In this study, procyanidins fractions of dimers and trimers (F1–F2) from the Leucosidea sericea total extract (LSTE) were investigated for their chemical constituents. The total extract and the procyanidins were employed in the synthesis of gold nanoparticles (Au NPs) and fully characterized. Au NPs of 6, 24 and 21 nm were obtained using LSTE, F1 and F2 respectively. Zeta potential and in vitro stability studies confirmed the stability of the particles. The enzymatic activity of LSTE, F1, F2 and their corresponding Au NPs showed strong inhibitory alpha-amylase activity where F1 Au NPs demonstrated the highest with IC₅₀ of 1.88 µg/mL. On the other hand, F2 Au NPs displayed the strongest alpha-glucosidase activity at 4.5 µg/mL. F2 and F2 Au NPs also demonstrated the highest antioxidant activity, 1834.0 ± 4.7 μM AAE/g and 1521.9 ± 3.0 μM TE/g respectively. The study revealed not only the ability of procyanidins dimers (F1 and F2) in forming biostable and bioactive Au NPs but also, a significant enhancement of the natural products activities, which could improve the smart delivery in future biomedical applications.

We review the hepatocarcinogenic effects of fungal cultures of Fusarium verticillioides(= Fusarium moniliforme) strain MRC 826 in male BD IX rats. Subsequent chemical analyses of the fumonisin B (FB) mycotoxin content in the culture material used and long-term carcinogenesis studies with purified FB1 provide information about dose-response effects, relevance of hepatotoxicity during FB1-induced carcinogenesis, and the existence of a no-effect threshold. Fumonisin intake levels of between 0.08 and 0.16 mg FB/100 g body weight (bw)/day over approximately 2 years produce liver cancer in male BD IX rats. Exposure levels < 0.08 mg FB/100 g bw/day fail to induce cancer, although mild toxic and preneoplastic lesions are induced. The nutritional status of the diets used in the long-term experiments was marginally deficient in lipotropes and vitamins and could have played an important modulating role in fumonisin-induced hepatocarcinogenesis. Short-term studies in a cancer initiation/promotion model in rat liver provided important information about the possible mechanisms involved during the initial stages of cancer development by this apparently nongenotoxic mycotoxin. These studies supported the findings of long-term investigations indicating that a cytotoxic/proliferative response is required for cancer induction and that a no-effect threshold exists for cancer induction. The mechanisms proposed for cancer induction are highlighted and include the possible role of oxidative damage during initiation and the disruption of lipid metabolism, integrity of cellular membranes, and altered growth-regulatory responses as important events during promotion.