NAC-OLEANDER PROTOCOL questions??

[Guest guest]

Following excerpt is from a paper studying oleander, explaining its mechanism of

effect against cancer cells. It is explained here that oleander needs oxygen

species for anticancer effects, and NAC inhibits formation of -oleander induced-

oxygen species. that means it is not beneficial to use antioxidants during

oleander treatment. NAC stops oleander killing cancer cells. it increases

gluthation and serves as antioxidant. I wonder why it is favored in this group

to use NAC as it interferes whith oleander? any ideas?

 

best wishes to all,

 

 

excerpt:

 

 

J Exp Ther Oncol. 2006;5(3):167-81.

 

Oleandrin-mediated oxidative stress in human melanoma cells.

 

Newman RA, Yang P, Hittelman WN, Lu T, Ho DH, Ni D, Chan D, Vijjeswarapu M,

Cartwright C, Dixon S, Felix E, Addington C.

 

Department of Experimental Therapeutics, Univ. Texas M. D. Anderson Cancer

Center, Houston, TX 77054, USA. rnewman

 

While certain cardiac glycoside compounds such as oleandrin, bufalin and

digitoxin are known to be associated with potent cytotoxicity to human tumor

cells, the mechanisms by which this effect is produced are not clear. We now

demonstrate that incubation of human malignant melanoma BRO cells with oleandrin

results in a time-dependent formation of reactive oxygen species (ROS). Use of

Mito-SOX and dihydroethidine dyes revealed the presence of oleandrin-mediated

superoxide anions. Formation of superoxide anions correlated with a loss in

cellular viability, proliferation and cellular defense mechanisms such as GSH

content. Oleandrin also resulted in an unusual time-dependent mitochondrial

condensation in BRO cells that could be blocked with use of N-acetyl cysteine

(NAC). NAC was also shown to block ROS formation and partially prevent

oleandrin-mediated loss of cellular GSH. Taken as a whole, the data suggest that

exposure of human tumor cells such as BRO to oleandrin results in the formation

of superoxide anion radicals that mediate mitochondrial injury and loss of

cellular GSH pools. These mechanisms play a role in cardiac glycoside mediated

tumor cell injury. Conversely, incubation of NAC, a precursor to GSH, largely

prevents oleandrin-mediated inhibition of proliferation and mitochondria

structural changes.

 

PMID: 16528968 [PubMed - indexed for MEDLINE]