Muramyl dipeptide is a powerful potentiator of the antitumor action of various tumor-necrotizing agents

1984 ◽  
Vol 17 (3) ◽  
Author(s):  
Nanne Bloksma ◽  
FransM.A. Hofhuis ◽  
JanM.N. Willers
2018 ◽  
Vol 8 (8) ◽  
pp. 1048-1072
Author(s):  
Abdou Saad El-Tabl ◽  
Moshira Mohamed Abd-El Wahed ◽  
Seham Abd-El Rafea El-Saied

2018 ◽  
Vol 18 (6) ◽  
pp. 784-804 ◽  
Author(s):  
Georg Bauer

Background: Application of cold atmospheric plasma to medium generates “plasma-activated medium” that induces apoptosis selectively in tumor cells and that has an antitumor effect in vivo. The underlying mechanisms are not well understood. Objective: Elucidation of potential chemical interactions within plasma-activated medium and of reactions of medium components with specific target structures of tumor cells should allow to define the active principle in plasma activated medium. Methods: Established knowledge of intercellular apoptosis-inducing reactive oxygen/nitrogen species-dependent signaling and its control by membrane-associated catalase and SOD was reviewed. Model experiments using extracellular singlet oxygen were analyzed with respect to catalase inactivation and their relevance for the antitumor action of cold atmospheric plasma. Potential interactions of this tumor cell-specific control system with components of plasma-activated medium or its reaction products were discussed within the scope of the reviewed signaling principles. Results: None of the long-lived species found in plasma-activated medium, such as nitrite and H2O2, nor OCl- or .NO seemed to have the potential to interfere with catalase-dependent control of apoptosis-inducing signaling of tumor cells when acting alone. However, the combination of H2O2 and nitrite might generate peroxynitrite. The protonation of peroxnitrite to peroxynitrous acid allows for the generation of hydroxyl radicals that react with H2O2, leading to the formation of hydroperoxide radicals. These allow for singlet oxygen generation and inactivation of membrane-associated catalase through an autoamplificatory mechanism, followed by intercellular apoptosis-inducing signaling. Conclusion: Nitrite and H2O2 in plasma-activated medium establish singlet oxygen-dependent interference selectively with the control system of tumor cells.


1988 ◽  
Vol 53 (11) ◽  
pp. 2897-2906 ◽  
Author(s):  
Jan Ježek ◽  
Milan Zaoral ◽  
Miloš Buděšínský ◽  
Jiří Günther ◽  
Jiří Rotta

In the search for immunoadjuvant active compounds without pyrogenic activity we prepared N-Ac-norMur-L-Abu-D-Gln-O-Bu (V), N-Ac-Mur-L-Abu-D-Gln-O-Bu (VII) and their respective α-benzylglycosides VI and VIII. All the prepared compounds are nonpyrogenic. In the delayed hypersensitivity test, compound V is inactive, VI is comparable to MDP, VII is more and VIII is less active than MDP.


2021 ◽  
Author(s):  
Christina S. Kim ◽  
Anne M. Brown ◽  
Tijana Z. Grove ◽  
Felicia A. Etzkorn

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Muh. Akbar Bahar ◽  
Tsugunobu Andoh ◽  
Keisuke Ogura ◽  
Yoshihiro Hayakawa ◽  
Ikuo Saiki ◽  
...  

Chemotherapy-induced peripheral neuropathy is a major dose-limiting side effect of commonly used chemotherapeutic agents. However, there are no effective strategies to treat the neuropathy. We examined whether Goshajinkigan, a herbal medicine, would prevent paclitaxel-induced allodynia without affecting the anticancer action in mice. Murine breast cancer 4T1 cells were inoculated into the mammary fat pad. Paclitaxel (10 and 20 mg/kg, intraperitoneal, alternate day from day 7 postinoculation) inhibited the tumor growth, and Goshajinkigan (1 g/kg, oral, daily from day 2 postinoculation) did not affect the antitumor action of paclitaxel. Mechanical allodynia developed in the inoculated region due to tumor growth and in the hind paw due to paclitaxel-induced neuropathy. Paclitaxel-induced allodynia was markedly prevented by Goshajinkigan, although tumor-associated allodynia was not inhibited by Goshajinkigan. These results suggest that Goshajinkigan prevents paclitaxel-induced peripheral neuropathy without interfering with the anti-cancer action of paclitaxel.


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