Inhibition of mouse urinary bladder carcinogenesis by açai fruit (Euterpe oleraceae Martius) intake.

Açai, fruit from Euterpe oleraceae Martius, is consumed in natura and in a variety of beverages and food preparations and possesses several potential antioxidant compounds. In a first study for anticarcinogenicity screening, male Swiss mice (n = 20/per group) were chemically-induced to urothelial bladder carcinogenesis for 10 weeks and received a standard diet or a standard diet containing 2.5 and 5 % spray-dried açai pulp (AP) for 10 weeks. At week 20, the incidence of simple and nodular hyperplasia and the incidence and multiplicity of transitional cell carcinoma (TCC) were evaluated. In a second study for antigenotoxicity screening, male Swiss mice (n = 6/per group) were fed standard diet or standard diet containing 5 % AP for three weeks. Urothelial cell suspensions were obtained and challenged with H(2)O(2) for induction of DNA damage and analyzed by comet assay. Overall, dietary 5 % AP reduced TCC incidence and multiplicity (p = 0.019 and p = 0.015, respectively) and tumor cell proliferation and p63 expression (p = 0.02 and p = 0.007, respectively), Furthermore, the group fed the 5 % AP presented a significant reduction (p < 0.01) in DNA damage induced by H(2)O(2), a notable oxidant agent. The results suggest that the spray-dried açai pulp used here inhibits the TCC development in male Swiss mice, probably due to its potential antioxidant action.

Coffee and caffeine protect against liver injury induced by thioacetamide in male Wistar rats.

Coffee intake has been inversely related to the incidence of liver diseases, although there are controversies on whether these beneficial effects on human health are because of caffeine or other specific components in this popular beverage. Thus, this study evaluated the protective effects of coffee or caffeine intake on liver injury induced by repeated thioacetamide (TAA) administration in male Wistar rats. Rats were randomized into five groups: one untreated group (G1) and four groups (G2-G5) treated with the hepatotoxicant TAA (200 mg/kg b.w., i.p.) twice a week for 8 weeks. Concomitantly, rats received tap water (G1 and G2), conventional coffee (G3), decaffeinated coffee (G4) or 0.1% caffeine (G5). After 8 weeks of treatment, rats were killed and blood and liver samples were collected. Conventional and decaffeinated coffee and caffeine intake significantly reduced serum levels of alanine aminotransferase (ALT) (p < 0.001) and oxidized glutathione (p < 0.05), fibrosis/inflammation scores (p < 0.001), collagen volume fraction (p < 0.01) and transforming growth factor ß-1 (TGF-ß1) protein expression (p ≤ 0.001) in the liver from TAA-treated groups. In addition, conventional coffee and caffeine intake significantly reduced proliferating cellular nuclear antigen (PCNA) S-phase indexes (p < 0.001), but only conventional coffee reduced cleaved caspase-3 indexes (p < 0.001), active metalloproteinase 2 (p ≤ 0.004) and the number of glutathione S-transferase placental form (GST-P)-positive preneoplastic lesions (p < 0.05) in the liver from TAA-treated groups. In conclusion, conventional coffee and 0.1% caffeine intake presented better beneficial effects than decaffeinated coffee against liver injury induced by TAA in male Wistar rats.