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Mehanizam delovanja Cordycepina na ćelije raka i virus

U časopisu Journal of Biological Chemistry,  objavljeno je istraživanje, dr Cornelia de Moor sa Univerziteta u Notingemu i njenog tima o Kordicepinu , koji je prvobitno izdvojen iz retke vrste divlje pečurke koja se zove Cordiceps Sinensis.

Dr de Moor je rekla : " Naše otkriće će otvoriti nove mogućnosti istraživanja  o lecenju  Kordicepinom   različitih oblika raka:

(http://www.bbsrc.ac.uk/news/archive/2009/091223-pr-new-insights-mushroom-derived-drug-for-cancer.aspx)

(http://www.sciencedaily.com/releases/2009/12/091223094729.htm)

Pored dobro poznate imuno-modulacije koju izazivaju jedinjenja polisaharida, postoje dokazi o još jednom mehanizmu kada je u pitanju dejstvo Cordycepsa na tumor. To je povezano sa strukturom nekih od izmenjenih nukleotida koje sadrži ova gljiva, a koje imamo u primeru jedinjenja kordicepina (3'deoksiadenozina).Ovaj molekul gotovo je jednak normalnom adenozinu, ali mu nedostaje atom kiseonika na riboznom delu molekula na 3-poziciji. Isti nedostatak tog 3-kiseonika može se videti i kod drugih jedinjenja Cordycepsa, poput Dideoksiadenozina (DidanosineTM, VidexTM). Smatra se da je nedostatak kiseonika na toj poziciji veoma značajan jer od njega zavisi struktura DNK koja uz njegovu pomoć stvara vezu sa susednim nukleotidima. Veza se nalazi između 3. i 5. pozicije na riboznim delovima nukleotida, koji na taj način stvaraju "strukturu lestvica" koji drži DNK zajedno.

Some-of-the-unique-nucleosides-found-in-Cordyceps

Prvi korak prilikom duplikacije bilo koje ćelije jeste razdvajanje DNK molekula po sredini, poput otkopčavanja rajsfešlusa, i raskidanja veze komplementarnih nukleotida. Sledi ubacivanje jednog po jednog novog, komplementarnog nukleotida koji formiraju hidrogenske veze između komplementarnih parova, i oblikuju veze fosfatnih – šećera između 3. i 5. ozicije na spoljašnjoj ivici molekula, odnosno riboznom delu.

Structural-Arrangement-of-DNA

Cordycepin-Halts-DNA-Replication

Sinteza novih molekula DNK brzo napreduje, novi komplementarni nukleotidi se jedan po jedan sekvencijalno umeću u novi molekul DNK, sve dok se prvobitni niz DNK ne umnoži dvaput, a svaki od nizova je identična kopija, i formira genetski kod za novu generaciju ćelija. Odnosno, sinteza se nastavlja umetanjem novih nukleotida, sve dok se ne povuče molekul 3. deoksiadenozina (kordicepina). Kada se to desi, na poziciji od vitalnog značaja više nema kiseonika pomoću koga bi se stvorila 3.- 5. veza, i duplikacia molekula DNK prestaje. Tada ćelija ne može da nastavi sa deobom, i ne dolazi do formiranja novih ćelija. Kod normalnih ćelija sisara, to umetanje deoksigenovanog adneozina i nije od nekog značaja, pošto zdrave ćelije u sebi sadrže mehanizam popravke DNK. Kada dođe do ovakve greške, izmenjeni nukleotid (kordicepin) uklanja se iz niza nukleotida, i umeće se novi segment adenozina. Nasuprot zdravim ćelijama, ćelije raka po definiciji gube svoj mehanizam popravke DNK. (Da mogu da isprave greške u svojoj DNK, ne bi bile ćelije raka).

Većina bakterija i svi virusi (uključujući i virus HIV-a) nemaju mehanizam popravke DNK. Kada pogledamo brzinu kojom se ćelije raka dupliciraju, jasno nam je kako bi takav mehanizam mogao da izazove značajnu reakciju protiv tumora. Na primer, normalne ćelije zdravog tkiva dojke imaju prosečan životni vek od oko 10 dana, i nakon tog vremena se dupliciraju. S druge strane, ćelije raka razmožavaju se mnogo brže od zdravih ćelija. Dupliciraju se, u proseku, svakih 20 minuta. To znači da se množe otprilike 750 puta brže od ćelija zdravog tkiva kojim su okružene. Da je kordicepin podjednako toksičan za oba tipa ćelija, ubijao bi ćelije raka 750 puta brže nego zdrave ćelije. Ipak, kordicepin se zbog pomenutog mehanizma popravke DNK kod zdravih ćelija ne meša u njihovu replikaciju, a brzina kojom ubija ćelije tumora mnogo je veća od 750:1.

Ista vrsta mehanizma prekida DNK odgovorna je i za antitumorni efekat nekih od agensa koji se koriste u procesu hemoterapije. Mehanizam koji sprečava sintezu DNK verovatno je odgovoran i za antiviralne efekte kordicepina. Za strukturalnu analizu ovog mehanizma pogledajte sledeće ilustracije. (Holliday, 2004.b) (Liu i Zheng, 1993,.i ostali na osnovu zaključaka).

Ovaj tekst i sajt su edukativnog karaktera, namenjeni za opšte obrazovanje i u informativne svrhe, nisu zamena za profesionalni medicinski savet, ispitivanje, dijagnozu ili lečenje.

Tekst  preuzet sa:  "Cancer Research UK" Društvo za istraživanje raka Ujedinjenog Kraljevstva:

Link ka:  Cancer Research UK : Medicinal Mushrooms: Their therapeutic properties and current medical usage with special emphasis on cancer treatments:

by

Table of Contents  (PDF 8.87 kb)

Preamble (PDF 15.5)

Chapter 1 - Introduction (PDF 36.3 kg)

Chapter 2 - The Nature of Fungi with Special Emphasis on Mushrooms  (PDF 1.41 mb)

Chapter 3a - Medicinally Important Mushrooms Part 1  (PDF 8.12 mb)

Chapter 3b - Medicinally Important Mushrooms Part 2  (PDF 8.75)

Chapter 3c - Medicinally Important Mushrooms Part 3  (PDF 8.33)

Chapter 4 - Technology of Mushroom Cultivation (PDF 338 kg)

Chapter 5 - Extraction, Development and Chemistry of Anti-Cancer Compounds from Medicinal Mushrooms (PDF 399 kg)

Chapter 6 - Immunomodulatory Activities of  Mushroom Glucans and Polysaccharide-Protein Complexes in Animals and Humans (PDF 216 kg)

Chapter 7 - The Role of Polysaccharides Derived from Medicinal Mushrooms in Cancer (PDF 133 kg)

Chapter 8 - Additional Medicinal Properties (PDF 84.2 kg)

Chapter 9 - Regulatory and Safety Criteria (PDF 67.8 kg)

Chapter 10 - Conclusions(PDF 49.5 kg)

Appendix 1 - Overview of Human Immune System (PDF 603 kg)

Appendix 2 - Standard Antitumor Activity Test (PDF 12.7 kg)

Appendix 3 - Medicinal Mushrooms and Cancer Prevention (PDF 17.0 kg)

Author Biographies (PDF 21.6 kg)

Executive Summary (PDF 32.7 kg)

Acknowledgment (PDF 6.89 kg)

Front Cover (PDF 6.17 kg)

Back Cover (PDF 26.29 kg)

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