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Whey protein isolates (WPI) have been indicated to have potent cholesterol lowering and antioxidative properties. Such effects, however, are not consistently observed, which could be the result of major differences in the processing, isolation and composition of WPI. Moreover, the mechanisms of action or the bioactive component(s) in WPI are poorly understood although the relatively high cysteine content in WPI has been suggested to play an important role. Although high dietary cysteine has been shown to lower plasma homocysteine concentrations, the impact of WPI in this regard has not been investigated. The overall objective of this thesis was to examine the antioxidative and plasma cholesterol and homocysteine lowering properties of two WPI that were produced via different industrial processing and isolation techniques with the milk protein, casein, used as the control protein. We also examined for the mechanism(s) of action of WPI in terms of possible antioxidative, and plasma cholesterol and homocysteine lowering effects. In this regard, the intake of bovine serum albumin (BSA), a major cysteine-rich whey protein was also studied since this protein has been implicated as a key bioactive component for the antioxidant effects of WPI. Four studies were performed. The first involved the characterization of a variety of commercially prepared WPI by high performance capillary electrophoresis for identification of two WPI products that showed major differences in protein composition for subsequent feeding trials. Most of the WPI had similar characteristic electrophoretic profiles, however, significant differences in protein and macronutrient (Ca, Mg, P) composition were noted in two commercial WPI that were chosen as the test proteins in subsequent feeding trials. In the first two feeding studies, hamsters were fed different commercial WPI or milk protein (BSA or casein) containing diets that were either matched or unmatched in terms of macro

Dietary phytochemicals such as saponins have been suggested to have therapeutic uses in the prevention and alleviation of hypercholesterolemia. Thus, twelve Tanzanian plant additives hypothesized to contain saponins and used in soup by the Batemi, were investigated for in vitro hypocholesterolemic potential by: (1) screening for likelihood of detectable saponins using TLC, hemolysis, frothing ability and molluscicidal activity. (2) using changes in hemolytic activity to indirectly examine interactions of plant extracts with cholesterol, cholesterol-analogues, conjugated bile salts and non-conjugated bile salts. (3) using radiolabelled cholesterol to examine direct binding capacity of extracts with cholesterol. Albizia anthelmintica, Myrsine africana and Acacia goetzii were most likely to contain saponins and had significant (p $<$ 0.05) hemolytic activity that was effected by the presence of cholesterol, cholesterol analogues, conjugated and non-conjugated bile salts (p $<$ 0.05). Methanol, ethyl acetate, aqueous and n-butanol extracts of A. anthelmintica and methanol, ethyl acetate and aqueous extracts of A. goetzii bound significant amounts of cholesterol solubilized in ethanol (p $<$ 0.05). Thus, saponins are a detectable component of the Batemi diet and extracts likely containing saponins do interact with chemicals that have been proposed to be involved in in vivo mechanisms of saponin induced hypocholesterolemia. A. anthelmintica and A. goetzii seem likely to have hypocholesterolemic potential as dietary additives.

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No description available.

Enzymatic and lipid transfer reactions involved in reverse cholesterol transport were studied in HDL deficient plasma systems. Fasting plasma samples were obtained from control and cholesterol fed guinea pigs as well as from a fish eye disease patient and were used to localize the enzyme LCAT among plasma lipoproteins (VLDL, LDL, and HDL). In both guinea pig and fish eye disease patient plasma, the LCAT activity was found in association with the HDL type particles. Cholesterol feeding in guinea pigs altered the properties of lipoprotein substrates for LCAT resulting in some changes, specifically: 1) decreased fractional rate of plasma cholesterol esterification and, 2) lower transfer of free cholesterol (FC) and esterified cholesterol (CE) within the lipoprotein fractions.