The aim of the present study was to verify whether the oral administration of cyanidin 3-O-b-D-glucoside (C3G) might counteract damage inducedby chronic exposure (28 d) to ochratoxin A (OTA) in rats and if its effect may be mediated by haeme oxygenase-1 (HO-1). Forty male Sprague–Dawley rats, individually caged, were divided into four groups of ten animals. A control group received a commercial diet, group C3G received thecontrol diet supplemented with C3G (1 g/kg feed), group OTA received the control diet supplemented with 200 parts per billion of OTA, and groupOTA þ C3G received the OTA group diet supplemented with C3G (1 g/kg feed). After 4 weeks of treatment animals were killed and the liver,kidneys and brain of each rat were collected and homogenised to evaluate non-proteic thiol groups (RSH), lipid hydroperoxide (LOOH) levels,HO-1 expression and DNA fragmentation. Rats of the OTA group showed a significant (P,0·001) decrease in RSH content of kidney and liverand a significant (P,0·001) increase of LOOH in all the examined tissues compared with the control group. In the OTA þ C3G group both RSHcontent and LOOH levels were similar to those observed in the control group, demonstrating that C3G was able to counteract the effects of OTA.A significant (P,0·001) induction of HO-1 was evident in kidney and liver of both OTA and C3G groups. DNA damage occurred in all the examinedtissues of the OTA group, whereas C3G was able to prevent it. The present study confirmed that the effects of OTA are mediated by oxidativestress and demonstrated that C3G efficiently counteracted deleterious effects of OTA because of its antioxidant and HO-1-inducing properties.

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Protective effect of cyanidin 3-O-beta-d-glucoside on ochratoxin A-mediated damage in the rat

DI GIACOMO, Claudia;ACQUAVIVA, ROSARIA;SORRENTI, Valeria;VANELLA, LUCA;GALVANO, Fabio
2007-01-01

Abstract

: : s:
The aim of the present study was to verify whether the oral administration of cyanidin 3-O-b-D-glucoside (C3G) might counteract damage inducedby chronic exposure (28 d) to ochratoxin A (OTA) in rats and if its effect may be mediated by haeme oxygenase-1 (HO-1). Forty male Sprague–Dawley rats, individually caged, were divided into four groups of ten animals. A control group received a commercial diet, group C3G received thecontrol diet supplemented with C3G (1 g/kg feed), group OTA received the control diet supplemented with 200 parts per billion of OTA, and groupOTA þ C3G received the OTA group diet supplemented with C3G (1 g/kg feed). After 4 weeks of treatment animals were killed and the liver,kidneys and brain of each rat were collected and homogenised to evaluate non-proteic thiol groups (RSH), lipid hydroperoxide (LOOH) levels,HO-1 expression and DNA fragmentation. Rats of the OTA group showed a significant (P,0·001) decrease in RSH content of kidney and liverand a significant (P,0·001) increase of LOOH in all the examined tissues compared with the control group. In the OTA þ C3G group both RSHcontent and LOOH levels were similar to those observed in the control group, demonstrating that C3G was able to counteract the effects of OTA.A significant (P,0·001) induction of HO-1 was evident in kidney and liver of both OTA and C3G groups. DNA damage occurred in all the examinedtissues of the OTA group, whereas C3G was able to prevent it. The present study confirmed that the effects of OTA are mediated by oxidativestress and demonstrated that C3G efficiently counteracted deleterious effects of OTA because of its antioxidant and HO-1-inducing properties.
yanidin-3-O-b-glucoside; Ochratoxin A; Non-proteic thiol groups; Lipid hydroperoxides:; Haeme oxygenase-1
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11769/26434
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