Monday, 19 June 2017

Phytoalexin glyceollins (Glycine max) kháng LNCaP

Molecular effects of soy phytoalexin glyceollins in human


Phytoalexin glyceollins (Glycine max) kháng  LNCaP

Phytoalexin

From Wikipedia, the free encyclopedia

Capsidiol is a phytoalexin produced by certain plants in response to pathogenic attack
Phytoalexins are antimicrobial and often antioxidative substances synthesized de novo by plants that accumulate rapidly at areas of pathogen infection. They are broad spectrum inhibitors and are chemically diverse with different types characteristic of particular plant species. Phytoalexins tend to fall into several classes including terpenoidsglycosteroids and alkaloids; however, researchers often find it convenient to extend the definition to include all phytochemicals that are part of the plant's defensive arsenal.

Function[edit]

Phytoalexins produced in plants act as toxins to the attacking organism. They may puncture the cell wall, delay maturation, disrupt metabolism or prevent reproduction of the pathogen in question. Their importance in plant defense is indicated by an increase in susceptibility of plant tissue to infection when phytoalexin biosynthesis is inhibited. Mutants incapable of phytoalexin production exhibit more extensive pathogen colonization as compared to wild type. As such, host-specific pathogens capable of degrading phytoalexins are more virulent than those unable to do so.[1]
When a plant cell recognizes particles from damaged cells or particles from the pathogen, the plant launches a two-pronged resistance: a general short-term response and a delayed long-term specific response.
As part of the induced resistance, the short-term response, the plant deploys reactive oxygen species such as superoxide and hydrogen peroxide to kill invading cells. In pathogen interactions, the common short-term response is the hypersensitive response, in which cells surrounding the site of infection are signaled to undergo apoptosis, or programmed cell death, in order to prevent the spread of the pathogen to the rest of the plant.
Long-term resistance, or systemic acquired resistance (SAR), involves communication of the damaged tissue with the rest of the plant using plant hormones such as jasmonic acidethyleneabscisic acid or salicylic acid. The reception of the signal leads to global changes within the plant, which induce genes that protect from further pathogen intrusion, including enzymes involved in the production of phytoalexins. Often, if jasmonates or ethylene (both gaseous hormones) is released from the wounded tissue, neighboring plants also manufacture phytoalexins in response. For herbivores, common vectors for disease, these and other wound response aromatics seem to act as a warning that the plant is no longer edible (source?). Also, in accordance with the old adage, "an enemy of my enemy is my friend," the aromatics may alert natural enemies of the plant invaders to the presence thereof.

Recent research[edit]

Allixin (3-hydroxy-5-methoxy-6-methyl-2-pentyl-4H-pyran-4-one), a non-sulfur-containing compound having a γ-pyrone skeleton structure, was the first compound isolated from garlic as a phytoalexin, a product induced in plants by continuous stress.[2] This compound has been shown to have unique biological properties, such as anti-oxidative effects,[2] anti-microbial effects,[2] anti-tumor promoting effects,[3] inhibition of aflatoxin B2 DNA binding,[4] and neurotrophic effects.[4] Allixin showed an anti-tumor promoting effect in vivo, inhibiting skin tumor formation by TPA in DMBA initiated mice.[3] Herein, allixin and/or its analogs may be expected useful compounds for cancer prevention or chemotherapy agents for other diseases.

Role of natural phenols in the plant defense against fungal pathogens[edit]

Polyphenols, especially isoflavonoids and related substances, play a role in the plant defense against fungal and other microbial pathogens.
In Vitis vinifera grape, trans-resveratrol is a phytoalexin produced against the growth of fungal pathogens such as Botrytis cinerea[5] and delta-viniferin is another grapevine phytoalexin produced following fungal infection by Plasmopara viticola.[6] Pinosylvin is a pre-infectious stilbenoid toxin (i.e. synthesized prior to infection), contrary to phytoalexins which are synthesized during infection. It is present in the heartwood of Pinaceae.[7] It is a fungitoxin protecting the wood from fungal infection.[8]
Sakuranetin is a flavanone, a type of flavonoid. It can be found in Polymnia fruticosa[9] and rice, where it acts as a phytoalexin against spore germination of Pyricularia oryzae.[10] In Sorghum, the SbF3'H2 gene, encoding a flavonoid 3'-hydroxylase, seems to be expressed in pathogen-specific 3-deoxyanthocyanidin phytoalexins synthesis,[11] for example in Sorghum-Colletotrichum interactions.[12]
6-Methoxymellein is a dihydroisocoumarin and a phytoalexin induced in carrot slices by UV-C,[13] that allows resistance to Botrytis cinerea[14] and other microorganisms.[15]
Danielone is a phytoalexin found in the papaya fruit. This compound showed high antifungal activity against Colletotrichum gloesporioides, a pathogenic fungus of papaya.[16]
Stilbenes are produced in Eucalyptus sideroxylon in case of pathogens attacks. Such compounds can be implied in the hypersensitive response of plants. High levels of polyphenols in some woods can explain their natural preservation against rot.[17]

Glyceollin

From Wikipedia, the free encyclopedia
  (Redirected from Glyceollins)
Glyceollins are a family of prenylated pterocarpan found in ineffective types of nodule in soybean in response to symbiotic infection.[1]
It possesses two chiral centers and can be asymmetrically synthesized chemically at a gram level scale.[2]
They are phytoalexins with an antiestrogenic activity.[3]
Molecules found in the family are :

Metabolism[edit]

Glycinol is the direct precursor of glyceollins through the action of a prenyltransferaseGlyceollin synthase then transforms those prenylated precursors into glyceollins.

