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BETHY NGUYEN CHEMISTRY 12B SPRING, 2006. INTRODUCTION Green tea is natural dried leaves of the tea plant, camellia sinensis. Green tea is natural dried.

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Presentation on theme: "BETHY NGUYEN CHEMISTRY 12B SPRING, 2006. INTRODUCTION Green tea is natural dried leaves of the tea plant, camellia sinensis. Green tea is natural dried."— Presentation transcript:

1 BETHY NGUYEN CHEMISTRY 12B SPRING, 2006

2 INTRODUCTION Green tea is natural dried leaves of the tea plant, camellia sinensis. Green tea is natural dried leaves of the tea plant, camellia sinensis. Most of the polyphenols in green tea are Most of the polyphenols in green tea are flavanols, commonly known as catechins. The primary catechins in green tea are epicatechin, epicatechin-3-gallate (ECG), epigallocatechin (EGC), and epigallocatechin-3-gallate (EGCG). The primary catechins in green tea are epicatechin, epicatechin-3-gallate (ECG), epigallocatechin (EGC), and epigallocatechin-3-gallate (EGCG).

3 INTRODUCTION (CONT.) http://www.micronutrient.org/IDPAS/pdf/447GreenTea.pdf#search='mechanism%20of%20phenol%20in%20green%20tea'

4 What are Antioxidants? Green tea is regarded as an antioxidant. The polyphenols, especially EGCG. Green tea is regarded as an antioxidant. The polyphenols, especially EGCG. The human body constantly produces unstable molecules called oxidants, also commonly referred to as free radicals. The human body constantly produces unstable molecules called oxidants, also commonly referred to as free radicals. These free radicals readily react and damage other molecules and cell DNA. Antioxidants "mop up" these free radicals and eliminate them before they can damage healthy tissue. These free radicals readily react and damage other molecules and cell DNA. Antioxidants "mop up" these free radicals and eliminate them before they can damage healthy tissue. Furthermore, oxidative damage by free radicals on low density lipoproteins (LDL) is believed to be a precursor in the development of atherosclerosis and coronary heart disease. Furthermore, oxidative damage by free radicals on low density lipoproteins (LDL) is believed to be a precursor in the development of atherosclerosis and coronary heart disease. Oxidation to cell membranes and other cell components is also theorized to be part of the aging process. Oxidation to cell membranes and other cell components is also theorized to be part of the aging process. http://www.imperialteagarden.com/greenteaantioxidants.html http://www.imperialteagarden.com/greenteaantioxidants.html http://www.imperialteagarden.com/greenteaantioxidants.html

5 MECHANISM OF ANTIOXIDANTS Antioxidants are molecules that can neutralize free radicals by accepting or donating an electron to eliminate the unpaired condition Antioxidants are molecules that can neutralize free radicals by accepting or donating an electron to eliminate the unpaired condition Example of Formation of a complex between the lipid radical and the antioxidant radical (free radical acceptor). Example of Formation of a complex between the lipid radical and the antioxidant radical (free radical acceptor).

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7 http://class.fst.ohio-state.edu/fst821/Lect/AA.pdf

8 Mechanisms of Metals in Accelerating Lipid Oxidation http://class.fst.ohio-state.edu/fst821/Lect/AA.pdf

9 MECHANISMS OF FATTY ACID OXIDATION Autoxidation by free radical reaction, In a peroxide- free lipid system. 1.Initiation: the initiation of a peroxidation sequence refers to the attack of a ROS able to abstract a hydrogen atom from a methylene group (- CH2-). This attack generates easily free radicals from polyunsaturated fatty acids. OH is the most efficient ROS to do that attack, whereas O2.- is insufficiently reactive.

