http://www.cnr.it/ontology/cnr/individuo/prodotto/ID5346
Methylglyoxal causes strong weakening of detoxifying capacity and apoptotic cell death in rat hippocampal neurons. (Articolo in rivista)
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- Methylglyoxal causes strong weakening of detoxifying capacity and apoptotic cell death in rat hippocampal neurons. (Articolo in rivista) (literal)
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- 2008-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.biocel.2007.07.019 (literal)
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S. Di Loreto a; V. Zimmitti b; P. Sebastiani a; C. Cervelli c; S. Falone d; F. Amicarelli b (2008)
Methylglyoxal causes strong weakening of detoxifying capacity and apoptotic cell death in rat hippocampal neurons.
in International journal of biochemistry & cell biology; Pergamon-Elsevier Science Ltd., Oxford (Regno Unito)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- S. Di Loreto a; V. Zimmitti b; P. Sebastiani a; C. Cervelli c; S. Falone d; F. Amicarelli b (literal)
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- a CNR, ITIO, I-67100 Laquila, Italy
b Univ Aquila, Dept Basic & Appl Biol, I-67100 Laquila, Italy
c Reg Ctr Immunohaematol & Tissue Typing ASL 4, Laquila, Italy
d Fac Med G Annunzio, Excellent Ctr Aging Studies, Dept Biomed Sci, I-66013 Chieti, Italy (literal)
- Titolo
- Methylglyoxal causes strong weakening of detoxifying capacity and apoptotic cell death in rat hippocampal neurons. (literal)
- Abstract
- The hippocampus is known to play a crucial role in learning and memory. Recent data from literature showthat cognitive problems,
common to aged or diabetic patients, may be related to accumulation of toxic ?-oxoaldehydes such as methylglyoxal. Thus, it is
possible that methylglyoxal could be, at least in part, responsible for the impairment of cognitive functions, and the knowledge of
the mechanisms through which this compound elicits neuronal toxicity could be useful for the development of possible therapeutic
strategies.
We previously reported a high susceptibility of hippocampal neurons to methylglyoxal, through an oxidation-dependent mechanism.
In the present study,we extend our investigation on the molecular mechanisms which underlie methylglyoxal toxicity, focusing
on possible effects on expression and activity of glyoxalases, its main detoxifying enzymes, and glutathione peroxidase, as well as
on the levels of reduced glutathione. We also investigate methylglyoxal-induced modulation of brain derived neurotrophic factor
and proinflammatory cytokines.
Our results show that methylglyoxal causes a dramatic depletion of reduced glutathione and a significant inhibition of both glyoxalase
and glutathione peroxidase activities. Furthermore, methylglyoxal treatment seems to affect the expression of inflammatory
cytokines and survival factors.
In conclusion, our findings suggest that methylglyoxal-induced neurotoxicity occurs through the impairment of detoxification
pathway and depletion of reduced glutathione. This, in turn, triggers widespread apoptotic cell death, occurring through the
convergence of both mitochondrial and Fas-receptor pathways. (literal)
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