Sunday, 18 June 2017

Curcumin kháng LNCaP

The effect of curcumin on proliferation and apoptosis in LNCaP

Curcumin kháng LNCaP

From Wikipedia, the free encyclopedia
Curcumin
Skeletal formula
Enol form
Skeletal formula
Keto form
Ball-and-stick model
Ball-and-stick model
Names
Pronunciation/ˈkɜːrkjᵿmɪn/
Preferred IUPAC name
(1E,6E)-1,7-Bis(4-hydroxy-3-methoxyphenyl)hepta-1,6-diene-3,5-dione
Other names
(1E,6E)-1,7-Bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione
Diferuloylmethane
Curcumin I
C.I. 75300
Natural Yellow 3
Identifiers
3D model (JSmol)
ChEBI
ChemSpider
E numberE100 (colours)
PubChem CID
UNII
Properties
C21H20O6
Molar mass368.39 g·mol−1
AppearanceBright yellow-orange powder
Melting point183 °C (361 °F; 456 K)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
 verify (what is Yes ?)
Infobox references
Curcumin is a bright yellow chemical produced by some plants. It is the principal curcuminoid of turmeric (Curcuma longa), a member of the ginger family (Zingiberaceae). It is sold as an herbal supplementcosmetics ingredient, food flavoring, and food coloring.[1] As a food additive, its E number is E100.[2]
It was first isolated in 1815 when Vogel and Pierre Joseph Pelletier reported the isolation of a "yellow coloring-matter" from the rhizomes of turmeric and named it curcumin.[3] Although curcumin has been used historically in Ayurvedic medicine,[4] its potential for medicinal properties remains unproven and is questionable as a therapy when used orally.[5][6][7]
Chemically, curcumin is a diarylheptanoid, belonging to the group of curcuminoids, which are natural phenols responsible for turmeric's yellow color. It is a tautomeric compound existing in enolic form in organic solvents and as a keto form in water.[8]

Applications[edit]

The most common applications are as a dietary supplement, in cosmetics, as a food coloring, and as flavoring for foods such as turmeric-flavored beverages (Japan).[1]
Curcumin
Annual sales of curcumin have increased since 2012, largely due to an increase in its popularity as a dietary supplement.[1] It is increasingly popular in skincare products that are marketed as containing natural ingredients or dyes, especially in Asia.[1] The largest market is in North America, where sales exceeded US$20 million in 2014.[1]

Chemistry[edit]

Curcumin incorporates several functional groups whose structure was first identified in 1910.[9] The aromatic ring systems, which are phenols, are connected by two α,β-unsaturated carbonyl groups. The diketones form stable enols and are readily deprotonated to form enolates; the α,β-unsaturated carbonyl group is a good Michael acceptor and undergoes nucleophilic addition.
Curcumin is used as a complexometric indicator for boron.[10] It reacts with boric acid to form a red-colored compound, rosocyanine.

Biosynthesis[edit]

The biosynthetic route of curcumin is uncertain. In 1973, Roughly and Whiting proposed two mechanisms for curcumin biosynthesis. The first mechanism involves a chain extension reaction by cinnamic acid and 5 malonyl-CoA molecules that eventually arylized into a curcuminoid. The second mechanism involves two cinnamate units coupled together by malonyl-CoA. Both use cinnamic acid as their starting point, which is derived from the amino acid phenylalanine.[11]
Plant biosyntheses starting with cinnamic acid is rare compared to the more common p-coumaric acid.[11] Only a few identified compounds, such as anigorufone and pinosylvin, build from cinnamic acid.[12][13]
Curcumin biosynthesis diagram
malonyl-CoA (5)
Biosynthetic pathway of curcumin in Curcuma longa.[11]

Research[edit]

In vitro, curcumin exhibits numerous interference properties which may lead to misinterpretation of results.[5][6]
Although curcumin has been assessed in numerous laboratory and clinical studies, it has no medical uses established by well-designed clinical research.[14] According to a 2017 review of over 120 studies, curcumin has not been successful in any clinical trial, leading the authors to conclude that "curcumin is an unstable, reactive, non-bioavailable compound and, therefore, a highly improbable lead".[5]
Cancer studies using curcumin conducted by Bharat Aggarwal, formerly a researcher at the MD Anderson Cancer Center, were deemed fraudulent and subsequently retracted by the publisher.[15]

Pharmacology[edit]

Curcumin, which shows positive results in most drug discovery assays, is regarded as a false lead that medicinal chemists include among "pan-assay interference compounds" attracting undue experimental attention while failing to advance as viable therapeutic or drug leads.[5][6][16] In vitro, curcumin inhibits certain epigeneticenzymes (the histone deacetylasesHDAC1HDAC3HDAC8), transcriptional co-activator proteins (the p300 histone acetyltransferase)[17][18][19] and the arachidonate 5-lipoxygenase enzyme.[20]
In Phase I clinical trials, curcumin had poor bioavailability, was rapidly metabolized, retained low levels in plasma and tissues, and was extensively and rapidly excreted, factors that make its in vivo bioactivity unlikely and difficult to accurately assess.[5][21] Curcumin appears to reduce circulating C-reactive protein in human subjects, although no dose-response relationship was established.[22] Factors that limit the bioactivity of curcumin or its analogs include chemical instability, water insolubility, absence of potent and selective target activity, low bioavailability, limited tissue distribution, extensive metabolism, and potential for toxicity.[5]

Toxicity[edit]

Two preliminary clinical studies in cancer patients consuming high doses of curcumin (up to 8 grams per day for 3–4 months) showed no toxicity, though some subjects reported mild nausea or diarrhea.[23]

Alternative medicine[edit]

Some alternative medicine practitioners give curcumin (as turmeric) intravenously as a treatment for a wide range of health problems, leading to a death in California in 2017[24] despite the absence of reliable clinical research and concerns about safety or efficacy.[5][6]