10 The carbon radical tends to be stabilized by a molecular rearrangement to form a conjugated diene.

11 Under aerobic conditions conjugated dienes are able to combine with O2 to give a peroxyl (or peroxy) radical, ROO..

12 2. Propagation As a peroxyl radical is able to abstract H from another lipid molecule (adjacent fatty acid), especially in the presence of metals such as copper or iron, thus causing an autocatalytic chain reaction. The peroxyl radical combines with H to give a lipid hydroperoxide (or peroxide). http://www.cyberlipid.org/perox/oxid0006.htm#3

13 TERMINATION Termination (formation of a hydroperoxide) is most often achieved by reaction of a peroxyl radical with a-tocopherol which is the main lipophilic "chain-breaking molecule" in the cell membranes.a-tocopherol

14 OXIDATIVE DAMAGE TO DNA: formation of 8−OHdG/8−oxoG 8−OHdG from Guanosine with Hydroxyl 8−oxoG 8−OHdG/8−oxoG is the most commonly studied biomarker of DNA oxidation [1] and is believed to constitute 5% of all oxidative DNA damage [2] 8−OHdG is mutagenic because it inhibits methylation and because it can be paired with adenosine rather than cytosine during DNA replication leading to GC-to-AT conversion http://www.benbest.com/lifeext/aging.html#mitochondria

15 BENEFIT OF GREEN TEA POLYPHENOLS Years of research, in the United States and Japan support the theory that Tea (Camellia Sinensis) has the ability to ward off many types of cancer Years of research, in the United States and Japan support the theory that Tea (Camellia Sinensis) has the ability to ward off many types of cancer The belief is that polyphenol (-)-epigallocatechin gallate (EGCG) have an inhibitory effect on the enzyme, urokinase, which is required for tumor formation. The belief is that polyphenol (-)-epigallocatechin gallate (EGCG) have an inhibitory effect on the enzyme, urokinase, which is required for tumor formation. help prevent the oxidation of LDL cholesterol. help prevent the oxidation of LDL cholesterol. The phenol groups in Green Tea polyphenols are extremely active, easily able to capture and neutralize free radicals and other pro-oxidants The phenol groups in Green Tea polyphenols are extremely active, easily able to capture and neutralize free radicals and other pro-oxidants

16 Conclusion In conclusion, green tea and its polyphenols (catechins)-- gallocatechin, epigallocatechin, epicatechin, epigallocatechin, and epicatechin gallate-- have been shown to not only inhibit carcinogenesis before it begins, and decrease the number of tumors, but also, amazingly, induce apoptosis and cell cycle arrest in carcinoma cells, as well. In conclusion, green tea and its polyphenols (catechins)-- gallocatechin, epigallocatechin, epicatechin, epigallocatechin, and epicatechin gallate-- have been shown to not only inhibit carcinogenesis before it begins, and decrease the number of tumors, but also, amazingly, induce apoptosis and cell cycle arrest in carcinoma cells, as well. Nevertheless, more work is required to elucidate the molecular and clinical chemopreventive effects of green tea on human colorectal cancer. Nevertheless, more work is required to elucidate the molecular and clinical chemopreventive effects of green tea on human colorectal cancer. http://carbon.hampshire.edu/~cjarvis/NS120/projects/gt&cancer.htm

17 REFERRENCES http://www.pdrhealth.com/drug_info/nmdrugprofiles/nutsupdrugs/gre_0319.shtml http://www.pdrhealth.com/drug_info/nmdrugprofiles/nutsupdrugs/gre_0319.shtml http://www.pdrhealth.com/drug_info/nmdrugprofiles/nutsupdrugs/gre_0319.shtml http://www.micronutrient.org/IDPAS/pdf/447GreenTea.pdf#search='mechanism%20 of%20catechins%20in%20green%20tea‘ http://www.micronutrient.org/IDPAS/pdf/447GreenTea.pdf#search='mechanism%20 of%20catechins%20in%20green%20tea‘ http://www.micronutrient.org/IDPAS/pdf/447GreenTea.pdf#search='mechanism%20 of%20catechins%20in%20green%20tea http://www.micronutrient.org/IDPAS/pdf/447GreenTea.pdf#search='mechanism%20 of%20catechins%20in%20green%20tea http://www.cyberlipid.org/perox/oxid0006.htm#3 http://www.cyberlipid.org/perox/oxid0006.htm#3 http://www.cyberlipid.org/perox/oxid0006.htm#3 http://class.fst.ohio-state.edu/fst821/Lect/AA.pdf http://class.fst.ohio-state.edu/fst821/Lect/AA.pdf http://class.fst.ohio-state.edu/fst821/Lect/AA.pdf http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/R/ROS.html http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/R/ROS.html http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/R/ROS.html JOURNALS: 1.MUTATION RESEARCH 424:51-58 (1999) 2. MUTATION RESEARCH; Dizdaroglu;M; 275(2-6):331-342 (1992)


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