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• W87622207 abstract "The high consumption of foods and beverages rich in flavonoids has been associated with lower risk of chronic degenerative diseases such as atherosclerosis and cancer due to both their direct antioxidant removal of free radicals, for their ability to act as an antioxidant indirectly by activating different pathways signaling against oxidative stress. Euterpe oleracea Mart. or acai palm is a native of the Amazon regions whose fruit is rich in flavonoids, especially anthocyanins and proanthocyanidins (cyanidin-3-glucoside and cyanidin-3-rutinosideo). Several recent studies have highlighted the antioxidant properties, pro-apoptotic, antiproliferative and pro-longevity of acai, both in vitro and in animal models. In this work, Caenorhabditis elegans was used as a model organism to test the in vivo antioxidant activities of different extracts of acai that could be exploited to enhance innate defenses to oxidative stress and longevity. Through the pH differential method, it was found that the amount of anthocyanins present in acai freeze-dried extract of two (AL-1 and AL-2) showed around 19.2 to 34.7 mg of anthocyanins monomericas/100g extract. To test whether treatment with extracts of freeze-dried acai (AL-1 and AL-2) increase resistance to oxidative stress, wild-type animals were treated for 48 hours of larval stage L1 to L4 with 100 and 200 mg / ml extract acai and then subjected to stress caused by tert-butyl hydroperoxide (t-Booher). Animals treated with 200 mg / ml do not develop and remain in L1. Since wild animals treated with 100 mg / ml of AL-1 AL-2 and were more resistant to oxidative stress caused by 5 mM t-Booher than untreated animals. On the other hand, treatment of wild-type animals with 100 mg / ml of AL-1 for 168 hours did not increase the resistance to heat stress at 35 ° C. Continuous treatment with 100 mg / ml of AL-1 did not increase the longevity of wild-type animals. Despite having a higher resistance to stress, the animals treated with 100mg/ml of the extract of acai for 48 hours did not show a significant difference to the biochemical markers (catalase activity) and indicators of resistance (total sulfhydryl and protein carbonyl) in relation to the control group. To verify that the increased resistance to oxidative stress promoted by treatment with acai extract depends on signaling pathways p38/SKN-1 and DAF-16, tests of resistance to oxidative stress were repeated using deletion mutants of sek-1 (ku7 ), the p38 MAPKK, skn-1 (RNAi) and daf-16 (mgDf46). Apparently, treatment with 100 mg / ml AL-1 did not increase oxidative stress resistance mutants of sek-1 and daf-16, suggesting that this increase depends on the activation of SEK-1 and DAF-16. On the other hand, no significant induction of nuclear localization in treated animals containing reporter gene DAF-16:: GFP. These data suggest that the increased resistance to oxidative stress induced by treatment with acai extract possibly depends on p38 MAPK and DAF-16, but occurs without activation of the nuclear localization of DAF-16." @default.
• W87622207 created "2016-06-24" @default.
• W87622207 creator A5057312362 @default.
• W87622207 date "2011-01-01" @default.
• W87622207 modified "2023-09-27" @default.
• W87622207 title "Avaliação dos efeitos antioxidantes e pró-longevidade do extrato de açaí (Euterpe oleraceae Mart.) no organismo modelo Caenorhabditis elegans" @default.
• W87622207 hasPublicationYear "2011" @default.
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