Several polyphenolic constituents of the leaf and bark materials of Mangifera indica, have been isolated and identified (E 1 S i s s i and S a 1 e h , 1964, 1965, 1970). N o information related to the plant-acids and amino-acids of this plant, as far as we are aware, has yet been published. The underlying communication deals with the identification of both the plant-and amino-acids, present in both the leaf and bark materials of M. indica. Four varieties of M. indica, namely, hindi-sinnara, mabrouka, pyri and taimour were thus investigated. A modified method based on both procedures given by Hathway (1956) and R e d d y et al. (1964) was applied, and the extracts, freed from their polyphenolics were then paper chromatographically investigated for plant-and amino-acids. The isolated amino-acids present in the leaf materials of the four varieties were shown to be alanine, glycine, leucine, tryosine, valine and an amino-acid with RFvalues rather similar to those of Y-amino-butyric acid (S m i t h , 1961 d). O n the

IntroductionAtherosclerosis is the underlying cause of cardiovascular diseases (CVD), the major cause of death worldwide [1,2]. Atherosclerosis is an inflammatory disease of the arteries in which activated macrophages are abundant in the atherosclerotic lesions [3]. Macrophages and their oxidative status play key roles during early atherogenesis [3,4]. After differentiating from peripheral monocytes, the formed intimal macrophages incorporate oxidized lipoproteins and are transformed into lipid-rich foam cells, the hallmark feature of early atherosclerosis [3]. In addition to lipoprotein uptake, lipid accumulation in macrophages can also result from alterations in cellular lipid metabolism, e.g. attenuated reverse cholesterol transport or enhanced rates of lipid biosynthesis; all are considerably affected by the oxidative status of the cells [4].High intake of added sugars increases the risk of CVD and type 2 diabetes mellitus (T2DM) [5]. T2DM and hyperglycemia are associated with accelerated atherosclerosis mediated by enhanced macrophage foam cell formation [6]. Numerous studies have demonstrated the detrimental role of high glucose on macrophage oxidative status or lipid metabolism leading to foam cell formation. Accelerated atherosclerosis in diabetic mice was associated with macrophage lipid peroxidation and increased generation of reactive oxygen species (ROS) via induction of NADPH oxidase [7,8]. In addition, macrophages from diabetic mice or under high glucose conditions exhibit lipid accumulation mediated by various mechanisms that regulate intracellular lipid metabolism [7][8][9][10][11][12][13][14][15]. These include enhanced uptake of oxidized (ox)-LDL via up-regulation of the scavenger receptors CD36 and SR-A [7-9,11], enhanced cholesterol or triglyceride biosynthesis rates via induction of lipid biosynthesis regulators e.g. the sterol regulator elements binding proteins (SREBPs), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) or diacylglycerol acyltransferase1 (DGAT1) [12,14], and attenuation of HDL-mediated cholesterol efflux from macrophages via suppression of ATP-binding cassette (ABC) transporters ABCA1 and ABCG1 [10,13,15].Although the pro-oxidative and pro-atherogenic role of glucose in macrophage foam cell formation has been established, little is Abstract Background: Glucose is known to enhance macrophage foam cell formation and atherosclerosis development. However, the role of other monosaccharides, disaccharides or artificial sweeteners in macrophage atherogenicity remains unclear.