According to epidemiologic studies, dietary phenolic antioxidants, such as chlorogenic acid (CQA), could prevent coronary heart diseases and some cancers. Coffee is the main source of CQA in the human diet. The aim of this study was to assess the effect of usual coffee consumption conditions, such as the addition of milk, on CQA bioavailability. Interactions between CQA and milk proteins were shown, using an ultrafiltration technique. These interactions proved to be slightly disrupted during an in vitro digestion process. CQA absorption and bioavailability were then studied in vitro using a Caco-2 cell model coupled with an in vitro digestion process, and in vivo, in a chronic supplementation study in which rats were fed daily coffee or coffee and milk for 3 weeks. Both experiments showed that CQA absorption under its native form is weak, but unmodified by the addition of milk proteins, and slightly reduced by the addition of Maillard reaction products. These data show that there are some interactions between coffee phenolics and milk proteins, but these have no significant effect on CQA bioavailability from coffee in the rat. CQA is poorly absorbed under its native form in the body, when ingested in a realistic food matrix.

: In the human diet, coffee is the major source of caffeoyl‐quinic acids known as powerful antioxidants. The aim of this study was to assess the effect of usual coffee consumption, such as the addition of milk, and of processing conditions, such as spray‐drying, on beverage antioxidant power and potential polyphenol bioavailability impairments. When 25% milk was added to coffee, up to 40% of coffee chlorogenic acid were found to be bound to dairy proteins, using an ultrafiltration technique. However, neither milk addition nor spray‐drying had a significant effect on beverage antioxidant power, evaluated using 2,2‐diphenyl‐1‐pycrylhydrazyl (DPPH), 2‐2′‐azobis (2‐amidinopropane) dihydrochloride (AAPH), and total antioxidant capacity (TAC) tests. Moreover, these interactions tended to decrease during in vitro gastric and intestinal digestion, thus suggesting that interactions between chlorogenic acid and milk proteins in coffee and milk beverage may not have any significant effect on coffee antioxidant power before and after consumption.

The aim of this study was to determine the metabolic fate of phospholipid hydroperoxides (PLOOH) in rat gastric mucosa. Here we report evidence concerning the mechanism for PLOOH detoxification in gastric mucosa homogenate. Analysis by the TLC blot technique showed that the gastric mucosa has the highest potential to eliminate 1-palmitoyl-2-linoleoyl-phosphatidylcholine hydroperoxides (PL-PtdChoOOH) compared with the intestinal mucosa and liver. Major products detected after incubation with gastric mucosa were the partially reduced linoleic acid hydroperoxides (LAOOH) and lysophosphatidylcholine, indicating the involvement of phospholipase A2 (PLA2) in the elimination pathway. Using unilamellar vesicles, we demonstrated that gastric mucosal PLA2 does not distinguish between PLOOH and intact phospholipids. Although gastric mucosal PLA2 activity efficiently eliminated excess amounts of PLOOH, the complete reduction of LAOOH was dependent on the supply of exogenous GSH. In a separate experiment, administration of egg yolk PtdChoOOH to rats for 6 d significantly elevated GSH peroxidase (GPx) activity in the gastric mucosa. We concluded that excess amounts of PLOOH are efficiently eliminated through the hydrolysis by PLA2, and the subsequent reduction of FA hydroperoxide by GPx is the critical step for complete detoxification of oxidized phospholipids in the stomach.

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