Data di Pubblicazione:
2012
Citazione:
A high fructose diet induces protein glycoxidation and HNE protein modifications in rats / L. Cannizzaro, G. Rossoni, F. Savi, M. Orioli, M. Carini, G. Aldini - In: Atti del congresso: 16th Biennial Meeting of the Society for Free Radical Research International[s.l] : Society for Free Radical Research International, 2012 Sep 09. - pp. 24-24 (( Intervento presentato al 16. convegno Biennial Meeting of the Society for Free Radical Research International tenutosi a London nel 2012.
Abstract:
Protein oxidative modifications are involved in the onset and progression of cell and tissue damage induced by a high fructose diet (HFD) (1) (2). The aim of the present
work is to investigate the glycoxidative protein pattern as well as the formation of lipid derived reactive carbonyl species (RCS) protein adducts in rats fed HFD. Sprague
Dawley rats (n=20) were divided into two groups: one group was fed with 60% HFD and the other received a standard diet (control). After 42 days of HFD, blood,
urine and tissue samples were collected. CML and CEL protein modifications in plasma and urine were determined by ELISA while HNE protein adducts
formation in plasma was determined by a validated western-blot analysis, using HSA-HNE adducts as external standard, prepared as previously described (3)
and fully characterized by ESI-MS analysis. HFD ratscompared to control rats showed metabolic syndrome conditions, characterized by hypertension, dyslipidemia
(increase of plasma TG and cholesterol), insulin resistance, kidney damage (increase of urinary albumin and protein and plasma creatinine), inflammatory
response and a sustained systemic oxidative stress as measured by urinary isoprostanes. CEL and CML increased in urine of HFD rats by 2.5 and
2 fold (p<0.001) in respect to control rats. HNE protein adducts content in plasma was determined by a validated western-blot approach showing a dynamic
range of 46pmoL-1.4pmoL, and a calibration curve with a correlation coefficient greater than 0.99885. HNEalbumin
content significantly increased almost 12 fold in the plasma of HFD in respect to controls (p<0.05). In conclusion, HFD induces AGEs formation, which most
likely through RAGE activation, gives an inflammatory response and oxidative damage, which in turn promotes
HNE formation which further sustains the damage induced by HFD.
Tipologia IRIS:
03 - Contributo in volume
Elenco autori:
L. Cannizzaro, G. Rossoni, F. Savi, M. Orioli, M. Carini, G. Aldini
Link alla scheda completa:
Titolo del libro:
Atti del congresso: 16th Biennial Meeting of the Society for Free Radical Research International