## 2 Bioactive Compounds Commonly Found in Green-Colored Fruits and Vegetables
### General Characteristics, Structure, and Food Sources
The conjugated HA is inaccessible to the digestive enzymes and thus presents poor bioaccessibility and bioavailability. Most of the metabolized HAs are excreted in urine instead of feces. Recently, [PERSON] and [PERSON] reported that the ingested HAs, except for CGA, were primarily excreted as free or conjugated forms in the urine within 0-6 h [159]. The total urinary excretion rate (% of the dose) at 48 h followed the order FA (73.2%) \(>\) CA (61.6%) \(>\)\(p\)-CA (54.1%) \(>\) CGA (4.9%). The percentages of the conjugates in the urine differed among the rats gavage-fed with individual HAs (74% for CGA, 83% for CA, 68% for \(p\)-CA, and 96% for FA), which may be explained by their distinct bioactivities. The urinary excretion rate of various HAs, including \(p\)-CA, in non-fasted rats under normal physiological conditions was 54.1% of the dose at 48 h [159]. Among the four HAs (i.e., CGA, CA, \(p\)-CA, and FA), CA, \(p\)-CA, and FA are much more bioavailable than CGA, although they are excreted more rapidly than CGA. FA and \(p\)-CA are absorbed by the monocarboxylic acid transporter (MCT) in Caco-2 cells, although gallic acid (GA) is not [160]. Low bioavailability of HAs limits the exhibition of their beneficial bioactive effects. Therefore, many studies have focused on developing the appropriate food processing technologies that can facilitate the release and/or increase the accessibility of conjugated phenolic compounds in green-colored foods, primarily through fermentation, breakdown of cereal matrices, or degradation of fiber polymers. Potential Health Benefits  
HAs, including CA, CQA, GA, and FA, exert a wide variety of biological antioxidant, anti-inflammatory, antimicrobial, antiallergic, hepatotoxicity, anticarcinogenic, antithrombotic, and antiviral activities. Studies in rats and piglets suggest that HAs play a role in increasing sperm viability, vasodilatory actions, enzyme activity modulation, transcriptional factor activation, gene expression, and signal transduction [161; 162; 163; 164]. **CA** has a wide range of pharmacological activities similar to most phenolic compounds. It exerts its antioxidant effect by scavenging free radicals, such as 2,2'-azino-bis3-ethylbenzothazoline-6-sulphonic acid (ABTS) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) [165], reducing iron ions and chelating metal ions [166]. Additionally, CA ex erts potential cardiovascular benefits through antioxidant mechanisms associated with LDL oxidation, NO bioavailability, and blood pressure lowering. Daily use of CA in moderate amounts can reduce the incidence of CVDs such as atherosclerosis and coronary heart disease of humans [167]. Furthermore, CA could fight diabetes and hyperglycemia through multiple mechanisms, including the antibiotic effect of CA in animal models, promotion of islet survival, reduction of serum fibrinogen levels in diabetic animals, and regulation of \(\beta\) cell and adipocyte glucose transporter type 4 (GLUT4) performance [168]. Furthermore, consuming CA every day is beneficial in the treatment of CVDs because of its anti-hypertensive properties and its ability to lower blood pressure throughout the body of rats [169]. Furthermore, it could increase the number of platelets by increasing the content of granulocytes and megakaryocytes, thus speeding up coagulation to achieve hemostasis [167]. Additionally, some human and animal bioactivities of CA are closely related to gut microbial community. Studies have shown that dietary CA interacts with human and/or animal intestinal microbes and thus produces various metabolites that affect host metabolism and cardiovascular health [170]. In anaerobic conditions, bacteria possessing tyrosine decarboxylase could induce the decarboxylation of CA, generating [3-(3-hydroxyphenyl)-propionic acid], a product with higher antioxidant activity compared with CA [169]. **CQA** has a lipid-lowering activity that improves metabolic dysregulation in diet-induced obesity models partially by regulating peroxisome proliferatorator-activated receptor (PPAR)?2 expression.