Cranberry Extract 25% Proanthocyanidins

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Cranberry Extract 25% Proanthocyanidins Cranberry extract 25% Proanthocyanidins Cambridge Commodities Chemwatch Hazard Alert Code: 2 Part Number: P31139 Issue Date: 10/09/2020 Version No: 1.1.23.11 Print Date: 28/09/2021 Safety data sheet according to REACH Regulation (EC) No 1907/2006, as amended by UK REACH Regulations SI 2019/758 S.REACH.GB.EN SECTION 1 Identification of the substance / mixture and of the company / undertaking 1.1. Product Identifier Product name Cranberry extract 25% Proanthocyanidins Chemical Name Not Applicable Synonyms Not Available Chemical formula Not Applicable Other means of P31139 identification 1.2. Relevant identified uses of the substance or mixture and uses advised against A flavonoid. Many of the biological effects of flavonoids appear to be related to their ability to modulate a number of cell-signaling cascades. Flavonoids have been shown to exhibit antiallergic, antimicrobial, antiinflammatory, antithrombogenic, antidiabetic, anticancer, antitumorigenic, and antimutagenic and neuroprotective activities through different mechanisms of action in vitro and in animal modes.Flavonoids are regarded as vitamins that are important in the regulation of oxidative stress and act as antioxidants. Flavonoids potentially prevent cancer, heart disease, bone loss, and a number of other diseases Flavonoids are able to reduce plasma levels of low-density lipoproteins, inhibit platelet aggregation, and reduce cell proliferation. These properties result, inter alia, from their mechanisms of action: inhibiting the cell cycle, diminishing oxidative stress, improving detoxification enzymes, inducing apoptosis, and stimulating the immune system. The parent compound , flavanone, is involved in several enzymatic reactions to yield several different flavonoid sub-classes or types, e.g., flavones, flavonols, flavanonols (dihydroflavonols), isoflavones, and anthocyanins. Antioxidant activity Flavonoids are characterized by a molecular frame of two phenyl rings linked by a three carbon chain, making them good Relevant identified uses electron donators or acceptors. Their anti-oxidant capacity depends on this framework, the number and pattern of substitutions (primarily with hydroxyl groups), their ability to chelate with metal ions, and on their specific environment. Flavonoids can readily combine with free radicals, including reactive oxygen species (*ROS) by way of the hydroxyl groups on their structure, ultimately forming resonance-stabilized phenoxyl radicals.The antioxidant properties of flavonoids are related to their potential to prevent disorders associated with oxidative stress caused by free radicals and other reactive oxygen species (ROS). Flavonoids are phytamines with a common chemical structure and a broad range of activities, the most prominent being their radical scavenging ability. Reactive oxygen species (ROS) damage cells by different mechanisms. Direct cytotoxic effects include destruction of the cell membrane by causing radical chain reactions or induction of mutagenic changes in the nuclear and mitochondrial DNA. Indirect changes involve modification of intracellular signal transduction pathways that regulate inflammatory or proliferative activities. Hyperglycaemia results in the generation of free radicals, which may lead to disruption of cellular functions, oxidative damage to cell membranes and enhanced susceptibility to lipid peroxidation. Product code: P31139 Version No: 1.1.23.2 Page 1 of 27 S.REACH.GB.EN Lancaster Way Business Park Safety Data Sheet (Conforms to Regulation (EU) No 2020/878) Ely, Cambridgeshire, CB6 3NX, UK. Chemwatch: 9-775582 +44 (0) 1353 667258 Issue Date: 10/09/2020 [email protected] Print Date: 28/09/2021 www.c-c-l.com Reactive oxygen species (ROS) refers to a diverse group of reactive, short-lived, oxygen-containing species, such as superoxide (O2• -), hydrogen peroxide (H2O2), hydroxyl radical (• OH), singlet oxygen (1O2), and lipid peroxyl radical (LOO• ). ROS serve as second messengers for cellular signaling . However, excessive production of ROS results in oxidative stress and damage to DNA, lipids, and protein that is involved in cancer as well as cardiovascular and neurodegenerative diseases It is believed that flavonoids could behave as antioxidants or pro-oxidants, depending on the concentration and the source of the free radicals. Structures essential to flavonoid's antioxidant activity: 3', 4' hydroxylation, the presence of a double bond between carbons 2 and 3, and a carbonyl group on carbon 4 . The hydrogen atom from an aromatic hydroxyl group can be donated to free radicals. Pro-oxidant activity: Although the ability of flavonoids to protect cells from oxidative stress has been well-documented, there is increasing evidence for their pro-oxidant