2162332580 @default.
• W2059646751 cites W2163694606 @default.
• W2059646751 cites W2168323764 @default.
• W2059646751 cites W2178933626 @default.
• W2059646751 cites W2182200562 @default.
• W2059646751 cites W2334570807 @default.
• W2059646751 cites W2413694818 @default.
• W2059646751 cites W2471605942 @default.
• W2059646751 cites W4237140970 @default.
• W2059646751 cites W88059348 @default.
• W2059646751 doi "https://doi.org/10.1021/tx8001753" @default.
• W2059646751 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18729331" @default.
• W2059646751 hasPublicationYear "2008" @default.
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