property . The pro-oxidant activity of flavonoids may be related to their ability to undergo autoxidation catalyzed by transition metals to produce superoxide anions . In other reports, however, it was observed that the phenol rings of flavonoids are metabolized by peroxidase to form pro-oxidant phenoxyl radicals, which are sufficiently reactive to co-oxidize glutathione (GSH) or nicotinamide-adenine hydrogen (NADH) accompanied by extensive oxygen uptake and ROS formation . The structure- activity relationship study on pro-oxidant cytotoxicity of flavonoids shows that flavonoids with a phenol ring are generally more bioactive than the catechol ring-containing ones . Cytotoxicity induced by flavonoids is correlated with their electrochemical oxidation susceptibility and lipophilicity Anti-cancer activity: Plant flavonoids have been shown to decrease the risk of development of cancers and have been widely researched for chemoprevention. An epidemiological study in men has indicated the consumption of five flavonoids including apigenin, myricetin, quercetin, kaempferol, and luteolin decreases the incidence of all types of cancer, as well as the mortality from gastrointestinal and respiratory cancers One study also reported that, in both women and men, consuming a diet rich in flavonoids decreases the risk of cancers, more so in lung cancer, over a 24-year-long follow-up period. Flavonoids have been found to inhibit the proliferation of many cancer cells by arresting cell cycle progression either at the G1/S or G2/M checkpoint . The G1 cell cycle arrest is associated with inhibition of the cyclin dependent(CDK2) activity in melanoma and colorectal cancer cells. This arrest is achieved by up-regulation of the CDK inhibitors p27/kip1 and p21/waf1, or direct inhibition on the CDK2 activity Carcinogens activate cell survival pathways such as NF-kB and MAPK during the course of carcinogenesis; these pathways could be additional targets for flavonoids in anti-carcinogenesis Phyto-oestrogen activity: Flavonoids are naturally occurring phytoestrogens because they can bind to estrogen receptors (ERs) and activate their signaling pathways Flavonoids bind and activate ERs when estrogen is deficient. However, due to their relative weak estrogenic activity they may function as anti-estrogenic agents through competition with natural estrogens for binding to ERs Another mechanism of anti-estrogenic activity iinvolves inhibition of aromatase whose function is to aromatize androgens and produce estrogens . Additionally, one flavonoid, luteolin, reduces the ER expression level through inhibiting transcription of the ER gene or potentiating degradation of the ER protein. Finally, some alternative signaling mechanisms unrelated to ERs could also be involved . Although the interaction of estrogen agonists and antagonists with the ER is a primary event in estrogen action, mammalian cells contain a second binding site (type II site) for estrogen to control cell growth, which resides in endogenous proteins such as histone . Luteolin was found to bind to nuclear type II sites irreversibly and to compete for estradiol binding to these sites The etiology of breast, prostate, ovarian, and endometrial cancers is associated with estrogen activity. Flavonoids,are able to inhibit DNA synthesis and proliferation in mammary epithelial cells and breast cancer cells induced by estrogens, both in vitro and in vivo . Suppressing estrogen-induced cancer cell proliferation may contribute to flavonoids therapeutic and preventive activities against estrogen-associated cancer. Epidemiological studies suggest that dietary intake of flavonoids is inversely associated with risk of lung, prostate, stomach, and breast cancer in humans. Dietary intake of flavonols and flavones was found to be inversely associated with the risk of lung cancer. It should be noted that mixed bioactive compounds, such as different flavonoids that exist in foods, may impact each others’ biological effects. Lifestyle differences of the subjects in a study may interfere with the results. Furthermore, variations in epidemiological studies, including differences in questionnaire design, databases for flavonoid content in foods, and methods for data analysis, may substantially vary the outcomes of different studies. Thus, caution should be exercised when interpreting epidemiological study results Anti-inflammatory activity: Experiments with animals show that some flavonoids suppresses lipopolysaccharide (LPS) or bacteria-induced inflammation in vivo . LPS-induced-high mortality was effectively alleviated by luteolin, which is associated with reduction of LPS-stimulated TNFalpha release in serum and intercellular adhesion molecule-1 (ICAM-1) expression in the liver . Inflammation is one of the body's defense mechanisms that guard
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